Program

<p>Systemic lupus erythematosus (SLE) is characterized by pathogenic autoantibodies production due to loss of B cell tolerance. Yet, tissue injury persists despite blockade of autoreactive T-cell dependent B-cell maturation in the spleen and other secondary lymphoid organs after onset of kidney and skin inflammation. We therefore propose targeting T cell maladaptation in the inflamed tissue as the new avenue of therapeutic approach. In our previous publications, T cells in the inflamed kidney and skin presented with high Hypoxia-Inducible Factor (HIF)-1 in response to stressed tissue microenvironment, and either conditional knockout or small molecule inhibitor reverse organ damage. </p><p>We further found that T cell stress response to quintessential for the transition of circulatory memory T cells to tissue stem-like precursor T cells, an important population giving rise to the majority of tissue damaging effector T cells. These data highlight how the immune system respond to environmental stress, triggering a vicious cycle of tissue damage, increased microenvironment stress, and heightened T cell mediated damage.</p>

<p>Kidney fibrosis is poorly understood because of the organ’s cellular diversity. We used single-cell RNA sequencing not only in resolving differences in injured kidney tissue cellular composition but also in celltype-specific gene expression in mouse models of kidney fibrosis. This analysis highlighted major changes in cellular diversity such as immune cells in kidney fibrosis, which markedly impacted whole-kidney transcriptomics outputs. Proximal tubule (PT) cells are highly vulnerable to dysfunction in fibrosis and show altered differentiation. Nuclear receptors such as ESRRA maintain both PT cell metabolism and differentiation by directly regulating PT-cell-specific genes. </p><p>In second part of my presentation, I will present our novel single cell long-read sequencing method and its potential application to the kidney fibrosis. Although single-cell multi-omics technologies have enabled groundbreaking research in the field of biomedical science, there have been limited studies on expression patterns of transcript isoforms, one of the critical layers of cellular information, due to technical limitations. We developed Ouro-Seq, a novel single-cell long-read sequencing framework that can characterize intact full-length mRNA species of varying sizes (up to 6 kbp) at a single-cell resolution. Using Ouro-Seq, we constructed the Mouse Single-Cell Splicing Atlas by collecting full-length transcriptomes of 12 major organs of adult mice including kidney. With the resolution of single cells and single mRNA species, our atlas captured previously unappreciated complexity of functional heterogeneity across individual cells. Particularly, our atlas revealed that the three distinct Slc12a1 mRNA isoforms, encoding functionally distinct Na–K–Cl cotransporters (NKCC2-B, NKCC2-A, and NKCC2-F), are exclusively expressed by the three distinct cell populations in the thick ascending limb of the kidneys. Our long-read scRNA-seq technology and whole-organism single-cell splicing atlas will help advance the understanding of alternative splicing and enhance our comprehension of various healthy and diseased cells.</p>

<p>The autonomic nervous system is widely distributed throughout the body and plays an indispensable role in regulating vital physiological functions such as circulation, respiration, thermoregulation, and digestion. The kidney is a richly innervated organ, and sympathetic neural activity is critical for modulating renal circulation and hormonal output involved in fluid regulation. Furthermore, recent evidence highlights that anti-inflammatory effects mediated by neuroimmune interactions—specifically the “inflammatory reflex” via the parasympathetic nervous system— ameliorate kidney injury.</p><p>Our lab has extensively studied neuroimmune modulation and renal protective effects, beginning with the discovery that cervical vagus nerve stimulation ameliorates acute kidney injury. We demonstrated that these protective effects are mediated via the vagus nerve, the neurotransmitter acetylcholine, and immune cells. While vagus nerve stimulation was initially thought to suppress systemic inflammation through the “cholinergic anti-inflammatory pathway” mediated by the spleen, its specific role in kidney protection remained unclear. Recently, using single-cell RNA sequencing, we elucidated that macrophages receiving acetylcholine signals interact with other immune cells in the spleen, thereby enhancing anti-inflammatory responses. We also discovered that acetylcholine signaling directly acts on renal tubular epithelial cells, exerting kidney-protective effects.</p><p>Beyond the parasympathetic pathway, activation of adrenergic receptors via the sympathetic nervous system has also been shown to confer protection against kidney injury. These findings suggest that both branches of the autonomic nervous system—cholinergic and adrenergic—can contribute to renal protection through distinct yet complementary mechanisms.</p><p>To more precisely analyze these neural circuits, we recently succeeded in applying optogenetic techniques to selectively stimulate specific renal nerves. By targeting distinct neural circuits and their receptors within the kidney, this approach enables precise investigation of how autonomic inputs influence renal physiology and injury responses, independent of systemic effects.</p><p>In this presentation, I will introduce our latest findings integrating optogenetics and single-cell transcriptomics to gain a deeper understanding of how autonomic control modulates kidney inflammation and protection, and to explore its potential for novel therapeutic strategies in kidney disease.</p>

<p>Ureteral obstruction is marked by disappearance of the vasopressin-dependent water channel aquaporin-2 (AQP2) in the renal collecting duct and polyuria upon reversal. Most studies of unilateral ureteral obstruction (UUO) models have examined late time points, obscuring the early signals that trigger loss of AQP2. We performed RNA-Seq on microdissected rat cortical collecting ducts (CCDs) to identify early signaling pathways after the establishment of UUO. Results showed vasopressin V2 receptor (AVPR2) mRNA was decreased 3 hours after UUO, identifying one cause of AQP2 loss. The collecting duct principal cell differentiation markers were lost, including many that were not regulated by vasopressin. Immediate early genes in CCDs were widely induced 3 hours after UUO, including Myc, Atf3, and Fos (confirmed at the protein level). Simultaneously, expression of NF-kB signaling response genes known to repress Aqp2 increased. RNA-Seq for CCDs at an even earlier time point (30 minutes) showed widespread mRNA loss, indicating a “stunned” profile. Immunocytochemical labeling of markers of mRNA-degrading P-bodies DDX6 and 4E-T indicated an increase in P-body formation within 30 minutes. Immediately after establishment of UUO, collecting ducts manifest a stunned state with broad disappearance of mRNAs. Within 3 hours, there is upregulation of immediate early and inflammatory genes and disappearance of the V2 vasopressin receptor, resulting in loss of AQP2 (confirmed by lipopolysaccharide administration). The inflammatory response seen rapidly after UUO establishment may be relevant to both UUO-induced polyuria and long-term development of fibrosis in UUO kidneys.</p>

<p>Background </p><p>Mechanisms involved in compensatory hypertrophy of the kidney remain incompletely understood. New ‘-omic’ methodologies have been recently introduced that have the potential of identifying complex mechanisms. Here we seek to identify the earliest signaling changes in the contralateral kidney after unilateral nephrectomy (UNx) in mice using next-generation sequencing and proteomics techniques combined with lipid analysis.</p><p>Method</p><p>Experiments were done in mice undergoing UNx and sham nephrectomy. At specific time points (24 hours and 72 hours) after surgery, the earliest first portion of the kidney proximal tubule (PT-S1) was manually micro-dissected and utilized for transcriptomic analysis by single-tubule small sample RNA-Seq and single-tubule ATAC seq. Furthermore, quantitative proteomic analysis and lipidomics analysis were carried out using whole kidney.</p><p>Results</p><p>Kidney volume was already increased 24 hours after UNx, reaching a plateau at 72 hours. Quantitative morphometry in microdissected proximal tubules showed significant increases in outer diameter and mean cell volume, but no clear increase in the cell count per unit length. Measurements of DNA accessibility (ATAC-seq), transcriptome (RNA-seq) and proteome (quantitative protein mass spectrometry) independently identify patterns of change that are indicative of activation of the lipid-regulated transcription factor, PPARα. Lipid analysis shows an increased abundance of PPARα ligands in the hypertrophied kidney. Activation of PPARα by fenofibrate administration increases proximal tubule cell size, while genetic deletion of PPARα decreases it. </p><p>Conclusions </p><p>Compensatory growth of the kidney is associated with increased proximal tubule cell size, but not cell number. PPARα is an important determinant of proximal tubule cell size and is a likely mediator of compensatory proximal tubule hypertrophy. Early stages of compensatory hypertrophy are associated with altered fatty acid and cholesterol metabolism including anabolic pathways required for synthesis of new membranes needed for cell growth.</p>

<p>The year 2025 marks the 60th anniversary of the isolated tubule perfusion technique, invented by Maurice Burg and his colleagues at the National Heart, Lung, and Blood Institute, NIH. The successful perfusion of individual nephron segments for transepithelial flux measurements not only provided the proof of concept for how the kidney works, confirming earlier theories, but also greatly advanced our knowledge of the fundamental functions of each nephron segment. Nowadays, it remains a gold standard methodology for assessing the functional transport properties of specific nephron segment. This presentation will briefly review three indispensable elements of this state-of-the-art technique: the microdissection of nephron segments, the in vitro perfusion of single tubules, and the nanoliter analysis of fluid composition. The presentation will also highlight various applications utilizing microdissected nephron segments to elucidate intracellular physiological events relevant to tubular function. These applications include, but are not limited to, studies of changes in intracellular signaling (e.g., cyclic AMP and calcium), changes in enzyme activity, and changes in the intracellular localization of transporter proteins. In addition to these classic physiological approaches, microdissected nephron segments have emerged as valuable samples for modern -omics studies aimed to identify altered gene expression or protein changes associated with disease or pathophysiological conditions.</p>

<p>Water balance relies on aquaporin-2 (AQP2) in kidney collecting ducts, regulated by both gene transcription and protein trafficking. Dysregulation of AQP2 abundance contributes to various water balance disorders, including polyuria and water retention. To identify kinases regulating Aqp2 transcription, we performed a CRISPR screening targeting the entire kinome in mouse cortical collecting duct cell (mpkCCD). </p><p>A CRISPR knockout library targeting 713 proteins (four gRNAs per gene) was introduced into mpkCCD cells expressing GFP as a reporter for Aqp2 transcription, ensuring < 1 gRNA per cell. Cells treated with vasopressin analog dDAVP were sorted based on GFP intensity, and integrated gRNAs were identified by DNA sequencing. Based on these results, individual kinase knockout cell lines were generated.</p><p>The screening identified 29 kinases affecting Aqp2 transcription: 16 positive and 13 negative regulators. Known regulators, such as positive regulator PKA catalytic subunit alpha (Prkaca) and negative regulator PKA regulatory subunit (Prkar1a), were identified. Additional positive regulators include Dyrk1a, Akt1, Cdk10, Cdk12 and Mark2, while negative regulators include Tgfbr1, Tgfbr2, and Tgfbr3 (implicated in vasopressin escape), and components of the stress-activated MAP kinase pathway (Map3k1, Map2k4, and Map2k7). Knockout of the novel positive regulator Dyrk1a resulted in a complete loss of AQP2 abundance. Transcriptome analysis of Dyrk1a-deficient cells revealed widespread gene expression changes enriched in cell cycle-related pathways, suggesting a role of Dyrk1a in repressing cell cycle and maintaining cellular quiescence. </p><p>Overall, CRISPR/Cas9 screening identified multiple protein kinases involved in Aqp2 gene transcription. Our findings highlight that Dyrk1a is required for Aqp2 transcription and cellular quiescence. These results provide a foundation for further research into the roles of kinases in Aqp2 transcription in the kidney.</p>

<p>There are four phases in fluid resuscitation, and de-escalation is the last step in the resuscitation-optimization-stabilization-evacuation (ROSE) concept. This lecture will focus on the evacuation or de-escalation of fluid in the critically ill patients receiving kidney replacement therapy. Currently, there is no standardized and universal protocol on de-escalation; therefore, who, when, and how to remove fluid in critically ill settings remains controversial, and a personalized approach depending on the critical illness and comorbidities is suggested. This lecture will review several recent studies on this topic and discuss best practices of de-escalation for better patients and kidney outcome.</p>

<p>Critical care nephrology is moving from static thresholds toward continuous, context-aware bedside decisions. The most effective approach integrates trajectory-based risk prediction, actionable prevention bundles, ultrasound-guided congestion assessment, and individualized kidney replacement therapy (KRT) triggers. Serial multivariate trajectories—combining vitals, lab trends, medications, and stress biomarkers—identify patients likely to develop significant AKI before creatinine rises. Explainable ML or simple trend rules can drive EHR alerts but must be locally calibrated to stay clinically useful. When predictions activate a prevention bundle (hemodynamic optimization, nephrotoxin stewardship, dose adjustment, glycemic control, and early reassessment), AKI progression and dialysis rates decline.</p><p>Bedside ultrasound reveals the often-missed component of congestive nephropathy. The Venous Excess Ultrasound (VExUS) score integrates IVC size and hepatic, portal, and intrarenal venous Doppler patterns to grade venous hypertension. Incorporating VExUS into daily rounds guides whether to continue resuscitation, hold fluids, intensify diuresis, or begin ultrafiltration, aligning renal management with right-heart physiology rather than static CVP or weight. Coupled with lung ultrasound, capillary refill, and lactate, it distinguishes congestion from hypovolemia and prevents reflex fluid loading.</p><p>KRT decisions benefit from composite triggers rather than single lab cutoffs. Functional reserve testing with a furosemide stress test, alongside biomarkers such as TIMP-2·IGFBP7, proenkephalin, or NGAL, refines risk of metabolic failure or fluid harm and avoids both premature dialysis and harmful delays. Timing should be individualized based on (1) acid–base, potassium, and nitrogenous waste trajectories; (2) severity and rate of fluid accumulation with organ congestion; and (3) hemodynamic tolerance for modality and dose. Continuous therapy suits unstable patients needing ultrafiltration; intermittent or prolonged-intermittent therapy fits those requiring solute control with stable hemodynamics. Adjunctive cytokine hemoadsorption may aid stabilization in select phenotypes but warrants outcome-based audits until survival benefits are proven. Checklists, dashboards, and audit systems close the loop from prediction to intervention to outcomes, forming a roadmap: anticipate AKI using trajectories, guide de-resuscitation with VExUS, and start KRT using composite triggers for safer, physiology-aligned renal support.</p>

