Clinical and Experimental Nephrology最新文献

{"title":"Urinary albumin fraction and tubulointerstitial injury: an association shaped by diagnostic composition.","authors":"Shun Minatoguchi, Yoshitaka Tatematsu, Toshiyuki Narimiya, Akira Yamashita, Masayasu Kojima, Ryosuke Umeda, Yuka Sato, Shigehisa Koide, Midori Hasegawa, Hiroki Hayashi, Daijo Inaguma, Naotake Tsuboi","doi":"10.1007/s10157-026-02942-6","DOIUrl":"https://doi.org/10.1007/s10157-026-02942-6","url":null,"abstract":"<p><strong>Background: </strong>Urinary protein composition provides qualitative information not captured by total protein excretion alone. Prior studies have linked low urinary albumin fraction to tubulointerstitial diseases and lesions, but whether this reflects pathology itself or diagnostic composition remains unclear. We investigated the association of urinary albumin fraction with tubulointerstitial lesions and diagnostic composition.</p><p><strong>Methods: </strong>We conducted a multicenter cross-sectional study of patients who underwent kidney biopsy at three referral centers. Urinary albumin fraction was obtained by urinary protein fraction analysis. Associations with interstitial fibrosis/tubular atrophy (IFTA) and inflammatory cell infiltration were examined overall and by diagnostic group. We also evaluated diagnostic composition in low urinary albumin fraction subgroups and the diagnostic performance for identifying tubulointerstitial disease.</p><p><strong>Results: </strong>A total of 462 patients was included. In the overall cohort, urinary albumin fraction differed significantly across IFTA grades (ANOVA p <0.001). In linear regression, IFTA grade 4 was associated with a significantly lower urinary albumin fraction than IFTA grade 0 (β - 22.10, 95% CI - 29.77 to - 14.43, p <0.001), but this association was no longer evident after adjustment for diagnostic group (β 4.13, 95% CI - 2.98 to 11.23, p = 0.294). The low urinary albumin fraction subgroups included not only tubulointerstitial diseases but also a substantial number of vasculitis cases.</p><p><strong>Conclusion: </strong>In this study, the apparent association between low urinary albumin fraction and tubulointerstitial lesions was largely explained by diagnostic group composition. Low urinary albumin fraction may serve as a supplementary clue to tubulointerstitial disease, but is neither disease-specific nor interpretable in isolation.</p>","PeriodicalId":10349,"journal":{"name":"Clinical and Experimental Nephrology","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pediatric IgA vasculitis nephritis: Japanese guidance in the context of IPNA and KDIGO recommendations.","authors":"John Dotis","doi":"10.1007/s10157-026-02932-8","DOIUrl":"10.1007/s10157-026-02932-8","url":null,"abstract":"","PeriodicalId":10349,"journal":{"name":"Clinical and Experimental Nephrology","volume":" ","pages":"1380-1381"},"PeriodicalIF":2.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148700954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Energy metabolism in the kidney and its role in chronic kidney disease.","authors":"Hiroaki Kikuchi, Tomohiro Tsuboya, Jinming Hu, Mari Sugimoto, Miyu Yoshikawa, Maho Usui, Takefumi Suzuki, Mark A Knepper, Shinichi Uchida, Eisei Sohara","doi":"10.1007/s10157-026-02923-9","DOIUrl":"10.1007/s10157-026-02923-9","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) is associated with dysregulated lipid metabolism, particularly in proximal kidney tubules, where fatty acid oxidation serves as the primary energy source. The proximal tubules' reliance on fatty acid oxidation rather than glycolysis underscores their unique metabolic profile, consistent with the absence of key glycolytic enzymes. This dysregulation contributes to maladaptive hypertrophy in CKD, where surviving nephrons exhibit compensatory hypertrophy to maintain kidney function. Here, we focus on two key regulators of lipid metabolism: peroxisome proliferator-activated receptor alpha (PPARα) and adenosine monophosphate (AMP)-activated protein kinase (AMPK). Recent multi-omics studies have identified PPARα as an important determinant of proximal tubule cell size and a mediator of compensatory hypertrophy. In CKD models, AMPK activity decreases, impairing cellular responses to energy stress, as indicated by altered AMP/ATP ratios. This defective energy sensing may be exacerbated by uremic metabolites that diminish AMPK function. Unc-51-like autophagy activating kinase 1 (ULK1) has been identified as a regulator of AMPK activity through specific phosphorylation sites that enhance AMP sensitivity. Future research should assess whether targeting these pathways restores metabolic homeostasis and mitigates CKD progression by enhancing AMPK activity and lipid metabolism.</p>","PeriodicalId":10349,"journal":{"name":"Clinical and Experimental Nephrology","volume":" ","pages":"1261-1269"},"PeriodicalIF":2.