<p>Autosomal dominant polycystic kidney disease (ADPKD) the most common inherited cystic kidney disease that affects 1 in every 4,000~10,000 people. </p><p>From May 2019 to June 2024, we recruited a total of 1,628 probands in the Korean genetic cohort study of inherited cystic kidney diseases. Among them, 1,495 patients were clinically ADPKD.</p><p>The study results showed a mutation detection rate of 57.5% in the Phase 1 cohort of 725 patients, 62.3% in typical ADPKD patients, and 41.8% in atypical cases. Of the 100 patients who had no mutations identified in the gene panel, additional PKD1 mutations were detected by long-range PCR in 79, increasing the overall detection rate to 62%. WES was performed on 125 patients, including those who had no mutations or VUS detected in the initial test, and IFT140 was identified as a new candidate gene.</p><p>In Phase 2, 770 patients were enrolled, of whom 761 underwent targeted gene panel testing. The mutation detection rate was 69.5%, and the additional long-range PCR or WES increased the detection rate to 80%. In addition to the primary mutations in PKD1 and PKD2, other genetic alterations were found in 8% of typical ADPKD cases and 57% of atypical ADPKD cases.</p><p>Baseline characteristics analysis by genotype revealed that the PKD1 mutation group (n=818) was diagnosed at a significantly younger age compared to other groups, including the PKD2 mutation group (p<0.001). The PKD1 mutation group had the highest serum creatinine at 1.41±1.32 mg/dL (p=0.001), and the highest TKV at 1,564±1,209 mL (p<0.001). When analyzing disease severity by genotype, patients with PKD1-protein-truncating (PT) mutations tended to have more advanced CKD stages. PKD1-PT mutations were the most common genotype in high-risk Mayo classification stages 1D and 1E, indicating a more progressive disease course.</p><p>This study systematically elucidated the genetic characteristics of Korean ADPKD patients and significantly increased the diagnostic rate through stage-specific genetic testing.</p>

<p>Individualizing Peritoneal Dialysis (PD) prescriptions means tailoring the dialysis regimen to each patient's unique needs, preferences, and medical status. This involves considering factors like residual kidney function, nutritional status, and lifestyle, rather than simply following a "one-size-fits-all" approach. The goal is to optimize dialysis adequacy, minimize complications, and improve patient well-being.</p>

<p>Patients undergoing long-term dialysis experience a large number of symptoms and patients and caregivers place a high priority on identifying interventions that improve well being. Improvement of such symptoms is important to maximize life participation by patients, yet research on such treatments is limited. We will review the literature of the symptom burden in patients undergoing long-term dialysis and the opportunities to improve patient well being and their quality of life</p>

<p>Peritoneal dialysis (PD) is increasingly chosen by patients for its flexibility and potential to improve quality of life. However, home-based PD also presents challenges, including limited self-care ability, poor treatment adherence, caregiver burden, and gaps in healthcare resources and policy. Nurses play a pivotal role in overcoming these barriers. This presentation highlights five key roles of nurses: educators and trainers, technical supporters and problem solvers, remote monitors, emotional and psychological supporters, and connectors to family and community resources. Through these roles, nurses not only equip patients with essential skills but also foster confidence, ensure treatment safety, and enhance quality of life. Ultimately, nurses serve as comprehensive guides throughout the PD journey, enabling patients to successfully and safely continue dialysis at home.</p>

<p>The rising prevalence of chronic kidney disease (CKD) within the aging global population presents a considerable challenge to healthcare systems, demanding effective and sustainable management strategies. For older adults with CKD, an individualized approach is essential, with primary goals focused on minimizing cardiovascular risk and slowing the progression to kidney failure.</p><p>The cornerstone of modern treatment is an integrated strategy that combines advanced pharmacotherapies with non-pharmacological interventions. Newer medications, such as SGLT-2 inhibitors and GLP-1 receptor agonists, have shown significant promise in protecting both the heart and kidneys and are generally well-tolerated in older populations. Alongside these drugs, non-pharmacological approaches are critically important. Tailored nutritional plans and regular exercise not only enhance the efficacy of medications but also play a vital role in preserving cognitive function, physical strength, and overall quality of life, which are paramount concerns in geriatric care.</p><p>When CKD advances to kidney failure, treatment decisions must move beyond outdated criteria based solely on chronological age or cognitive status. It is crucial that all options are considered through a process of shared decision-making. These options include not only dialysis and transplantation but also conservative kidney management (CKM), an approach that prioritizes comfort and quality of life without dialysis. This patient-centered model ensures that the chosen treatment path aligns with the individual’s personal values and life goals.</p><p>Looking forward, the integration of digital technologies, such as wearable devices and telehealth, is poised to further enhance the personalization and effectiveness of CKD care for this growing demographic.</p>

<p>Quality of life (QOL) in older adults with kidney failure is an increasingly important clinical issue, as a growing proportion of CKD patients are aged 65 years and older. This demographic shift means more individuals are now facing the prospect of kidney failure and its treatment at an advanced age. Decision making around dialysis and conservative management are complex, and involve considerations including the significant symptom burden in kidney failure, potential for functional decline, and co-morbidities, but selected older patients may achieve comparable QOL outcomes with either approach. The high prevalence of frailty, cognitive impairment, and treatment-related burdens further complicates QOL for this group. The aging population in the Asia Pacific region means that there is a pressing need for more research and individualised strategies to optimise supportive care and guide treatment choices in this vulnerable population.</p>

<p>End-of-life (EoL) decision-making is a critical and challenging issue in nephrology, especially regarding dialysis withdrawal and the provision of palliative care. In Korea, the Act on Decisions on Life-Sustaining Treatment (2018) legally permitted withholding or withdrawal of dialysis, prompting active debate among nephrologists.</p><p>Nationwide surveys revealed that most Korean nephrologists consider withholding (87.3%) and withdrawing (86.2%) dialysis at EoL ethically appropriate, even for maintenance dialysis patients. Key factors influencing such decisions include dialysis intolerance, poor performance status, and patient request, while age and dementia are less decisive. However, limited access to palliative care services and the absence of clear clinical guidelines remain major barriers.</p><p>Shared decision-making (SDM) has been recognized as essential for aligning treatment with patient values. Yet only a minority of physicians in Korea have received formal SDM training. Those trained are more confident in applying SDM, but lack of time, educational tools, and institutional support hinder its effective implementation in practice.</p><p>To address these gaps, Korean experts developed consensus recommendations on withholding and withdrawing dialysis in older adults, published in 2024, emphasizing individualized, ethically grounded decisions, advance care planning, and the expansion of palliative care infrastructure.</p><p>This lecture will review the evolving perspectives of Korean nephrologists on EoL care, highlight the role of SDM in bridging ethical principles and clinical practice, and discuss future directions in policy, education, and guideline development. The Korean experience provides valuable insights for shaping palliative nephrology across the Asia-Pacific region.</p>

<p> Chronic kidney disease (CKD) is often accompanied by cognitive decline and higher risks of cardiovascular and renal complications, both of which drive excess morbidity and mortality. Physical activity (PA) has gained recognition as a pivotal modifiable factor that may protect brain function and mitigate adverse cardiorenal outcomes in this population. This talk will highlight the broad benefits of PA in CKD, with a focus on how exercise can enhance cognitive resilience, preserve kidney function, and improve survival and quality of life.</p><p> Emerging evidence indicates that patients who engage in regular PA experience slower cognitive decline, even at later stages of CKD. Proposed mechanisms include enhanced cerebral blood flow, vascular protection, and reductions in systemic inflammation, underscoring the interconnection between kidney and brain health.</p><p> In parallel, dose-response analyses indicate that moderate amounts of PA are strongly associated with reduced risks of all-cause mortality, end-stage kidney disease, and major cardiovascular events. Benefits are most pronounced when activity levels meet or exceed current recommendations, such as those equivalent to brisk walking, reinforcing the importance of structured exercise interventions.</p><p> Overall, PA represents a promising strategy to break the cycle of cognitive impairment and progressive cardiorenal disease in CKD. This presentation will outline current evidence, mechanistic insights, and clinical applications, and will advocate for integrating tailored exercise programs into multidisciplinary CKD care to improve long-term outcomes.</p>

<p>With the recent new cardiovascular-kidney-metabolic health paradigm suggested by the American Heart Association, the ISPD is revising and updating the last 2015 ISPD cardiovascular and metabolic guideline for patients receiving peritoneal dialysis. </p><p>This is an important area to be addressed in the talk for improving outcomes of patients receiving peritoneal dialysis. Several innovations have been incorporated into this 2025/26 ISPD update. Bioimpedance spectroscopy is reinforced as an objective tool for longitudinal assessment of extracellular volume status, while previously strong recommendations for rigid dietary sodium restriction have been downgraded in light of emerging data questioning its long-term effectiveness and feasibility. In managing atrial fibrillation, direct oral anticoagulants (DOAC) — particularly apixaban — are now conditionally endorsed for stroke prevention in PD patients based on real-world evidence supporting their safety and efficacy over warfarin. Furthermore, continuous glucose monitoring (CGM) is increasingly recognized as a valuable adjunct for glycemic management in diabetic PD patients, particularly those receiving glucose-based or icodextrin-containing dialysis solution. </p><p>We understand the practical issue of regional consistencies and variabilities, when devices (such as CGM) or drugs (such as sodium-glucose cotransporter 2 SGLT2 inhibitor) are unavailable to clinicians implementing evidence-informed guidelines in low-resource settings. Some deviations from current ISPD guidelines may be due to variability in local settings including cost, training, availability, and policy. Collectively, these guidelines reflect a decisive shift toward individualized, evidence-informed cardiometabolic care in PD. By integrating contemporary pharmacotherapies, refined monitoring strategies, and flexible implementation across diverse resource settings, this update aspires to mitigate the disproportionate cardiovascular burden borne by PD patients worldwide — advancing both clinical excellence and health equity.</p>

<p>Glucose-sparing strategies in peritoneal dialysis (PD) aim to reduce the harmful effects of prolonged exposure to glucose-based dialysis solutions. Long-term exposure to high glucose concentrations in conventional PD solutions can lead to several complications, including peritoneal membrane damage, systemic metabolic issues (such as hyperglycemia, weight gain, dyslipidemia and other metabolic disturbances) and reduced ultrafiltration efficiency; all of which are factors that contribute to increased cardiovascular risks, morbidity and mortality.</p><p>Glucose-sparing strategies focus on minimizing glucose exposure while maintaining adequate ultrafiltration, which is crucial for fluid and waste removal. This is achieved through various approaches including optimizing dialysis prescriptions, utilizing alternative osmotic agents like icodextrin or amino acids, and preserving residual kidney function – all of which allow the avoidance of increasing the tonicity of PD solutions used for the daily exchanges. By implementing these glucose-sparing strategies, the aim is to improve the long-term outcomes of PD patients by reducing the detrimental effects of glucose exposure while maintaining or improving the effectiveness of dialysis.</p>

<p>Diabetic Kidney Disease (DKD) is one of leading cause of end-stage renal disease that becomes a tremendous healthcare burden in Taiwan. Dysfunction of mesangial cells and podocytes in renal glomerular micro-compartments contribute to DKD. Compared with conventional mechanisms of diabetic nephropathy, the Dickkopf-1(DKK1)/Wnt/ β-catenin signaling pathway is virgin land in this field. By searching the PubMed at that time (2006), there is no research group in the world studies on molecular mechanism of DKK1/Wnt/GSK-3β/β-catenin signaling pathways that mediated diabetic nephropathy. In 10th Anniversary of Chang-Gung Memorial Hospital, Chiayi, international symposium on DKD, we are clearly have demonstrated that embryonic stem cell signaling in DKD are important cellular events underlying diabetes-mediated renal injury. Although the new era of KDCRT in DKD research has made great progress in the first 10 years (2004-2014), the studies related the underlying mechanisms in DKD are still ongoing within last 10 years (2014-2024). KDCRT are trying to put much effort to establish and understand this molecular frame-signaling model in DKD. Furthermore, in 20th Anniversary of Chang-Gung Memorial Hospital, Chiayi, on Precision medicine in the Kidneys, we would like to demonstrate that miR-29a and HDAC4 is an important regulator in the maintenance of podocyte ultra-structure integrity and renal homeostasis. This study highlights an emerging view of an epigenetic mechanism underlying nephrin acetylation in podocytes and suggests that the addition of the miR-29a function is beneficial for improving diabetic podocytopathy. Our hypothesis in this paper was selected to be the cover page of this top journal “JASN” which recognized the importance of our theory. Furthermore, we would have also demonstrated that targeting the KDM6A-KLF10 feedback loop may be beneficial to attenuate diabetes-induced kidney injury which is publish in top journal EMBO Molecular medicine. In this talk, our group KDCRT would orchestrate Epigenetic-Based Precision Medicine for Diabetic Kidney Disease from Chiayi CGMH prospective, and provide precision platform of epigenetic against diabetic kidney disease and exciting new venues for improving renal outcome by retarding the progression of DKD, which are regarded as the therapeutic hope in the future.</p>

<p>Podocytes are specialized epithelial cells that form a key component of the glomerular filtration barrier and play a critical role in blood filtration. Podocytes adhere to the glomerular basement membrane through integrin-mediated focal adhesions (FAs) and generate actomyosin contractility to counteract mechanical stress from filtration. We previously demonstrated the critical role of ROCK2 regulation by Shp2 at FAs in mediating cellular responses to extracellular mechanical stimuli. Furthermore, we identified alpha-actinin-4 as a key factor in recruiting Shp2 to FAs, enhancing cell adhesion and cytoskeletal organization in podocytes. Given that mechanical stress caused by filtration has been recognized as a major physical challenge for podocytes in various glomerular diseases, we established an in vitro cell filtration system to investigate its impact on podocytes. Differentiated podocytes were seeded onto collagen IV-coated filter membranes, exposed to varying flow rates, and analyzed by immunofluorescence and RNA sequencing. Our data showed significant increases in FAs, stress fibers, interdigitating intercellular junctions, and microtubule acetylation as filtration flow rates increased. RNA sequencing revealed distinct transcriptional changes associated with mechanosensing and cytoskeletal adaptation. These results provide direct evidence that podocytes dynamically sense and adapt to the mechanical stress of filtration through coordinated cytoskeletal remodeling and transcriptional regulation. While our primary focus has been on mechanical stress, we have also demonstrated that various nephrotoxic factors can disrupt the podocyte cytoskeleton. Our findings highlight the importance of podocyte biomechanical resilience and offer new insights into glomerular disease mechanisms.</p>

<p>The precision estimation on prevalence of anti-HCV was 2.86 % in Taiwan. Studies have shown that iatrogenic behavior was the major transmission route in geriatric patients. Moreover, it is highest in the specific groups including end stage renal disease during hemodialysis, human immunodeficiency virus infection, person who inject drug (PWID), and those under opioid substitution therapy. The estimated chronic hepatitis C (CHC; HCV RNA positive) patients were 188,126 who need to be treated.</p><p>Taiwan has accelerated its efforts to eliminate HCV infection since 2017, and the government claims to reach the programmatic and impact targets set by WHO indicating HCV elimination by 2025. The most important and successful factor is government will. The Ministry of Health and Welfare (MOHW) conquer several barriers of diagnosis and linkage to care including finance a national program, implementing a harm reduction program, expanding treatment capacity beyond specialists, remove treatment restriction, implement monitoring and evaluation, implement awareness and national screening program and implement national link-to-care program during 2017-2024. Fortunately, the calculated diagnostic and treatment rates are 90.6% and 92.8% respectively in the general population and achieve full HCV elimination programmatic targets which is diagnostic rate >90% and treatment rates >80% based on the WHO definition.</p>

<p>Acute kidney injury (AKI) is a prominent feature of leptospirosis, characterized by tubulo-interstitial nephritis and tubular dysfunction. The association of leptospirosis kidney disease with CKD has recently been discovered. Two pathways have been hypothesized, including first, AKI to CKD due to acute infection leading to chronic kidney injury if not treated as early and as effectively. Secondly, AKI on CKD by secondary AKI superimposed on the subclinical chronic kidney injury of leptospirosis leading to progression of CKD.</p><p>AKI to CKD: It has been reported that CKD may be a consequence of acute leptospirosis. Recently, we studied 2145 patients with leptospirosis over an 8-year follow-up from the National Health Insurance Research Database. Four hundred and forty-three (20.6%) patients had AKI; among them 77 (3.6%) patients received replacement therapy (AKI-RRT). Long-term mortality is increased in AKI-RRT group while compared to the AKI group and the non-AKI group using the multivariate logistic regression model. Along the same line, the rate of CKD is increased in the AKI-RRT group, followed by AKI and non-AKI group. Single cell analysis and spatial transcriptome analysis indicate proximal tubule injury associated with immune reaction are the initiators kidney fibrosis in leptospirosis. </p><p>AKI on CKD: In a survey of human CKD, populations with anti-leptospira seropositivity were associated with lower eGFR and higher prevalence of CKD in endemic areas. In animal, adenine-induced kidney injury in a chronically leptospira-infected murine model was performed to evaluate renal function, inflammation, and fibrosis gene expression in comparison to controls. Results showed that an increased gene expression of immune/inflammatory genes and fibrosis may be aggravated by adenine nephrotoxic injury. A system biology study with transcriptome analysis indicated highly aggravated and synergistic gene expressions of kidney injury may be induced whenever secondary injury is superimposed on the subclinical kidney injury in this chronic leptospirosis model. This model explained how AKI on CKD may aggravate the progression of kidney disease. </p><p>In summary, leptospirosis kidney disease helps to understand how infection can induce CKD via AKI and provides a model to decipher the mechanism of AKI to/on CKD and a possible cause of CKDu. Early recognition of leptospirosis by rapid screening and timely appropriate antibiotics will rescue patients not only from AKI to/on CKD but also from multiple organ failure in acute settings.</p>

<p>Taiwan offers a distinctive and globally relevant model where three landmark laws—the Human Organ Transplant Act, the Hospice Palliative Care Act, and the Patient Right to Autonomy Act—are implemented in synergy under a single publicly funded institution: the Taiwan Organ Sharing Registry and Patient Autonomy Promotion Center (TOSR-PAPC). This integration enables a coherent continuum from end-of-life care to posthumous organ donation, ensuring that the final stage of life can be both dignified and meaningful. It represents a paradigm shift in public health governance that bridges ethical, legal, and clinical dimensions of care, turning “unexpected death” into “a meaningful life.”</p><p>In recent years, particularly in the wake of the COVID-19 pandemic, Taiwan has strengthened care for critically ill and end-stage patients through innovations in shared decision-making, virtual family meetings, and structured time-limited trials. These practices provide a framework for balancing aggressive treatment with timely transitions to palliative care, prioritizing total symptom control, psychosocial support, and family inclusion in medical decisions. Yet, the expanding societal and clinical interest in donation after circulatory death (DCD) has generated new ethical and procedural complexities. Communication among clinical teams, forensic investigators, and judicial authorities remains a sensitive frontier, highlighting the need for interdisciplinary consensus on definitions of death, consent validity, and professional accountability.</p><p>TOSR-PAPC continues to champion the concept of the “Three Acts for a Good Death” through nationwide public education, legal literacy campaigns, and cultural transformation. Key initiatives include online platforms for advance care planning (ACP), organ donation pledges, and individualized palliative preferences, fostering an environment where patients and families can engage in early, informed discussions about end-of-life decisions.</p><p>Looking ahead, Taiwan’s strategy focuses on expanding ACP into community and home-based care, promoting equitable access, and strengthening the competency of healthcare professionals through simulation-based education on ethical dilemmas such as DCD. This approach aims to consolidate public trust while ensuring transparency and ethical rigor in organ donation practices.</p><p>Ultimately, this presentation offers a contemporary perspective on how integrated legislation, cultural engagement, and clinical innovation—complemented by education on ethically challenging issues—can reshape end-of-life care, reinforce societal compassion, and transform loss into a legacy of life through organ donation.</p>

<p>　　IgA nephropathy (IgAN) is the most common primary glomerulonephritis in the world, particularly in East Asia, including Japan. Untreated, approximately 40% of cases progress to end-stage kidney disease, resulting in poor prognosis. It has been designated an intractable disease in Japan. Over half a century has passed since the disease was first described, and its pathogenesis is gradually clarified.</p><p>　　There is increasing evidence that aberrantly glycosylated IgA1 (Gd-IgA1) have a key role in the pathogenesis of IgAN. It is thought that autoantibodies (IgG and IgA subclasses) specific to Gd-IgA1 form high-molecular-weight immune complexes, which are deposited in the mesangium. In fact, serum levels of Gd-IgA1 containing immune complexes elevate in patients with IgAN. Recently, the presence of IgA antibodies with specificity for mesangial cells are reported and identified β2-spectrin (SPTBN1) and CBX3 as target antigens. Activation of mesangial cells and complement activation by the deposited IgA1 immune complexes induces nephritis, which progresses to podocyte and tubular damage.</p><p>　　In recent years, several promising curative therapies based on the pathogenesis have emerged, aimed at suppressing the production of Gd-IgA1 containing immune complexes and controlling inflammation after glomerular deposition. Abundant clinical trials of these drugs are in progress worldwide. This symposium will provide an overview of treatment options for each drug based on the stage of the disease.</p>

<p>IgA nephropathy (IgAN) is the most common biopsy-proven glomerulonephritis globally, characterized by the mesangial deposition of IgA in the glomeruli, leading to varying degrees of kidney failure. Until recently, the primary treatment strategies for IgAN for many years had only focused on controlling blood pressure, particularly through the use of renin-angiotensin-aldosterone system (RAAS) inhibitors. New drug approvals, including targeted therapies, have expanded treatment options beyond traditional approaches. The latest KDIGO guidelines, revised in 2025, incorporate new evidence on the efficacy of various interventions. For the first time, the guidelines have articulated therapeutic targets which included reducing proteinuria below 300mg/day and slowing annual eGFR decline to less than 1ml/min/1.73m2. In addition, the revised guidelines advocate for:</p><p>• Managing IgAN as a chronic kidney disease with proteinuria reduction therapy that included RAAS inhibition, SGLT-2 inhibitors and endothelin receptor antagonists.</p><p>• Ameliorating the deleterious insults of glomerular inflammation through anti-inflammatory agents such as corticosteroids.</p><p>• Addressing IgAN-specific drivers of nephron loss by reducing pathogenic forms of IgA and IgA immune complex formation with targeted release budesonide. </p><p>The evolution of IgA nephropathy treatment reflects ongoing research and the incorporation of new findings into clinical practice. Since the release of this update, at least 2 new drugs have received, and an additional 2 other drugs are being considered for accelerated approval by the US FDA for the treatment of IgAN. The KDIGO guidelines serve as a framework for improving patient outcomes through evidence-based recommendations and the adoption of innovative therapies. Continued updates to these guidelines will ensure that practitioners are equipped with the most current strategies for managing this complex condition.</p>

<p>C3 glomerulopathy (C3G) represents a rare and complex glomerular disease driven by dysregulation of the alternative pathway (AP) of the complement cascade. The diagnosis is made on renal biopsy, which is characterized on immunofluorescence (IF) by the hallmark dominance of glomerular C3 deposition in the absence of significant immunoglobulins. A 2013 C3G Consensus Report (PMID: 24172683) established guidelines defining C3G histologically as a proliferative glomerulonephritis with C3 staining that is at least two orders of magnitude greater than other immune reactants. Electron microscopy (EM) facilitates the recognition of two main entities: dense deposit disease (DDD), marked by highly electron-dense intramembranous deposits, and C3 glomerulonephritis (C3GN), which features mesangial and capillary wall deposits of lesser intensity.</p><p>Per KDIGO Practice Guidelines (2021, PMID: 34556256), definitive diagnosis requires the exclusion of other C3-dominant lesions, such as postinfectious glomerulonephritis (PIGN) and monoclonal gammopathy of renal significance (MGRS). The former is typically acute and non-recurrent while the latter should be considered in older patients presenting with a paraprotein. </p><p>The diagnostic workup of the C3G patient must include a comprehensive assessment of the AP. This evaluation is built on four pillars: (1) assays of complement components and their cleavage products (e.g., C3, C4, C3d, sC5b-9); (2) functional tests of complement integrity (e.g., CH50, AP50); (3) screening for acquired drivers of complement dysregulation (e.g., C3-, C4-, and C5-nephritic factors); and (4) testing for genetic mutations in complement activating and regulating genes (e.g., C3, CFB, CFH, CFI, CFHRs). </p><p>In summary, the diagnosis of C3G requires a multidisciplinary approach that integrates histopathology, IF, EM, comprehensive complement studies, and age-specific considerations for monoclonal protein evaluation. Best practices emphasize ruling out PIGN prior to diagnosing C3G and evaluating for MGRS in older adults. Accurate classification has never been more critical for guiding management and distinguishing C3G from mimicking conditions. Two novel anti-complement drugs – iptacopan and pegcetacoplan – have recently been approved for C3G and the availability of these two disease-specific agents is changing the treatment algorithm for C3G patients.</p>

<p>The major academic societies for renal and renal replacement therapy in Japan are the Japanese Society of Nephrology (JSN) founded in 1959 and the Japanese Society for Dialysis Therapy (JSDT) founded in 1968, both of which are historical organizations. On the other hand, the Japanese Society for Dialysis Access (JSDA) founded in 1998, and the Japanese Society of Interventional Nephrology (JSIVN) founded in 2013, are societies that focus on the creation and management of dialysis access (ex. vascular and peritoneal access). Among them, especially JSDA has been collaborating with JSDT since its inception, and has exchanged the MOU for overseas mutual cooperation with the Vascular Access Society (VAS), Vascular Access Society of the Americas (VASA), Asia Pacific Society of Dialysis Access (APSDA), Korean Society of Diagnostic Interventional Nephrology (KSDIN). </p><p>In 2000, since the establishment of American Society of Diagnostic Interventional Nephrology (ASDIN), the concept of “Interventional Nephrology” has been advocated and widely spread in the world, and it’s one of the main mission is strongly related to management and creation of dialysis access. </p><p>On the other hand, private medical facilities are taking the lead in dialysis treatment in Japan, which is characterized by less sectionalism compared to other medical organizations, and doctors from many specialties such as nephrology, general internal medicine, urology, and vascular surgery etc. are involved in dialysis management as dialysis specialists. This is the major characteristic of dialysis treatment in Japan. According to a JSDA survey conducted in 2016, multiple professions are involved in the field of vascular access (VA), and about 40% of VA creation and repair is performed by Nephrologists engaged in dialysis management. In other words, Nephrologists are already actively intervened in the field of dialysis access treatment and play a significant role in this field in Japan. And their involvement will contribute to improving the prognosis of dialysis treatment in Japan.</p><p>We expect that the number of nephrologists participating in dialysis care alongside interventional nephrology activities will continue to increase. The most important aspect is that interventional nephrologists participating in these activities will be experts well-versed in dialysis care. We believe that without a fully understanding of the dialysis care environment, it is impossible to provide appropriate VA treatment. Therefore, interventional nephrologists who manage VA also be dialysis specialists.</p>

<p>Endovascularly created arteriovenous fistula (endoAVF) creation represents a transformative, minimally invasive technique for establishing vascular access in hemodialysis patients. Two systems are currently in clinical use: the Ellipsys system (Medtronic), which employs thermal resistance energy to create a percutaneous anastomosis between the proximal radial artery and perforating vein, and the WavelinQ system (BD), which utilizes dual intraluminal catheters and radiofrequency energy to connect paired radial/ulnar arteries with adjacent veins. While both devices demonstrate high technical success, patient selection is the critical determinant of durable maturation and long-term usability. Careful pre-procedural assessment with duplex ultrasound is essential, with particular emphasis on the “rule of two”: target arteries and veins for anastomosis, size of perforator and upper arm veins should be ≥2 mm in diameter and target cannulation veins ≤6 mm in depth to optimize outcomes. In this session, we will outline key anatomical and physiological criteria for candidate selection, compare considerations unique to Ellipsys and WavelinQ, and highlight strategies to maximize success rates and long-term patency with this breakthrough technology.</p>

<p>Aldosterone, synthesized in the zona glomerulosa (ZG) via aldosterone synthase (CYP11B2), regulates sodium retention, blood volume, and blood pressure. In adult adrenals, ZG cells expressing CYP11B2 are sparse. Given modern high-salt diets, we hypothesize this is due to aldosterone production influencing ZG cell fate. Herein, this study aims to examine the impact of CYP11B2 inhibition on human adrenal cell function. CYP11B2 was inhibited in HAC15 cells using siRNA (siCYP11B2) or Baxdrostat, a selective CYP11B2 inhibitor. 48 hours post-transfection, hormone levels, RNA sequencing, transcriptome analysis, and functional assays (EZMTT, xCELLigence, Annexin V/SYTOX Assays) were performed. siCYP11B2 cells had reduced aldosterone production (30+2.9%, n=18, P-value<0.001), and CYP11B2 (0.12±0.11-fold), HNRNPA1 (0.67±0.18-fold) and UHMK1 (0.58±0.14-fold) mRNA expression (n=9, P-value<0.05) compared to controls. In-depth analysis of the differentially expressed genes identified mitophagy and autophagy as the most enriched pathways. Treatment with U0126 (autophagy inhibitor) reduced AngII-stimulated aldosterone and cortisol synthesis in a dose-responsive manner (n=12, P-value=<0.001), while SB203580 (autophagy inducer) increased the aldosterone-to-cortisol ratio (4.5±0.5-fold, n=12, P-value=<0.001). No consistent apoptosis changes were observed with either siCYP11B2 or CYP11B2 inhibitor, though Baxdrostat treatment did significantly increased necrotic cells (FC=1.42+0.05, n=144 and P-value=1.3 x 10-10). The EZMTT assay showed a 0.141±0.02 increased in absorbance in siCYP11B2 cells at 96 hours (P-value<0.001), but not in Baxdrostat-treated cells. Similarly, no changes were seen with the xCELLigence assay (n=10-12). The findings suggest that aldosterone production capability modulates ZG cell fate potentially through autophagy and/or mitophagy, with pharmacological inhibition of CYP11B2 leading to ZG cell death.</p>