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13518396/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148668648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kidney outcomes of coenzyme Q10 supplementation in patients with genetically confirmed CoQ10 nephropathy in Japan.","authors":"China Nagano, Katsumi Ushijima, Yuko Tezuka, Takayuki Okamoto, Yasuhiro Inaba, Akinori Miyazono, Naoko Takeda, Taro Aoki, Akira Mizutani, Hiroki Miyano, Masaki Yamamoto, Mariko Imai, Takehiko Kawaguchi, Toshiyuki Komiya, Masayuki Ishihara, Yoshiki Nagao, Naoaki Mikami, Yuta Inoki, Nana Sakakibara, Tomoko Horinouchi, Tomohiko Yamamura, Shingo Ishimori, Kandai Nozu","doi":"10.1007/s10157-026-02917-7","DOIUrl":"10.1007/s10157-026-02917-7","url":null,"abstract":"<p><strong>Background: </strong>Coenzyme Q10 (CoQ10) nephropathy is a rare mitochondrial kidney disease caused by defects in CoQ10 biosynthesis and represents a unique form of steroid-resistant nephrotic syndrome with a disease-specific therapy. However, data on treatment outcomes of this disease in Japanese patients remain limited.</p><p><strong>Methods: </strong>We conducted a retrospective observational study of Japanese patients. Patients with a genetically confirmed diagnosis of CoQ10 nephropathy who received CoQ10 supplementation and had available longitudinal clinical data were included. Changes in the urinary protein-to-creatinine ratio (UPCR) and estimated glomerular filtration rate before and after treatment were evaluated, and adverse events were assessed.</p><p><strong>Results: </strong>Twelve patients were included in the analysis. The median age at treatment initiation was 9.0 years, and COQ8B was the predominant causative gene (n = 11). One patient harbored a COQ6 variant. CoQ10 supplementation was initiated at a median dose of 10.0 mg/kg/day. The median UPCR decreased from 1.66 g/gCr at baseline to 0.19 g/gCr at 12 months, and 6/7 (86%) patients with available 12-month data achieved a ≥ 50% reduction in proteinuria. Kidney function remained stable, and no patients progressed to end-stage kidney disease during a median follow-up of 28.8 months. Adverse events were mild and did not lead to treatment discontinuation.</p><p><strong>Conclusions: </strong>In Japanese patients with CoQ10 nephropathy, CoQ10 supplementation was associated with a substantial reduction in proteinuria and stabilization of kidney function. These findings indicate the importance of early genetic diagnosis and prompt initiation of targeted therapy for this treatable hereditary kidney disease.</p>","PeriodicalId":10349,"journal":{"name":"Clinical and Experimental Nephrology","volume":" ","pages":"1341-1349"},"PeriodicalIF":2.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13518395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nationwide epidemiological survey of autosomal dominant polycystic kidney disease in Japan in 2022.","authors":"Shinya Nakatani, Keiichi Matsuzaki, Ryousuke Aoki, Satoko Ohfuji, Saori Nishio, Junichi Hoshino, Tatsuya Suwabe, Toshio Mochizuki, Koichi Nakanishi, Ken Tsuchiya, Shigeo Horie, Yoshitaka Isaka, Wakaba Fukushima, Yusuke Suzuki, Satoru Muto","doi":"10.1007/s10157-026-02894-x","DOIUrl":"10.1007/s10157-026-02894-x","url":null,"abstract":"<p><strong>Background: </strong>Accurate epidemiological data on autosomal dominant polycystic kidney disease (ADPKD) are essential for healthcare planning and therapeutic strategies. However, nationwide prevalence estimates in Japan have not been updated for decades.</p><p><strong>Methods: </strong>This was a nationwide survey conducted in Japan. Departments at hospitals were selected using stratified random sampling based on specialty and hospital size. The number of patients with ADPKD not receiving kidney replacement therapy (KRT), defined in this study as those who did not receive dialysis and did not newly undergo kidney transplantation in 2022, was estimated by taking into account sampling fractions and response rates. Data on dialysis and kidney transplantation were obtained from the Web-Based Analysis of Dialysis Data Archives (WADDA) system and the Japanese Renal Transplant Registry.</p><p><strong>Results: </strong>Among 11,690 departments, 2,148 were selected (nephrology, n = 842; urology, n = 678; pediatrics, n = 628). The response rate was 32.9%. In 2022, the estimated number of patients with ADPKD not receiving KRT was 40,901 (95% confidence interval [CI], 29,543-52,259), corresponding to 32.7 per 100,000 population (1 in 3,055 individuals). Additionally, 12,487 patients with polycystic kidney disease (PKD) were receiving dialysis and 130 underwent kidney transplantation in 2022. After incorporating these data, the total population potentially representing ADPKD was estimated at 53,518 (42.8 per 100,000 population; 1 in 2,335 individuals).