<p>Context: Detecting patients with surgically curable aldosterone-producing adenoma (APA) among hypertensive individuals is clinically pivotal. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) is the ideal method of measuring plasma aldosterone concentration (PAC) because of the inaccuracy of conventional chemiluminescent enzyme immunoassay (CLEIA). However, LC-MS/MS is expensive and requires expertise. We have developed a novel noncompetitive CLEIA (NC-CLEIA) for measuring PAC in 30 minutes.</p><p>Objective: This work aimed to validate NC-CLEIA PAC measurements by comparing them with LC-MS/MS measurements and determining screening cutoffs for both measurements detecting APA.</p><p>Methods: We retrospectively measured PAC using LC-MS/MS and NC-CLEIA in 133 patients with APA, 100 with bilateral hyperaldosteronism, and 111 with essential hypertension to explore the accuracy of NC-CLEIA PAC measurements by comparing with LC-MS/MS measurements and determined the cutoffs for detecting APA.</p><p>Results: Passing-Bablok analysis revealed that the values by NC-CLEIA (the regression slope, intercept, and correlation coefficient were 0.962, -0.043, and 0.994, respectively) were significantly correlated and equivalent to those by LC-MS/MS. Bland-Altman plot analysis of NC-CLEIA and LC-MS/MS also demonstrated smaller systemic errors (a bias of -0.348 ng/dL with limits of agreement of -4.390 and 3.694 within a 95% CI) in NC-CLEIA than LC-MS/MS. The receiver operating characteristic analysis demonstrated that cutoff values for aldosterone/renin activity ratio obtained by LC-MS/MS and NC-CLEIA were 31.2 and 31.5 (ng/dL per ng/mL/hour), with a sensitivity of 91.0% and 90.2% and specificity of 75.4% and 76.8%, respectively, to differentiate APA from non-APA. PAC measured by LC-MS/MS and NC-CLEIA≧6.0 and renin activity ≦1.0 might be a good cutoff values for screening primary aldosteronism. </p><p>Conclusion: This newly developed NC-CLEIA for measuring PAC could serve as a clinically reliable alternative to LC-MS/MS.</p>

<p>Prediction and Management of Severe Antibody-Mediated Rejection in ABO-incompatible Kidney Transplantation</p><p>Hideki Ishida</p><p>Introduction</p><p>We still encounter a few cases in ABO incompatible kidney transplantation with immediate graft loss every year, despite reaching within acceptable titer less than x32, just before transplantation. We retrospectively performed sequential C1q assay using serum samples from recipients with or without immediate graft loss.</p><p>Materials and methods </p><p>We experienced three cases with immediate graft loss within 2022. As previous reported, our desensitized protocol in ABO incompatible transplantation includes rituximab administration and several sessions of plasmapheresis to remove anti-blood type antibodies until x32 titers under triplicate immunosuppressive regimen. We have just started flow cytometric analysis to measure anti-blood type antibodies, subtypes of IgG as well as C1q assay in the clinical setting.</p><p>Results</p><p>As shown in Table, all three recipients (baseline anti-blood type antibody titer; x32, x64 and x256) with graft loss showed high ratio of C1q binding IgG antibody, although the blood type antibodies’ titer dropped to acceptable titer x32 or less after desensitization. They have no preformed DSA. After declamping of renal artery anastomosis in surgery, transplanted grafts were not changed to pinky color filled with fresh blood flow, also resulting in no blood flow shown by ultrasonography. They had no urine output postoperatively with no response to any treatment including anti-rejection therapies, finally followed by removal of transplanted kidneys. Pathological findings in all three grafts showed TMA suspected of vigorous active acute antibody mediated rejection.</p><p>Conclusions</p><p>We experienced immediate graft losses in three recipients within one year. Complement activation has already been reported in recipients with HLA high risk barrier, however, it should be focused on in ABO incompatible kidney transplantation as well. Additionally, high dose IVIG treatment would be helpful to decrease this complement activation, probably by binding to complements.</p>

<p>BK polyomavirus (BKPyV) infection remains a major threat to long-term kidney allograft survival. In 2024, the Transplantation Society convened an international consensus group to review emerging evidence and issue updated, evidence-based guidelines using the GRADE framework. The guidelines reaffirm that BKPyV reactivation is driven by multiple risk factors including older recipient age, male sex, donor BKPyV viruria, donor-seropositive/recipient-seronegative pairings, tacrolimus use, episodes of acute rejection, and heightened corticosteroid exposure.</p><p>To detect BKPyV-DNAemia early and prevent irreversible injury, the panel recommends universal plasma BKPyV screening monthly until 9 months post-transplant, then every three months until two years (extended to three years in children). In resource-limited settings, urine cytology (decoy cells) may guide selective plasma testing. For persistent BKPyV-DNAemia (≥ 1,000 copies/mL for >2 weeks) or high-level (> 10,000 copies/mL), or biopsy-confirmed BKPyV nephropathy, a stepwise reduction of immunosuppression is advised—targeting antiproliferative agents, calcineurin inhibitors, or both. Biopsy is reserved for graft dysfunction or high immunologic risk (less so in adults). Immunohistochemistry is preferred to confirm viral inclusion in tissue. The guidelines discourage routine use of antivirals (e.g. leflunomide, cidofovir), IVIG, or quinolones, and strongly advocate enrolling patients in trials of novel therapies (antivirals, vaccines, adoptive T cells). Finally, retransplantation after BKPyV nephropathy is feasible if DNAemia is undetectable, and routine graft nephrectomy is not recommended.</p><p>These consensus recommendations aim to standardize BKPyV management globally, to optimize graft outcomes and patient safety.</p>

<p>The 2019 KDOQI Clinical Practice Guideline for Vascular Access emphasizes individualized, patient-centered strategies for surveillance and monitoring of hemodialysis access, and explicitly states that current evidence is insufficient to mandate routine surveillance (access-flow, pressure monitoring, or imaging) beyond careful clinical monitoring. </p><p>Randomized trials and controlled cohort studies, however, have produced mixed but promising signals that active surveillance—most commonly via access blood-flow measurement (ultrasound dilution or duplex) ± targeted imaging—can reduce rates of acute thrombosis and improve assisted-primary and secondary patency in selected settings. Notable randomized and controlled studies reported lower thrombosis rates with structured flow surveillance programs compared with clinical monitoring alone. </p><p>Meta-analyses and systematic reviews, however, judge the overall quality of the evidence to be low–very low because of heterogeneity in study design, surveillance modality, definitions of dysfunction, and downstream intervention thresholds; consequently, pooled estimates that suggest benefit for thrombosis reduction must be interpreted cautiously. </p><p>In routine clinical practice, several real-world constraints complicate guideline implementation and trial translation: variable availability of surveillance technology, differences in operator expertise (duplex interpretation, flow-measurement technique), logistical workflows in dialysis units, inconsistent thresholds for pre-emptive angioplasty, and concerns about false-positive detection driving unnecessary interventions and cost. Cost-effectiveness analyses are heterogeneous and depend heavily on local thrombosis rates, access to timely angioplasty, and the capacity to act on positive surveillance findings. </p><p>This presentation will (1) summarize the KDOQI recommendations and the evidence base with emphasis on randomized data addressing thrombotic outcomes, (2) dissect sources of heterogeneity across trials and their impact on pooled inference, and (3) offer practical, evidence-informed algorithms for integrating surveillance into clinical workflows—balancing potential thrombosis reduction against resource constraints and the risk of overtreatment. The goal is to provide nephrologists with a pragmatic framework to apply surveillance selectively where the greatest benefit is likely and to identify research gaps that remain before routine universal surveillance can be uniformly recommended.</p>

<p>Vascular access (VA) is essential for achieving adequate hemodialysis (HD) efficiency. However, VA-related complications, particularly stenosis and thrombosis, frequently result in suboptimal dialysis, which was associated with morbidity and mortality. The 2019 KDOQI guidelines recommend integrated, multidisciplinary VA care and management, yet practical implementation strategies remain underexplored in current research.</p><p>This lecture will cover key aspects of integrated VA care—from basic science to clinical application—with the goal of improving VA-related outcomes in patients. We will begin by reviewing common causes of VA dysfunction, followed by an exploration of the pathogenesis of VA stenosis and thrombosis. Upstream factors contributing to arteriovenous access (AVA) stenosis—including inflammatory stimuli, genetic predisposition, hemodynamic stress, and vascular injury—will be discussed. We will then examine downstream molecular and cellular responses that drive the development of intimal hyperplasia (IH).</p><p>With a mechanistic understanding of IH, we will discuss the role of access flow surveillance in the integrated care and management of VA. Finally, we will address how VA-related parameters correlate with hard clinical outcomes, including cardiovascular events and all-cause mortality, etc.</p>

<p>Diabetes is the leading cause of kidney disease that progresses to kidney failure. However, the key molecular and cellular pathways involved in diabetic kidney disease (DKD) pathogenesis are largely unknown. Here, we performed a comparative analysis of adult human kidneys by examining cell type-specific chromatin accessibility by single-nucleus ATAC-seq (snATAC-seq) and analyzing three-dimensional chromatin architecture via high throughput chromosome conformation capture (Hi-C</p><p>method) of paired samples. We mapped the cell type specific and DKD-specific open chromatin landscape and found that genetic variants associated with kidney diseases were significantly enriched in the proximal tubule- (PT) and injured PT-specific open chromatin regions in samples from patients with DKD. BACH1 was identified as a core transcription factor of injured PT cells; its binding target</p><p>genes were highly associated with fibrosis and inflammation, which were also key features of injured PT</p><p>cells. Additionally, Hi-C analysis revealed global chromatin architectural changes in DKD, accompanied by changes in local open chromatin patterns. Combining the snATAC-seq and Hi-C data identified direct target genes of BACH1, and indicated that BACH1 binding regions showed increased chromatin contact frequency with promoters of their target genes in DKD. Thus, our multi-omics analysis revealed BACH1 target genes in injured PTs and highlighted the role of BACH1 as a novel regulator of tubular inflammation and fibrosis.</p>

<p>Kidney disease progression remains a complex challenge, with limited biomarkers to predict outcomes or guide therapy. This talk explores metabolomic approaches to unravel the molecular underpinnings of chronic kidney disease (CKD) progression. By leveraging high-throughput mass spectrometry and advanced bioinformatics, investigators analyzed plasma and urine metabolomes from large patient cohorts to identify metabolic signatures associated with disease stages and outcomes. Their findings reveal distinct metabolic perturbations, including altered amino acid metabolism, dysregulated lipid profiles, and accumulation of uremic toxins, which correlate with declining renal function. Notably, specific metabolites, such as indoxyl sulfate and p-cresyl sulfate, emerge as potential predictors of progression to end-stage renal disease. This talk will also discuss how integrating metabolomics with genomic and proteomic data enhances our understanding of CKD pathophysiology and informs personalized therapeutic strategies. These insights pave the way for novel diagnostic tools and targeted interventions to slow disease progression.</p>

<p>The kidney has a higher order structure: multiple branched collecting ducts connected to numerous nephrons located in the periphery. Additionally, the kidney is connected to the ureter, which drains urine. Recapitulating such an organotypic structure in vitro is a major challenge in developmental biology and regenerative medicine. The kidney develops through the triad interactions of nephron progenitor, ureteric bud and stromal progenitor. We have previously established the induction protocols for the first two from mouse and human pluripotent stem cells (PSCs) (Cell Stem Cell 2014&2017). These protocols have been successfully applied to model inherited kidney diseases, including congenital nephrotic syndrome and autosomal polycystic kidney disease (Stem Cell Reports 2018, J Am Soc Nephrol 2020). We also established an in vitro induction protocol for the stromal progenitor from mouse PSCs. When the induced stromal progenitors were assembled with two differentially induced parenchymal progenitors (nephron progenitors and ureteric buds), the fully PSC-derived organoids reproduced the higher order kidney structure: branched collecting ducts connected to multiple nephrons with stromal cells distributed between the epithelia (Nat Commun 2022). Generation of a similar structure from human iPSCs is underway. Furthermore, we recently induced the ureteric stromal progenitor from PSCs. By combining this stromal progenitor with the epithelial progenitor (i.e., ureteric bud), we successfully generated ureteral organoids in both mice and humans (Nat Commun 2025). Thus, assembly of multiple progenitors will pave the way for recapitulation of organotypic architecture and functions. I will also discuss the hurdles that need to be overcome for the future clinical application of organoids for transplantation therapy.</p>

<p>Genetic kidney diseases represent a significant clinical challenge due to their progressive nature and limited therapeutic options. Recent advances in stem cell biology offer promising strategies for disease modeling and regenerative therapy. This presentation explores the application of induced pluripotent stem cells (iPSCs) and organoid technology to replicate key pathological features of hereditary nephropathies, enabling precise investigation of underlying genetic mechanisms. These innovations highlight the potential of stem cell platforms to transform personalized treatment paradigms for genetic kidney disorders.</p>

<p>Fibrosis is a hallmark of chronic kidney disease (CKD) that can compromise the viability and efficacy of transplanted stem cells post-administration. To overcome this, we have developed a combination therapy using bone marrow-derived mesenchymal stromal cells (BM-MSCs; the most clinically evaluated stem cells) and the anti-fibrotic drug, serelaxin (recombinant human relaxin; RLX). BM-MSCs express the RLX receptor, relaxin family peptide receptor 1 (RXFP1), which allows RLX to bind to RXFP1 on BM-MSCs and enhance their proliferation and migration in vitro[1]. The combined effects of RLX and BM-MSCs either prevented unilateral ureteric obstruction-induced tubulointerstitial fibrosis[1] or therapeutically attenuated uninephrectomy and deoxycorticosterone acetate/saline drinking (1K/DOCA-salt)-induced hypertensive kidney fibrosis and glomerulosclerosis[2] to a greater extent than BM-MSC treatment alone in murine models of disease in vivo. However, as RLX is a peptide drug, its continuous infusion via a microinfusion pump was required to maintain its activity, with BM-MSCs intravenously (i.v) administered 15-30 minutes later in the models established. To overcome the cumbersome nature of this combination therapy, we engineered BM-MSCs to express therapeutic levels of RLX, enabling the combination therapy to be administered via a single i.v injection of engineered cells[3]. 1-2x10E6 RLX-producing BM-MSCs attenuated the ischemia reperfusion injury-induced kidney fibrosis or therapeutically abrogated high salt (HS)-induced hypertension, tubular epithelial damage, fibrosis and proteinuria to an equivalent extent as the combined therapy administered separately; and to a greater extent than the ACE inhibitor, perindopril in HS-fed mice. Importantly though, no adverse effects of these RLX-producing BM-MSCs were found 9-months after cessation of cell therapy. Our current work is assessing the therapeutic effects and safety of RLX-producing BM-MSCs in aged (7-10 year old) and hypertensive marmosets (non-human primates) as a step towards the clinical evaluation of these engineered cells as a viable treatment option for CKD patients.</p><p>[1] Huuskes BM et al. FASEB Journal 2015; 29:54-553</p><p>[2] Li Y et al. British Journal of Pharmacology 2021; 178:1164-1181</p><p>[3] Li Y et al. Stem Cell Research & Therapy 2024; 15:375</p>

<p>Alport syndrome is the commonest genetic kidney disease and the second commonest genetic cause of kidney failure. XL Alport syndrome in affected males is characterised clinically by haematuria, proteinuria, kidney failure, hearing loss and minor ocular features. Autosomal dominant Alport syndrome is twenty times as common as XL disease but clinical manifestations in COL4A3 or COL4A4 heterozygotes are variable and include none, isolated haematuria, isolated proteinuria or steroid-resistant nephrotic syndrome, kidney failure, kidney cysts, and familial forms of IgA nephropathy. </p><p>The major challenges in the diagnosis of Alport syndrome are: the difficulty in recognising AD Alport syndrome clinically when the phenotype is so varied; understanding that up to 20% variants in Alport genes cannot detected by WES even when there is a strong clinical suspicion; and knowing that we do not know the risk factors for kidney failure in people with AD disease. However the major challenge for people with suspected AD Alport syndrome in low resource settings is that genetic testing itself is rarely available. </p><p>In contrast, current treatment for both XL and AD Alport syndrome (with ACE inhibitors and SGLT2 inhibitors) is widely available and inexpensive, and delays kidney failure but is not curative. We know that the earlier that this treatment is commenced, the longer that kidney failure is delayed. Many other treatments including gene therapies are currently undergoing evaluation in animal models, and we shall soon know of their efficacy and risks.</p>

<p>This talk will cover commons pitfalls and challenges in the diagnostic workup of genetic kidney diseases. This includes identifying probable genetic cases, selecting suitable genetic tests, interpretation of results and subsequent management.</p>

<p>Recent advancements in genetic research technologies have led to the identification of causative genes for hereditary tubular disorders. Along with this, details of tubular function associated with these genes have also been elucidated, highlighting the significant role that genetic testing has played in understanding tubular function. Among the hereditary tubular disorders with a higher prevalence that clinicians should be aware of are: 1. Gitelman syndrome and 2. Tubular proteinuria. Additionally, there are other disorders such as tubular acidosis and nephrogenic diabetes insipidus, among many others. This lecture will provide a summary of the prevalent hereditary tubular diseases, with an in-depth explanation of Gitelman syndrome and tubular proteinuria.</p><p>1. Gitelman syndrome is an autosomal recessive genetic disorder that is more common in East Asians, occurring at a frequency of about 1 in 10,000 people. Although it presents with hypokalemia and metabolic alkalosis, it is often considered a mild condition that rarely requires treatment. However, our data, as well as data from overseas, have shown that, compared to healthy individuals, patients experience significant quality of life (QOL) reductions due to symptoms like fatigue and nocturia. Furthermore, non-steroidal anti-inflammatory drugs have been found to be highly effective against fatigue, emphasizing the importance of identifying clinical symptoms in Gitelman syndrome patients and intervening with treatment when necessary.</p><p>2. Regarding tubular proteinuria, three diseases have recently been identified: Dent disease-1, Dent disease-2, and Chronic Benign Proteinuria (PROCHOB). Dent disease results from abnormalities in the CLCN5 or OCRL genes, leading to secondary dysfunction of megalin, while PROCHOB arises from abnormalities in the CUBN gene, which encodes for cubilin. OCRL gene abnormalities can lead not only to Dent disease-2 but also to Lowe syndrome, which presents with more severe systemic symptoms. We have clarified that while truncating variants from exons 1-7 cause Dent disease-2, variants from exon 8 onwards lead to Lowe syndrome, along with elucidating their mechanisms. PROCHOB is a benign disorder characterized by proteinuria without progressive renal dysfunction; however, due to the lack of diagnostic biomarkers, most patients undergo invasive renal biopsies. Our efforts are directed towards identifying biomarkers to enable early diagnosis.</p>

<p>Abstract </p><p>Renal tubular disorders represent a heterogeneous group of conditions characterized by impaired tubular function, resulting in disturbances of fluid, electrolyte, and acid-base balance. Clinical presentations vary from asymptomatic states to severe manifestations such as growth failure, nephrocalcinosis, and progression to chronic kidney disease. Early recognition hinges upon identifying characteristic biochemical abnormalities, clinical features (such as polydipsia, polyuria, salt craving, and growth retardation), and imaging findings. Distinguishing inherited from acquired etiologies requires integration of family history, age at onset, and exclusion of secondary causes including medications or systemic illness. Localization of the tubular defect can be guided by specific blood and urine electrolyte profiles, coupled with genetic analysis where indicated. </p><p>The presentation emphasizes the diagnostic approach through illustrative clinical cases, highlighting common inherited syndromes (Bartter’s, Gitelman’s, nephrogenic diabetes insipidus) and rare entities such as renal tubular dysgenesis. Modern diagnostic algorithms, including targeted gene sequencing, are also discussed to facilitate precise diagnosis, guide management, and prevent long-term complications.</p>

<p>Pericytes are interstitial mesenchymal cells found in many major organs. In the kidney, microvascular pericytes are defined anatomically as extensively branched collagen-producing cells in close contact with endothelial cells. Although many molecular markers have been proposed, none of them can identify the pericytes with satisfactory specificity or sensitivity. The roles of microvascular pericytes in kidneys were poorly understood in the past. Recently, by using genetic lineage tracing to label collagen-producing cells or mesenchymal cells, the elusive characteristics of the pericytes are illuminated. In the healthy kidney, pericytes are found to take part in the maintenance of microvascular stability. Detachment of the pericytes from microvasculature and loss of close contact with endothelial cells are observed upon kidney injury. Kidney pericytes are shown to be the major source of scar-forming myofibroblasts in progressive kidney disease. Targeting the crosstalk between pericytes and neighboring endothelial cells or tubular epithelial cells may inhibit the pericyte-myofibroblast transition, prevent peritubular capillary rarefaction, and attenuate kidney fibrosis. In addition, kidney pericytes produce erythropoietin in healthy kidneys by sensing the change of oxygenation and hemoglobin concentration. However, the ability of erythropoietin production decreases in pericytes-derived myofibroblasts in chronic kidney disease, leading to renal anemia. Recent advances on epigenetics create a new field to study erythropoietin gene expression at chromatin level. Demethylating agent has shown the restoration of erythropoietin expression as well as downregulation of alpha-smooth muscle actin in myofibroblasts. Through this talk I would like to share the knowledge in the physiology and pathophysiology of kidney pericytes, and our recent research on pericyte-specific drug delivery for kidney disease and complication.</p>

<p>Renal anemia remains a major challenge in chronic kidney disease (CKD), driven by reduced erythropoietin (EPO) production, functional iron deficiency, inflammation, and altered hepcidin regulation. Traditional strategies—erythropoiesis-stimulating agents (ESAs), intravenous iron, and red blood cell transfusions—have improved outcomes but are limited by safety concerns, including cardiovascular risks, iron overload, and infection. In recent years, advances in our understanding of oxygen sensing and iron metabolism have reshaped the therapeutic landscape. This presentation will revisit the evolution of renal anemia management, from the early ESA era to the present, and highlight emerging therapies that promise to bridge past experience with future innovations. Particular attention will be given to hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHIs), which stimulate endogenous EPO production, improve iron utilization, and modulate hepcidin. Clinical trial evidence will be discussed, addressing both efficacy in raising hemoglobin and potential pleiotropic benefits such as lipid modulation and reduced inflammation, while also critically examining safety concerns. In addition, we will briefly review other novel approaches, including hepcidin antagonists, anti-inflammatory strategies, and new iron formulations. By integrating mechanistic insights with clinical evidence, this lecture aims to provide a balanced perspective on the “future-past” of renal anemia therapy, emphasizing how next-generation agents may transform practice while reminding us of lessons learned from prior treatment eras.</p>

<p>Severe dyskalemia (hypokalemia and hyperkalemia) are potentially life-threatening emergency requiring prompt recognition and management. Their diagnosis almost always relies on the laboratory reports with the unexpected turnaround time. Since the cardiac tissue is very sensitive to dyskalemia, electrocardiography (ECG) as a non-invasive bedside tool may help detect the potentially fatal dyskalemia prior to laboratory report. Using a large data-driven deep learning model (DLM) with annotated ECGs, we have successfully developed the AI-ECG12NET to early recognize severe dyskalemia in a large retrospective and prospective cohort studies. Clinical applications of ECG12Net include early recognition of severe dyskalemia within 1 minute, much faster than laboratory testing, the identification of the underlying causes for dyskalemia (hypokalemic paralysis, thyrotoxic periodic paralysis, digoxin intoxication), rapid exclusion of pseudodyskalemia to avoid inappropriate management, the monitoring of serum potassium (K+) changes during the treatment of severe dyskalemia, and even the predication of adverse cardiovascular outcomes (previvor) associated with ECG-dyskalemia. Recently, our pragmatic randomized controlled trial on Artificial Intelligence enabled Dyskalemia using Electrocardiogram (AIDE) alert on K+ imbalance effectively provides the physicians for timely assessment of high-risk dyskalemia patients and prompt hyperkalemia treatment. Thus, the AI-ECG analysis provides both a quantitative indicator and prognostic predication for decision support. The ECG12Net model could be also incorporated into ECG machines in ambulances or remote areas to facilitate telemedicine and applied to a wearable device for dyskalemia.</p>

<p>In Taiwan, the phasing out of lead in petrol started in 1983, and the supply of leaded petrol was banned in 2000. Nevertheless, lead persists in the environment as a toxicant. The diagnosis of lead exposure is primarily based on an elevated blood lead level. The generally accepted normal blood lead level is less than 3.5 µg/dL for children under 6 years old, and less than 10 µg/dL for adults. Nevertheless, no level of lead is considered safe. Lead exposure, even at low-level, is associated with kidney impairment and progression of chronic kidney disease. In a series of studies, our group demonstrated that environmental exposure to lead was related to progressive kidney insufficiency in patients with and without diabetes, and chelation therapy may retard kidney disease progression in these patients. Moreover, our group reported that lead accumulates in patients with end-stage kidney disease, and that elevated blood lead level is associated with mortality in patients receiving chronic hemodialysis and peritoneal dialysis.</p>

<p>Arteriovenous (AV) fistulas are widely regarded as the preferred vascular access modality for hemodialysis patients due to their superior longevity and lower complication rates compared to other access types. Despite these advantages, primary failure rates remain high, with reported rates of 20–40% for upper arm fistulas and 40–60% for forearm (radiocephalic) fistulas. Such high failure rates represent a significant clinical challenge that necessitates innovative therapeutic strategies.</p><p>To address this issue, we have adopted an aggressive interventional approach for AV fistulas that have already been surgically created but never became usable for dialysis (primary failure). By employing advanced endovascular techniques, we aim to maximize fistula salvage and optimize clinical outcomes.</p><p>From an angiographic standpoint, these fistulas can be classified into two main categories: those with a clearly defined main trunk and those without. In cases lacking a main trunk, the angiographic appearance often reveals distinct morphological patterns, which we refer to as the "eighth note deformity" and the "caput medusae deformity."</p><p>During this presentation, I will illustrate, through clinical case examples, how even thrombotic immature fistulas, which had been abandoned—can be successfully rescued. Furthermore, I will demonstrate how to remodeling fistulas with these characteristic deformities, highlighting the potential for improved patient outcomes through precision care and innovative interventions.</p>

<p>The nephron is viewed as comprising a series of distinct segments, each of which expresses essential solute transport proteins. While cell diversity within these segments has been noted for many years, the more recent development of transcriptomic analyses has revealed previously unrecognized cell type diversity. We have used the INTACT approach to enrich for distal convoluted tubule and thick ascending limb cells for RNA-Seq. This approach confirmed that there are subsegments along the distal convoluted tubule that serve different functions with respect to solute transport. We found that magnesium transport is restricted to early parts of the distal convoluted tubule whereas calcium and potassium transport occurs in later segments. Dietary potassium restriction altered cell states along this segment, favoring potassium reabsorption but at the expense of more sodium reabsorption and hypertension. Along the thick ascending limb, we found that there are three distinct cell types, only one of which corresponds to the Burg/Greger model of apical potassium recycling. These cells are ringed by claudin 10, which mediates paracellular sodium reabsorption. A second cell type does not recycle potassium or generate a voltage, but instead reabsorbs the divalent cations, calcium and magnesium, through tight junctions that express claudin 16. A third cell type, found only in the inner stripe of the outer medulla also lacks an apical potassium channel, but appears prepared to reabsorb potassium across the cell. The recognition of cellular diversity along these segments provides important new insights into how the kidney responds to dietary challenge and maintains homeostasis.</p>

<p>Bartter syndrome (BS) is the most common congenital renal tubulopathy affecting infants and young children. BS type 3, which accounts for approximately 75% of BS cases, is caused by mutations in the CLCNKB gene, responsible for encoding the voltage-gated chloride channel ClC-Kb. This channel is highly expressed in the basolateral membrane of the thick ascending limbs (TAL) and distal convoluted tubules (DCT). The prevailing view of BS pathogenesis is that mutations impair transepithelial transport, resulting in early-onset renal salt wasting, hypovolemia, and failure to thrive. Our recent study shows that ClC-Kb plays a crucial role in the elongation of thick ascending limbs during mouse kidney development. When ClC-Kb is deleted after the developmental stage, the mouse phenotype is much milder, indicating that early effects of ClC-Kb on renal tubules are critical to BS pathogenesis. Next, multi-omics analyses of isolated TALs and DCTs reveal that ClC-Kb deficiency causes G2/M cell cycle arrest, delays cell proliferation, reduces mitochondrial biogenesis and bioenergetics, and induces apoptosis. These cellular responses can also be triggered by inhibitors of sodium chloride transporters, suggesting that decreased transport activity, coupled with downregulated mitochondrial mass and respiration, can lead to apoptosis, inflammation, and cell cycle arrest in TALs and DCTs during the neonatal stage of BS.</p>