</p><p><strong>Conclusions: </strong>This nationwide survey provides updated epidemiological estimates of ADPKD. Although registry data on KRT may not exclusively represent ADPKD, our findings suggest a higher disease burden than previously recognized, with prevalence consistent with estimates reported in other countries.</p>","PeriodicalId":10349,"journal":{"name":"Clinical and Experimental Nephrology","volume":" ","pages":"1332-1340"},"PeriodicalIF":2.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148027730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of Arhgap24 alters glomerular ultrastructure in zebrafish model.","authors":"Koji Saito, Fumiya Furukawa, Nagako Kawashima, Manabu Tanaka, Shokichi Naito","doi":"10.1007/s10157-026-02921-x","DOIUrl":"10.1007/s10157-026-02921-x","url":null,"abstract":"<p><strong>Background: </strong>ARHGAP24, a GTPase-activating protein (GAP) for the Rho family small GTPase Rac1, is highly expressed in podocytes and is thought to contribute to maintaining glomerular filtration barrier. Variants in ARHGAP24 have been implicated in human kidney diseases. However, the physiological requirement of ARHGAP24 in podocytes remains unclear. Here, we generated an arhgap24 knockout (KO) zebrafish, a well-established model organism, to investigate the in vivo role of ARHGAP24 in podocytes.</p><p><strong>Methods: </strong>An arhgap24 KO zebrafish was generated using the CRISPR/Cas9 double-nicking method with paired CRISPR RNAs targeting sequences flanking an arginine residue essential for GAP activity to increase target specificity and minimize off-target effects. Glomerular and podocyte morphology in adult arhgap24-deficient zebrafish was examined by light, immunofluorescence, and electron microscopy.</p><p><strong>Results: </strong>We obtained a homozygous arhgap24 KO mutant lacking the catalytic arginine residue. Microscopic observations of the glomerulus in arhgap24-deficient zebrafish revealed widening of podocyte foot processes and glomerular basement membrane structural changes, including thickening, lamellation, spike-like extensions, and small electron-dense granules, which are typical features of glomerular and podocyte injury associated with disrupted glomerular filtration barrier.</p><p><strong>Conclusion: </strong>arhgap24 deficiency altered glomerular ultrastructure in zebrafish. This study provides initial evidence for an in vivo role of ARHGAP24 and suggests a potential link to human kidney disease.</p>","PeriodicalId":10349,"journal":{"name":"Clinical and Experimental Nephrology","volume":" ","pages":"1282-1291"},"PeriodicalIF":2.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148577244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimizing low-dose rituximab protocol for ABO-mismatched kidney transplantation: long-term outcomes in a single-center retrospective cohort study.","authors":"Tomoaki Yamanoi, Takanori Sekito, Moto Tokunaga, Ichiro Tsuboi, Kasumi Yoshinaga, Yuki Maruyama, Tatsushi Kawada, Risa Kubota, Yusuke Tominaga, Takuya Sadahira, Satoshi Katayama, Takehiro Iwata, Shingo Nishimura, Kensuke Bekku, Yasuhiro Onishi, Hidemi Takeuchi, Katsuyuki Tanabe, Hiroshi Morinaga, Koichiro Wada, Motoo Araki","doi":"10.1007/s10157-026-02882-1","DOIUrl":"10.1007/s10157-026-02882-1","url":null,"abstract":"<p><strong>Background: </strong>ABO-mismatched kidney transplantation (KTx) expands donor availability but increases risks of antibody-mediated rejection and passenger lymphocyte syndrome (PLS). While rituximab (Rit) potentially mitigates these complications, conventional high-dose regimens (375 mg/m²) elevate infectious and hematologic toxicity. We implemented low-dose Rit induction (200 mg/body) for desensitization in minor/major ABO-mismatched and DSA-positive KTx, evaluating its efficacy and safety over 15-years.</p><p><strong>Methods: </strong>This single-center retrospective cohort (May 2009-April 2024) analyzed 161 adult KTx recipients: Rit (n = 107) and Non-Rit (n = 54) groups. All received tacrolimus, mycophenolate mofetil, prednisolone, and basiliximab; high-risk patients also underwent plasmapheresis. Outcomes included graft survival, biopsy-proven acute rejection, de novo donor-specific antibody (DSA) formation, infection, severe neutropenia, and PLS.</p><p><strong>Results: </strong>1-year graft survival was 100% in both groups. 5-year death-censored graft survival was 95.8% (Rit) vs 95.9% (Non-Rit), respectively (log-rank P = 0.43). Biopsy-proven acute rejection (7.5% vs 3.7%, P = 0.50) and de novo DSA production were equivalent (Class I: 5.5% vs 2.2%; Class II: 6.6% vs 8.7%; both P = 1.00), with lower mean fluorescent intensity (MFI) in the Rit group. Cytomegalovirus disease, urinary tract infection and fungal infection rates were comparable between both groups. Grade 4 neutropenia was not associated with Rit (OR 2.65; 95% CI 0.63-11.0; P = 0.18). Blood transfusion for hemoglobin declines occurred in 5.6% vs 7.4%, with preserved haptoglobin in all cases, indicating no PLS.