<p>The prevalence of hypertension increases with age and is a major risk factor for cardiovascular and cerebrovascular diseases, making its management an important clinical goal. However, the incidence of treatment-resistant hypertension is rising, and the use of antihypertensive medications frequently leads to orthostatic or postprandial hypotension in elderly individuals. These complications often result in suboptimal blood pressure control. Therefore, the development of new therapeutic strategies tailored to the pathophysiology of older adults is urgently needed.</p><p>Age-associated hypertension has long been suspected to involve increased salt intake and enhanced salt sensitivity; however, the precise mechanisms remain unclear. Clinical studies have shown that serum levels of the anti-aging factor Klotho decline with age. To investigate whether this serum Klotho deficiency contributes to enhanced salt sensitivity and hypertension with aging, we examined blood pressure responses in aged mice and Klotho heterozygous knockout mice with reduced circulating Klotho levels.</p><p>Upon administration of a high-salt diet, Klotho-deficient mice exhibited marked salt-sensitive hypertension. We further demonstrated that in the arteries of these models, the non-canonical Wnt5a–RhoA signaling pathway, which promotes vascular contraction, was activated in response to high salt intake, leading to augmented vasoconstriction and elevated blood pressure. In vascular smooth muscle, Wnt5a signaling modulates Angiotensin II-induced responses, suggesting a key role in the development of hypertension in aged animals.</p><p>Importantly, the elevation in blood pressure observed in aged mice during high-salt feeding was significantly suppressed by Klotho supplementation, Wnt5a inhibitor, or Rho kinase inhibitor. These findings indicate that dietary salt restriction is a beneficial preventive strategy for aging-associated hypertension and that novel therapies, such as Klotho replacement, Klotho-mimetic compounds, and Wnt5a pathway inhibitors, hold promise as effective treatments adapted to the pathophysiological characteristics of elderly hypertensive patients.</p>

<p>Selecting an appropriate dialysate sodium concentration is a critical issue in hemodialysis management. The optimal level depends on each patient’s clinical condition and baseline serum sodium status. Low-sodium dialysate has been proposed to improve blood pressure control, reduce interdialytic weight gain, and lessen cardiovascular stress from sodium overload. However, several disadvantages limit its broad application. First, low dialysate sodium increases the risk of intradialytic hypotension. By lowering plasma osmolality, it promotes rapid osmotic fluid shifts from the intravascular to the intracellular compartment, reducing effective circulating volume and predisposing patients to symptomatic blood pressure drops, cramps, nausea, and dizziness. These hemodynamic disturbances may require early termination of dialysis or additional nursing interventions. Second, rapid declines in plasma sodium may precipitate dialysis disequilibrium syndrome, especially in patients with markedly elevated pre-dialysis sodium or new dialysis initiates. Third, repeated exposure to low-sodium dialysate is associated with chronic hyponatremia, which has been linked to increased mortality, cognitive impairment, falls, and muscle weakness. Long-term use may also exacerbate the malnutrition–inflammation cycle through recurrent hypotensive episodes and gastrointestinal discomfort. Additionally, individualized sodium prescriptions demand frequent monitoring and adjustments, increasing clinical workload and limiting standardization. Evidence supporting long-term cardiovascular benefit remains inconsistent, with some studies suggesting potential harm from recurrent hypotension and electrolyte shifts.</p><p> Conversely, high dialysate sodium concentrations can improve intradialytic hemodynamic stability, reduce cramps, and lessen disequilibrium symptoms. By maintaining higher plasma osmolality, they help preserve intravascular volume and support blood pressure during treatment. Nevertheless, high-sodium dialysate can also increase thirst, promote greater interdialytic fluid intake, and lead to larger interdialytic weight gains. Over time, excessive sodium exposure may contribute to hypertension, left ventricular remodeling, and higher cardiovascular risk. Thus, while high-sodium dialysate mitigates acute symptoms, it may predispose patients to long-term fluid overload and cardiovascular complications.</p><p> In conclusion, both low and high dialysate sodium prescriptions carry important trade-offs. Individualized sodium profiling and further large-scale, high-quality trials are needed to optimize sodium targets and balance acute hemodynamic benefits against long-term cardiovascular outcomes. AI-based evaluation systems may also help determine patient-specific dialysate sodium levels to enhance precision and safety in hemodialysis care.</p>

<p>Hemodialysis is essential for patients with end-stage kidney disease, yet treatment-related complications remain a major challenge. Intradialytic hypotension (IDH) is among the most frequent and serious events, contributing to myocardial ischemia, cerebral hypoperfusion, cognitive decline, loss of residual kidney function, cardiovascular events, and increased mortality. Maintaining hemodynamic stability during dialysis is therefore a key clinical priority.</p><p>Dialysate temperature plays an important but often overlooked role in intradialytic hemodynamics. Traditionally, dialysate has been set at 36.5–37.0°C, approximating core body temperature and minimizing patient discomfort. However, standard temperatures may inadvertently cause heat accumulation, peripheral vasodilation, and reductions in plasma volume, thereby promoting IDH. In this context, cooled dialysate (≤35–36°C) has been proposed as a preventive strategy.</p><p>Clinical evidence indicates several potential benefits of cooling. Randomized controlled trials and meta-analyses consistently demonstrate a 30–70% reduction in IDH episodes, alongside evidence for organ protection through reduced myocardial stunning and cerebral ischemia. Some studies also suggest improvements in post-dialysis fatigue and cognitive decline.</p><p>However, cooled dialysis is not without limitations. Patient discomfort, including chills and shivering, is the most common barrier to acceptance. Furthermore, its impact on long-term outcomes remains uncertain. The MY TEMP trial, a large multicenter study, did not show significant reductions in mortality or major cardiovascular events with cooled versus standard temperatures, highlighting the gap between short-term hemodynamic benefits and long-term prognosis.</p><p>Recent discussion has shifted from a binary question of “to cool or not to cool” toward individualized temperature prescriptions. Strategies include tailoring dialysate to 0.5°C below baseline core temperature or applying real-time feedback systems that dynamically adjust temperature to balance stability and comfort. High-risk cardiovascular patients may benefit most, while elderly or thermosensitive patients may tolerate only modest reductions.</p><p>In summary, dialysate temperature is more than a technical setting; it is a therapeutic parameter that directly influences patient safety, quality of life, and potentially long-term outcomes. Cooled dialysis offers strong evidence for IDH prevention and organ protection, yet challenges of tolerability and uncertain survival benefit remain. This presentation will review current evidence, controversies, and future directions for optimizing dialysate temperature in personalized hemodialysis.</p>

<p>Expanded Hemodialysis (HDx), which employs medium cut-off (MCO) membranes, is an innovative dialysis modality introduced into clinical practice in the past decade. It enhances clearance of large middle molecules (15–60 kDa)—inefficiently removed by conventional high-flux hemodialysis (HD)—without requiring substitution fluid, thereby offering hemodiafiltration (HDF)-like efficacy through standard HD infrastructure. Owing to its ease of implementation and potential clinical benefits, HDx has garnered global attention as a next-generation renal replacement therapy.</p><p> Proponents of HDx highlight its enhanced removal of uremic toxins (e.g., β2-microglobulin, κ/λ free light chains, TNF-α), reduction in systemic inflammation, potential cardiovascular protection, better patient-reported outcomes, and possible healthcare cost savings. Observational studies report reduced hospitalizations and improvements in symptoms such as pruritus, fatigue, and recovery time. HDx may also preserve residual kidney function and offer environmental benefits compared to online HDF.</p><p> However, the evidence base remains insufficient to justify universal adoption. No large-scale randomized controlled trials (RCTs) have demonstrated significant reductions in mortality or cardiovascular events with HDx. Meta-analyses and cohort studies have not demonstrated superiority over high-flux HD or HDF in hard clinical outcomes. Although albumin loss with HDx is generally modest (1.5–2.5 g/session), it may pose a risk for malnourished patients. Additionally, the higher cost of MCO dialyzers and uncertainties regarding long-term safety and immunologic effects remain barriers to broader adoption. Given the heterogeneity of dialysis populations, a "one-size-fits-all" approach appears premature.</p><p> In conclusion, HDx is a promising and practical innovation with meaningful clinical potential. A tailored, patient-centered approach—guided by symptom profile, individual goals, and care context—remains the most prudent path forward. Specific patient subgroups—such as those with a high inflammatory burden, refractory pruritus, or preserved residual kidney function—may derive the greatest benefit. Broad implementation should await confirmatory evidence from large multinational trials demonstrating clear clinical advantage and cost-effectiveness, particularly in the Asia-Pacific region, where resource availability and reimbursement models vary considerably.</p>

<p>This consensus statement summarizes the recommendations from Taiwanese experts on vaccination strategies for patients with chronic kidney disease (CKD) and kidney transplant recipients. The guidance focuses on six key vaccines: respiratory syncytial virus (RSV), herpes zoster, pneumococcal, hepatitis B, influenza, and COVID-19 vaccines. These patient populations face heightened susceptibility to severe infections and suboptimal vaccine responses due to impaired immunity. Expert consensus highlights the importance of early vaccination planning, the preference for adjuvanted or recombinant formulations where applicable, and the timing of vaccination in relation to dialysis initiation or transplantation to maximize immunogenicity. The statement also addresses special considerations, including booster schedules, serologic monitoring for hepatitis B, and prioritization of vaccines during periods of intensified immunosuppression. Through these recommendations, the panel aims to reduce vaccine-preventable morbidity and mortality in CKD and kidney transplant populations in Taiwan and to harmonize clinical practice with evolving international evidence.</p>

<p>With the rapid increase in dialysis patients in South Korea, disaster preparedness for end-stage kidney disease (ESKD) patients has become a critical issue. Currently, approximately 127,000 patients require renal replacement therapy, with 78% undergoing hemodialysis. These patients are particularly vulnerable during disasters, necessitating specialized response strategies. In June 2022, the Korean Society of Nephrology (KSN) established the Disaster Preparedness and Response Committee, leveraging expertise from past experiences with MERS (2015) and COVID-19.</p><p>Key initiatives include infection control protocols such as cohort isolation strategies, which significantly reduced secondary transmission during the COVID-19 pandemic, as well as disaster response systems for dialysis units to address power outages, earthquakes, and emerging infectious diseases. Collaboration with national and international organizations, including the National Emergency Medical Center (NEMC) and the Japanese Society for Dialysis Therapy (JSDT), has been central to these efforts. A Korean-Style Disaster Response Dietary Plan for Hemodialysis Patients has been developed to ensure adequate nutrition during emergencies, incorporating traditional dietary patterns with evidence-based nutritional guidelines. Additionally, disaster preparedness surveys among dialysis staff revealed significant gaps in training and access to emergency response information, highlighting the need for realistic disaster drills and structured education programs.</p><p>Moving forward, the committee will strengthen collaboration with the ISN Renal Disaster Preparedness Working Group (ISN RDPWG) from 2025, reinforcing international cooperation in dialysis disaster management. Furthermore, within the Asian Pacific Society of Nephrology & Taiwan Society of Nephrology (APSN x TSN), closer collaboration between KSN is needed to enhance leadership and joint efforts in disaster response for dialysis patients. By integrating evidence-based policies, expanding professional networks, and strengthening regional cooperation, these efforts aim to improve the resilience of dialysis units and ensure continuity of care for ESKD patients in future disasters.</p>

<p>The impact of natural disasters on the provision of dialysis services has received increased attention following Hurricane Katrina devastating New Orleans in 2005. The Asia-Pacific is particularly vulnerable to earthquakes, tsunami, typhoons (also known as cyclones and hurricanes) or storms and flooding. These events can seriously interrupt provision of dialysis, especially haemodialysis, with adverse effects for patients including missed dialysis, increased hospitalization and post-traumatic stress disorder. Furthermore, haemodialysis patients may need to relocate and experience prolonged periods of displacement from family and social supports. In contrast to haemodialysis, most literature suggests peritoneal dialysis in a disaster situation is more easily managed and supported. It has become apparent that dialysis units and patients should be prepared for a disaster event and that appropriate planning will result in reduced confusion and adverse outcomes should a disaster occur. Numerous resources are now available to guide dialysis units, patients and staff in preparation for a possible disaster. The session will examine the disaster experiences of dialysis units in the Asia-Pacific, the impact on patients and staff, methods employed to manage during the disaster and suggested plans for reducing the impact of future disasters in the Asia-Pacific region.</p>

<p>Background: Gut dysbiosis is a well-recognized feature of chronic kidney disease (CKD). Modulating the gut microbiota has emerged as a potential therapeutic strategy to target the gut–kidney axis, yet the specific live biotherapeutic candidates and the mechanisms underlying their renoprotective effects remain insufficiently defined.</p><p>Methods: Fecal samples from 228 CKD patients (discovery cohort, 16S rRNA sequencing) and 93 CKD patients (validation cohort, shotgun metagenomic sequencing) were analyzed to identify candidate strains for live biotherapeutic product development. Bacteroides species were identified as the most discriminatory taxa associated with CKD. Clinical isolates of Bacteroides spp were subsequently obtained from 10 healthy individuals. High-fat diet (mild CKD) and adenine-induced (moderate CKD) mouse models were used to examine causal effects. Multi-omics profiling—including microbiome, immune profiling, single-cell RNA sequencing, and spatial transcriptomics—was performed to elucidate mechanisms of gut–kidney interaction following Bacteroides administration.</p><p>Results: Oral colonization with Bacteroides spp significantly improved renal morphology (reduced podocyte foot process effacement) and function (lower microalbuminuria) in both CKD models. Metabolically, treatment lowered glucose, cholesterol, TNF-α, IL-1α, and IL-1β levels. Single-cell and spatial transcriptomic analyses demonstrated that Bacteroides spp attenuated kidney immune dysregulation, reversing CKD-associated upregulation of inflammation-related and ferroptosis gene pathways. Metabolically, Bacteroides-treated CKD mice exhibited differential expression of genes involved in fatty acid metabolism, glycolysis and bile acid metabolism pathways.</p><p>Conclusion: These findings highlight Bacteroides spp as a compelling live biotherapeutic candidate for CKD, offering a promising microbiome-based approach to ameliorate renal dysfunction.</p><p>Keywords: Bacteroides spp, ferroptosis, inflammation, microbiome, single-cell sequencing, spatial transcriptomics.</p>

<p>Cardiovascular disease, kidney disease, and metabolic disorders like obesity and type 2 diabetes are closely linked. In 2023, the American Heart Association introduced cardiovascular-kidney-metabolic (CKM) syndrome to improve prevention, risk assessment, and management of these interconnected conditions. CKM syndrome arises from excess or dysfunctional adipose tissue, triggering inflammation, oxidative stress, insulin resistance, and vascular dysfunction. These processes drive metabolic risk factors, kidney disease progression, and cardiovascular complications. Additionally, the gut microbiome plays a key role in CKM syndrome. Over the past decade, research has highlighted trimethylamine-N-oxide (TMAO) as a contributor to cardiovascular and kidney disease. Beyond TMAO, two novel uremic toxins—phenylacetylglutamine and phenyl sulfate—have emerged as potential drivers of CKM syndrome, further linking gut microbial metabolism to disease progression.</p>

<p>Chronic kidney disease (CKD) is projected the 5th leading cause of death by 2040 and incurs an enormous health expenditure worldwide. A systematic analysis from the Global Burden of Disease study showed that 11 million global deaths and 255 million DALYs were attributable to poor diet and dietary risk factors. These dietary factors contributed significantly to a huge burden of non-communicable diseases including hypertension, cardiovascular disease and type 2 diabetes globally that are all closely associated with CKD. The pivotal role of nutrition management in preserving kidney health, slowing the progression of CKD and delaying the need for kidney replacement therapy (KRT) is well recognized. There is recent increased recognition of a precision medicine approach in implementing nutrition management. Due to ethnic differences in dietary and lifestyle habit, diversity in genetic make-up, intra-individual variations in implementing dietary therapy, psychosocial factors, and dietary adherence issues, these factors may all contribute to the heterogeneity in treatment responses and impacts clinical outcomes. It brings in the evolving concept of the need of a ‘precision medicine approach’ in</p><p>nutrition management, that is nutrition management should be tailored and individualized not only according to clinical manifestations but also to genetic make-up and biologic responses to therapy, which may vary depending on genetic composition and likelihood adherence to the dietary therapy. Precision nutrition management should also take into account patient demo graphics, social, psychological, education, and compliance factors, which may all influence the therapeutic needs and responses to the nutrition therapy prescribed. In this talk, I will discuss the novel precision medicine approach for nutrition management in patients with CKD including those with transition to dialysis.</p>

<p>In recent years, our understanding of IgA nephropathy has evolved rapidly, leading to significant updates in the KDIGO 2025 Clinical Practice Guideline. These new recommendations reflect both advances in disease mechanisms and results from pivotal randomized clinical trials.</p><p>The guideline now emphasizes a risk-based and patient-centered approach. Diagnosis still relies on kidney biopsy, but the International IgAN Prediction Tools have become valuable instruments to estimate each patient’s risk of progression and to guide shared decision-making. This reflects a move toward individualized management rather than a one-size-fits-all strategy.</p><p>Supportive care continues to be the foundation of therapy. Key elements include strict blood pressure control—ideally below 120 mmHg—reduction of proteinuria through optimized RAS inhibition, and lifestyle measures such as sodium restriction and regular exercise. The guideline also highlights the renal and cardiovascular benefits of SGLT2 inhibitors, which are now recommended for most proteinuric CKD patients, regardless of diabetes status.</p><p>For patients at higher risk despite optimal supportive care, targeted treatments are now formally included. A nine-month course of targeted-release budesonide (Nefecon) is suggested as first-line therapy to suppress mucosal IgA production and reduce proteinuria. When this is unavailable, reduced-dose systemic glucocorticoids remain an alternative. In addition, dual endothelin–angiotensin receptor blockade with sparsentan has demonstrated additive kidney protection.</p><p>Overall, the KDIGO 2025 guideline integrates traditional supportive therapy with new immunomodulatory and targeted approaches, providing a more precise and evidence-based roadmap for clinicians. In my presentation, I will summarize these key updates and discuss how they are changing the global standard of care for IgA nephropathy—moving from generalized treatment toward personalized, mechanism-guided therapy. </p>

<p>Hyperparathyroidism (HPT), particularly secondary hyperparathyroidism (SHPT) in chronic kidney disease (CKD), is associated with multiple systemic complications beyond bone disease. Excessive parathyroid hormone (PTH) contributes significantly to protein-energy wasting (PEW), sarcopenia, and nutritional decline in dialysis patients. Elevated PTH levels are linked to reductions in serum albumin and body mass index (BMI), indicating poor nutritional status. These effects are dose-dependent, with progressively worse outcomes observed in patients with higher PTH levels (≥1500 pg/mL). The pathophysiology of PEW in HPT involves increased resting energy expenditure due to PTH-induced browning of white adipose tissue. This process upregulates thermogenic genes, resulting in energy dissipation and skeletal muscle catabolism, ultimately contributing to sarcopenia and weight loss. Additionally, high PTH levels impair appetite and promote inflammation, further exacerbating nutritional deterioration. Evidence from observational studies demonstrates that patients who underwent parathyroidectomy (PTX) experienced improvements in nutritional markers compared to non-PTX counterparts. These improvements include significant increases in BMI, serum albumin, and creatinine indexed to body surface area (Cr/BSA), which reflect better muscle mass and nutritional recovery. Moreover, PTX has been associated with decreased mortality, particularly in patients with more severe HPT and PEW. While calcimimetics are effective medical therapies for SHPT, surgical PTX remains a critical option when medical management fails. PTX offers superior control of PTH and mineral metabolism, which translates into better clinical outcomes, including improved bone mineral density and reversal of PEW. Despite its benefits, guidelines lack specific recommendations regarding optimal timing and indications for PTX, underscoring the need for individualized clinical decision-making. </p><p>In conclusion, hyperparathyroidism plays a pivotal role in the development of PEW and sarcopenia in CKD. Timely and effective management can reverse nutritional impairment and improve survival in affected patients.</p>

<p>The role of diet in the management of chronic kidney disease (CKD) has traditionally centered around protein restriction and nutrient control in advanced stages. Over the years, observational and interventional studies have expanded this perspective, highlighting how overall dietary patterns, sodium and potassium intake, acid-base balance, and plant-based nutrition can influence CKD progression, metabolic health, and cardiovascular risk.</p><p>In this lecture, I will begin by revisiting key evidence on the impact of dietary factors in CKD, including previous findings from our KNOW-CKD cohort demonstrating the associations of sodium, potassium, and vegetable intake with kidney outcomes. I will then introduce recent epidemiologic data from large-scale cohorts, with a particular focus on the type of dietary protein—a question that remains under-addressed in clinical guidelines.</p><p>Building on this, I will present new findings from our UK Biobank study involving over 117,000 adults, showing that higher plant protein intake is independently associated with a lower risk of incident CKD, based on both ICD-coded outcomes and eGFR-based definitions. These associations were consistent across multiple models and sensitivity analyses, and were further supported by favorable metabolic profiles.</p><p>I will also discuss plausible biologic mechanisms—including reduced dietary acid load, improved blood pressure, inflammation, and gut microbiome health—as well as practical considerations regarding protein quality and adequacy in plant-based diets. Finally, I will reflect on how these findings fit within the context of current KDIGO and KDOQI guidelines, which remain cautious about protein type but increasingly recognize the value of plant-forward dietary patterns in CKD care.</p><p>This talk will provide a broad yet focused update on the evolving understanding of dietary protein quality in kidney health, with relevance to both prevention and clinical management.</p>

<p>Uremic sarcopenia is a complex and multifactorial condition commonly observed in patients with chronic kidney disease (CKD), particularly those undergoing dialysis. This presentation reviews the application of sarcopenia screening tools and diagnostic criteria—originally developed for older adults—to end-stage renal disease (ESRD) patients, highlighting unique considerations in this population. Beyond age-related factors, muscle wasting in uremic sarcopenia is driven by inflammation, myostatin overexpression, accumulation of uremic toxins, hyperparathyroidism, vascular dysfunction, and a complex interplay of other pathophysiological mechanisms. We emphasize that atherosclerotic cardiovascular disease and subclinical vascular dysfunction play significant roles in the pathogenesis of uremic sarcopenia. In clinical practice, multidisciplinary strategies—including tailored nutritional support, exercise interventions, patient education, and management of underlying conditions—are warranted to mitigate muscle loss. Nevertheless, treatment outcomes remain limited, underscoring the urgent need for novel therapeutic approaches.</p>

<p>The International Network of Chronic Kidney Disease (iNET-CKD) is a collaborative, multinational initiative designed to generate high-quality built on harmonized data from cohort studies worldwide, the iNET-CKD cohort provides a unique opportunity to examine regional similarities and differences in CKD progression, and mortality risk. Diagnosis, treatment uptake, and disparities in care, with a particular focus on the cardio–kidney–metabolic interface. We will also discuss the implications of these findings for clinical practice, research prioritization, and policy, emphasizing how iNET-CKD can serve as a platform for global learning in nephrology. The insights from this international cohort underscore the urgent need for earlier detection strategies, equitable access to effective therapies, and context-specific interventions to improve CKD outcomes across diverse populations.</p>

<p>The J-Kidney-Biobank was launched in 2020 under the auspices of the Japanese Society of Nephrology as the nationwide biobank dedicated to kidney diseases in Japan. Its mission is to establish a comprehensive research platform that accelerates mechanistic insights, enhances risk stratification, and ultimately advances precision medicine for patients with kidney disorders.</p><p>To date, approximately 2,600 patients have been recruited from 12 university hospitals across Japan. For each participant, detailed information has been systematically collected, including questionnaires, electronic health records, and biospecimens such as plasma, urine, and DNA. Nearly all participants are accompanied by genome-wide data generated through genotyping and imputation, enabling large-scale genetic analyses. In addition, metabolomic profiling has been performed in a subset of participants, creating a rich multi-omics resource. Importantly, the J-Kidney-Biobank has been developed in close collaboration with the Tohoku Medical Megabank, facilitating harmonization with broader national genomic initiatives and expanding opportunities for integrative research.</p><p>This talk will reflect on the conceptualization and development of the J-Kidney-Biobank, highlighting strategic approaches, innovations, and challenges encountered throughout its establishment. Particular emphasis will be placed on harmonizing clinical data collection across multiple sites, integrating diverse biospecimens with genomic information, ensuring robust data governance and ethical oversight, and fostering long-term sustainability through collaboration among clinicians, researchers, and the national society.</p><p>Beyond its infrastructure, I will also introduce ongoing research projects that are beginning to leverage this resource. These studies range from genetic epidemiology and biomarker discovery to integrative omics analyses, and are already yielding new insights into the molecular basis of kidney disease in the Japanese population. Looking ahead, the biobank is expected to contribute not only to research in Japan but also to global kidney research, by enabling international collaborations and data-sharing initiatives that place Japanese data in a worldwide context.</p><p>Through this journey, we have gained both a research resource of significant scientific value and key lessons about the organizational, ethical, and logistical dimensions of building disease-specific biobanks in Japan. By sharing our experiences, we hope to provide a model that will inform future biobank initiatives in nephrology and beyond.</p>

<p>With the steadily increasing prevalence of end-stage renal disease, the demand for efficient dialysis management continues to grow. The dialysis center at Taipei Veterans General Hospital (VGHTPE) operates with 75 outpatient beds, 15 inpatient beds, and an intensive care unit, providing three to four treatment sessions daily. Prior to digitization in 2015, dialysis scheduling relied entirely on manual documentation, requiring nursing staff to transcribe patient dynamics and treatment modalities onto individual cards. A comprehensive 2014 audit revealed dialysis scheduling completeness was only 54.7%, creating significant risks for incomplete scheduling and potential treatment delays that compromised patient safety and care quality.</p><p> Recognizing the growing trend toward electronic health systems, our hemodialysis center embarked on a comprehensive Digitalized Scheduling and Integration System in 2015. We implemented an Electronic Whiteboard Dialysis Scheduling System that seamlessly integrates dialysis treatment dynamics with advanced information management. This intelligent system automatically downloads dialysis schedules and physician orders, eliminating manual data entry. Treatment parameters are automatically transferred to electronic forms without human transcription, and the system provides automatic digital signatures immediately uploaded to the hospital's centralized electronic medical record system. This automation significantly reduces human error while improving both the timeliness and accuracy of documentation.</p><p> Expanding our digital capabilities, we implemented a specialized Digitalized Scheduling and Integration System in 2020 for intensive care dialysis. For patients receiving Continuous Veno-Venous Hemofiltration (CVVH), this system integrates and analyzes patient treatment information in real time. Healthcare providers can continuously monitor treatment parameter accuracy and immediately track physician order modifications during ongoing treatment.</p><p> Beyond operational improvements, this digital transformation enhanced patient and family experience through improved convenience and accuracy. The technology fostered better communication between healthcare providers and patients, creating favorable impressions of our hospital's digital infrastructure and commitment to quality care.</p><p>Keywords: Hemodialysis, Digitalized Scheduling, Continuous Veno-Venous Hemofiltration</p>

<p>The coronavirus disease pandemic has underscored the urgent need for efficient remote communication and innovative patient education strategies. With the increasing adoption of digital and social media platforms in Taiwan, we developed an Artificial Intelligence (AI)-based LINE Chatbot designed to improve the self-care capacity of patients undergoing peritoneal dialysis (PD). From May 1, 2021, to April 30, 2022, we implemented an automated Chatbot system that integrated six major interactive modules: instructional videos for PD techniques, clinical reminders, home care guidance, hospital registration services, dietary recommendations, and automated guidance for both continuous ambulatory and automated peritoneal dialysis. Patient satisfaction was evaluated three months after initiation using a Likert scale ranging from 1 to 5, with higher scores reflecting greater satisfaction.</p><p>A total of 440 PD patients participated in the program, of whom 297 completed the satisfaction survey. Among respondents, 91.7% reported overall satisfaction with the Chatbot, while 86.6% assigned scores higher than 4 points. Analysis of clickstream data across modules revealed valuable insights into patient needs and potential care scenarios. Furthermore, clinical outcomes demonstrated significant improvements: the rates of catheter exit-site and tunnel infections decreased significantly (p = .049 and .024, respectively), and the peritonitis rate declined from 0.93 to 0.80 episodes per 100 patient-months following Chatbot use. These findings suggest that the AI Chatbot is comparable to traditional face-to-face education in supporting effective self-management for PD patients.</p><p>In conclusion, the AI-driven LINE Chatbot successfully provided remote, personalized, and digital health education, thereby enhancing patient self-care ability while achieving high satisfaction levels. This innovative approach demonstrates strong potential for integration into PD care and warrants further investigation to determine its long-term impact and broader clinical applicability.</p>

<p>Kidney involvement is more common in childhood systemic lupus erythematosus (SLE), affecting more than 70% of Singapore children with SLE. Longitudinal studies have reported a rate of up to 15% of chronic kidney disease stage 5 in children with lupus nephritis. Currently steroid therapy is the standard of care of childhood lupus nephritis. In a large international cohort study of 382 children from 23 centers, induction therapy comprised of steroids in 95% of children, with 70% receiving intravenous methylprednisolone, together with other immunosuppressive agents such as cyclophosphamide (50%), mycophenolate (46%), azathioprine (14%) and rituximab (15%). A major concern in children with severe lupus nephritis treated with aggressive immunosuppression is therefore cumulative cyclophosphamide and steroid-related toxicities, in particular growth retardation. In our study, children with severe proliferative forms of lupus nephritis were treated with a multi-targeted regimen with monthly pulse methylprednisolone for 6 months, together with mycophenolate for induction and the addition of calcineurin inhibitor for children with moderate to severe proteinuria. This allowed oral prednisolone to be tapered rapidly to at least an alternate day dosing to minimize steroid toxicity. The majority had serological remission by 6 months, with more than 90% achieving complete renal remission by 1 year. 37.5% of patients were able to stop all steroid therapy, whereas another 50% were able to taper to low dose alternate day steroids. With long-term mycophenolate maintenance therapy, the cumulative relapse free survival at 10 years was 73.3%, with non-adherence to the twice daily medications being the main contributor to lupus relapses. This cohort of children were able to maintain normal height velocities compared to the older cohort using cyclophosphamide/azathioprine as maintenance therapy. The role of B cell therapies in childhood lupus nephritis is also well described, where rituximab has been shown to have a satisfactory profile regarding efficacy and safety, and may therefore also allow reduction of the steroid dose. Finally, therapy in childhood lupus nephritis should be individualized as the disease has a variable course and complications where modification of the standard protocols may be necessary.</p>

<p>Lupus nephritis remains one of the most severe manifestations of systemic lupus erythematosus, contributing to significant morbidity, mortality, and healthcare burden worldwide. This presentation will review its epidemiology, including geographic and ethnic variations. Clinical outcomes and latest treatment goals will be discussed, and the role of repeat kidney biopsies. Recent insights from real-world data will also be highlighted. Finally, ongoing challenges and opportunities for personalised management strategies for patients with lupus nephritis will be discussed.</p>

<p>Professor Huang Qiujin of the China Medical University Hospital began promoting home hemodialysis in 2008. It is the first hospital in Taiwan to implement home hemodialysis. After establishing a remote hemodialysis information transmission system in 2016, it can monitor patients' home hemodialysis treatment parameters online in real time, and provide abnormal warnings and abnormal processing feedback to the patient side for abnormal conditions, greatly increasing the safety of home hemodialysis. As of October 2025, a total of 30 patients have completed home hemodialysis training and returned home to perform home hemodialysis treatment. We would like to take this opportunity to share the current status of home hemodialysis in Taiwan and the experience of home hemodialysis training..</p>

<p>Before patients undergoing renal replacement therapy (KFRT) receive renal replacement therapy, they should engage in shared decision-making. Hospitals have a responsibility to provide patients with comprehensive KFRT dialysis mode selection education and implement shared decision-making to help them fully understand peritoneal dialysis. The Peritoneal Dialysis Center at National Taiwan University Hospital has developed a 3D-printed peritoneal dialysis educational tool that allows for a visual perspective of the peritoneal cavity to facilitate dialysis mode selection. The 3D-printed simulated peritoneal dialysis tool introduced clinical shared decision-making regarding dialysis mode selection, increasing the percentage of patients choosing peritoneal dialysis from 34.6% to 53.8%. The chi-square analysis (p-value = .027) was statistically significant. This tool helps patients choose a dialysis mode that meets their needs, enhances their understanding of peritoneal dialysis treatment, and allows them to choose a dialysis mode that is appropriate for them. When patients begin dialysis treatment, they improve their quality of life and return to social life at work.</p>

<p>Taiwan has continued to promote a nationwide on-site evaluation system for hemodialysis institutions. In 2023, a total of 724 facilities underwent evaluation. The nursing assessment focused on three main domains: nursing administration (including nursing management and material management), patient care (including nursing care and patient education), and nursing quality management (covering patient safety and dialysis care monitoring).The results showed stable performance in large hospitals. However, some clinic-level facilities still showed room for improvement in areas such as medication and material management, infection control, and quality monitoring documentation. On average, 87.41% of nursing staff had over three years of clinical dialysis experience, reflecting a stable and experienced nursing workforce.Overall satisfaction with the on-site evaluation process exceeded 95%, highlighting the positive value of this system in enhancing care quality and fostering professional dialogue.</p>

<p>This presentation outlines the nationwide on-site evaluation framework for peritoneal dialysis (PD) programs in Taiwan. The auditing system encompasses multiple domains, including patient safety, infection control, emergency preparedness, medical record integrity, dialysis adequacy monitoring, anemia and mineral-bone disorder management, cardiovascular surveillance, complication tracking, preservation of residual kidney function, nursing administration, PD training standards, home-care assessment, and incident-reporting mechanisms. By integrating these components, the evaluation provides a standardized, comprehensive approach to assessing PD practice quality across institutions. The audit structure also reflects Taiwan's commitment to strengthening home-based dialysis care, promoting consistent clinical standards, and aligning practice with international expectations for PD quality and safety.</p>

<p>Provide and an overview of regulatory T cell biology, clinical translation of regulatory T cells for prevention of rejection in kidney transplantation. Provide results of phase 1 and phase 2 trials</p>

<p>Artificial Intelligence (AI) and Deep Learning (DL) hold great promise to transform pathology practice. Currently, the vast majority of commercially available products and AI research focuses on cancer use cases and end-to-end AI, i.e., an approach in which the model learns all the steps between the initial input and the final output, providing qualitative or semiquantitative (class) data. A complementary or alternative approach to analyze histomorphology is using DL-based segmentation of relevant histological compartments and cells, followed by the extraction of relevant quantitative data (features). If done on a large scale, it is termed pathomics, representing a novel -omics approach for morphology at the microscopical level. Pathomics complements molecular omics, like genomics or transcriptomics, or radiomics, which aims at quantifying radiology images at the macroscopic level. This lecture will explore the potential of AI and pathomics in kidney transplant pathology and pathology in general.</p>

<p>For patients with end-stage renal disease, a kidney transplant is the best treatment. However, recipients must take lifelong immunosuppressive medications to prevent their bodies from rejecting the transplanted organ. These drugs carry significant side effects and increase the risk of infections and other diseases.</p><p>Cell therapy is an innovative and promising area of research aimed at improving kidney transplant outcomes and reducing the need for these medications. The goal is to induce immune tolerance, teaching the recipient's immune system to accept the donor kidney as its own. Hematopoietic stem cells and different regulatory cells have been studied to achieve immune tolerance in the recipients. Besides the immune tolerance goal, cell therapy is also used in infectious disease treatment. Virus-specific T cell therapy has been developed for various viral infections in patients with solid organ transplants.</p>

<p>In recent years, genome analysis has been rapidly advancing toward larger and more comprehensive scales. In the field of nephrology, large-scale international initiatives such as the UK Biobank and the CKDGen Consortium have already been established. However, in Japan, there had previously been no biobank specifically focused on kidney diseases.</p><p>To address this gap, the project titled “Risk stratification and establishment of personalized medicine for diabetic kidney disease and chronic kidney disease with elaborate disease registrations and a conprehensive analysis of genomic and environmental factors” was launched in fiscal year 2018 under the Japan Agency for Medical Research and Development (AMED) Genome Medicine Platform Program. Since then, this biobank has been referred to as the J-Kidney Biobank.</p><p>A distinctive feature of the J-Kidney Biobank is its comprehensive approach to analyzing multifactorial mechanisms involving not only genetic but also lifestyle and environmental factors. To this end, the biobank collects genomic data, metabolomic data (from plasma and urine), and detailed clinical information. All biospecimens are collected and managed by the Tohoku Medical Megabank Organization (ToMMo). Collaborative studies utilizing these samples and datasets have been conducted jointly with ToMMo, and several results have already been reported.</p><p>In one such study, data from 475 J-Kidney Biobank participants were integrated with data from approximately 13,000 participants of the Tohoku Medical Megabank Project’s Community-Based Cohort Study (Miyagi Prefecture). A genome-wide association study (GWAS) was then performed focusing on chronic kidney disease (CKD) and kidney function parameters such as estimated glomerular filtration rate (eGFR) and urinary albumin-to-creatinine ratio (UACR).</p><p>In this session, I will introduce the key characteristics of the J-Kidney Biobank and highlight part of our analytical findings.</p>

<p>The KOrea Renal Biobank NEtwoRk System TOward NExt-generation analysis (KORNERSTONE), the renal division of the Korea Biobank Project, has established a nationwide infrastructure enabling integrative multiomic research in glomerular diseases. This platform links systematically collected biospecimens—including snap-frozen and FFPE kidney biopsy tissues, peripheral blood mononuclear cells (PBMCs), plasma, and genomic DNA—with deep clinical phenotyping to support advanced omics pipelines.</p><p>Single-nucleus RNA sequencing is used to construct a disease-stratified, cell-type-resolved transcriptomic atlas of the kidney. PBMCs are analyzed with paired single-cell RNA and ATAC sequencing to uncover systemic immune perturbations and epigenetic states. Spatial transcriptomics (GeoMx, Xenium) preserves tissue architecture, enabling localization of transcriptional changes across glomerular and tubular compartments. Proteomic platforms such as Olink and imaging mass cytometry provide orthogonal protein-level validation in both tissue and blood samples. Recent additions to the platform include long-read RNA sequencing to identify full-length transcript isoforms and alternative splicing events in kidney tissue, and TCR/BCR 5′ repertoire sequencing to characterize adaptive immune landscapes across glomerular disease phenotypes.</p><p>Together, these pipelines enable integrative, high-resolution analysis of kidney disease biology and support biomarker discovery and therapeutic innovation. By anchoring molecular data to a robust biobank with detailed clinical context, the KORNERSTONE framework advances precision nephrology in an ethnically homogenous but clinically diverse population.</p>

<p>Childhood Idiopathic nephrotic syndrome is an important paediatric kidney disease associated with significant morbidities and even mortality. Anti-CD20 has now become an important therapeutic option in the management of this devastating condition. In the recent years, there are major breakthroughs in the disease management and the understanding of underlying pathogenesis through multi-omic investigations, including the identification of anti-nephrin autoantibodies, genetic susceptibility loci and the pathogenic role of B-cell subsets. Furthermore, several deep B cell depleting strategies have been described in the literatures and are being investigated in on-going trials. The aim of this talk is to summarise the recent major advancements in idiopathic nephrotic syndrome and attempt to provide potential therapeutic approaches in both steroid sensitive and steroid resistant nephrotic syndrome that may shape future therapeutic landscape.</p>

<p>The KDIGO definition and staging of acute kidney injury (AKI) has been used to guide clinical care in pediatric AKI. AKI is defined by an increase in serum creatinine to 1.5-1.9 times baseline within the prior 7 days or an increase of serum creatinine by ≥0.3 mg/dL (≥26.5 umol/L) within 48 hours. However, in the newborn, the serum creatinine in the first 2-3 days of life often reflects maternal levels, making it an unreliable marker of renal dysfunction. With regards to the serum creatinine criteria based on the large neonatal cohort study (AWAKEN), the optimal rise in serum creatinine that predicted mortality was 54.5 umol/L for gestational age ≤29 weeks, and 26.5 umol/L for gestational age >29 weeks. In addition, for newborns, the urine output criteria also differs from those >7 days. Another confounder to the use of serum creatinine is the long half-life of about 4 hours in the serum in patients with normal GFR. Following a 50% reduction in GFR where the half-life of serum creatinine is now doubled, it needs 3-5 half- lives to reach a new steady-state level of creatinine, resulting in delay in AKI diagnosis of up to 24-72 hours following the event that precipitated the reduction in GFR. Recently, the renal angina index has been proposed to try to detect early signs of AKI. This is based on a combination of AKI risk factors and early signs of kidney injury in order to predict severe AKI 3 days after PICU admission. </p><p>The frusemide stress test tests the functional reserve of the kidney and has been shown to predict development of AKI in children post cardiopulmonary bypass if the urine flow rate is <3.6 ml/kg/h at 2 hours post frusemide. </p><p>The early adaptive response of the stressed kidney can provide biomarkers that inform pathophysiology and early diagnosis. These include inflammatory biomarkers such as NGAL, IL6 and IL18, cell injury biomarkers such as KIM-1 and L-FABP, and cell cycle markers such as urinary TIMP-2 and IGFBP-7. A difficulty in using these biomarkers in pediatrics is the lack of age specific cut-offs.</p><p>In summary, early diagnosis of AKI is important in order to inform on potential therapeutic interventions.</p>

<p>Hemodiafiltration (HDF), a dialysis method that combines the two main principles of hemodialysis (HD) and hemofiltration — diffusion and convection — has had a positive impact on survival when delivered with a high convective dose. A number of biologically plausible explanations have been suggested for improved outcomes with HDF: HDF removes middle molecular weight uremic toxins including inflammatory cytokines, increases hemodynamic stability, and reduces inflammation and oxidative stress compared to conventional HD. </p><p>Randomized trials and meta-analyses in adults have shown improved survival with HDF compared to high-flux HD. A large prospective cohort study in children has shown that HDF attenuated the progression of cardiovascular disease, improved bone turnover and growth, reduced inflammation and improved blood pressure control compared to conventional HD. Importantly, children on HDF reported fewer headaches, dizziness and cramps and had increased physical activity and improved school attendance compared to those on HD.</p><p>In this talk I will discuss the technical aspects of HDF and results from pediatric studies, comparing outcomes on HDF vs conventional HD. Convective volume, the corner-stone of treatment with HDF, and a key determinant of outcomes in adult RCTs, is discussed in detail, including the practical aspects of achieving an optimal convective volume.</p>