</p><p><strong>Conclusions: </strong>Low-dose Rit induction achieves excellent graft survival and effective PLS prevention, without increasing toxicity, supporting its adoption as an optimal desensitization strategy.</p>","PeriodicalId":10349,"journal":{"name":"Clinical and Experimental Nephrology","volume":" ","pages":"1359-1367"},"PeriodicalIF":2.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13518381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148027703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical and functional evaluation of non-missense MYH9 variants in MYH9-related disease.","authors":"Seiya Inoue, China Nagano, Masafumi Matsuo, Shuhei Aoyama, Yuka Kimura, Yuta Inoki, Nana Sakakibara, Tomoko Horinouchi, Tomohiko Yamamura, Shingo Ishimori, Kandai Nozu","doi":"10.1007/s10157-026-02893-y","DOIUrl":"10.1007/s10157-026-02893-y","url":null,"abstract":"<p><strong>Background: </strong>MYH9-related disease (MYH9-RD) is an autosomal dominant disorder characterized by thrombocytopenia, giant platelets, and variable systemic manifestations including nephropathy. While most pathogenic MYH9 variants are missense substitutions causing dominant-negative effects, the pathogenic potential of non-missense variants, particularly those affecting splicing, remains unclear.</p><p><strong>Methods: </strong>MYH9 (NM_002473.6) variants registered as \"DM\" (disease-causing variant) or \"DM?\" (possible disease-causing variant) in HGMD® were curated. After excluding missense and non-analyzable variants, ten intronic or single-base deletions were selected. Splicing effects were assessed by minigene assays in HEK293T cells and compared with SpliceAI predictions. Clinical information was reviewed.</p><p><strong>Results: </strong>Aberrant splicing was confirmed in three variants: c.3838-2A>G, c.5765+2T>A, and c.5765+2T>G. The c.3838-2A>G variant caused in-frame skipping of exon 29, non-truncating variant, whereas the latter two induced inclusion of a cryptic 50-bp exon with premature termination codons in the final exon that can escape nonsense-mediated decay. These spliceogenic variants were associated with MYH9-RD phenotypes producing abnormal proteins that likely exert dominant-negative effects. The remaining seven variants showed no splicing abnormalities and were reported in non-MYH9-RD contexts, suggesting limited evidence for pathogenicity. SpliceAI predictions were concordant with experimental results.</p><p><strong>Conclusions: </strong>This study provides systematic evidence that some aberrant splicing MYH9 variants can lead to MYH9-RD with dominant-negative pathogenesis. Conversely, several variants previously annotated as \"DM?\" showed no functional or clinical relevance, arguing against a pathogenic role and supporting their consideration as likely benign or uncertain significance. Integrating in silico prediction with experimental validation improves variant interpretation and has implications for the clinical management of MYH9-RD.</p>","PeriodicalId":10349,"journal":{"name":"Clinical and Experimental Nephrology","volume":" ","pages":"1324-1331"},"PeriodicalIF":2.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148027738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationships of high mean corpuscular volume, low total iron binding capacity and protein-energy wasting in patients on maintenance hemodialysis.","authors":"Misa Ikeda-Taniguchi, Keiichi Hirao, Keigo Shibagaki, Hirokazu Honda","doi":"10.1007/s10157-026-02887-w","DOIUrl":"10.1007/s10157-026-02887-w","url":null,"abstract":"<p><strong>Background: </strong>Recent studies have reported that high mean corpuscular volume (MCV) may be associated with mortality in chronic kidney disease patients. A high MCV is caused by erythropoietin-stimulating agent (ESA). Most patients with protein-energy wasting (PEW) have functional iron deficiency (FID) and need a high ESA dose. FID is associated with low total iron binding capacity (TIBC), which is a marker of iron status, malnutrition, and inflammation, and it may be a predictor of muscle loss. The relationships between high MCV and iron status markers in patients on hemodialysis (HD) are not well known. The aim of this study was to assess the relationships between high MCV and iron status markers in a cross-sectional and longitudinal study considering nutritional status, inflammation, muscle mass, and hydration status.</p><p><strong>Methods: </strong>A prospective cohort of 39 HD patients was examined for 12 months. The relationships between MCV and iron status markers (TIBC, ferritin, hepcidin-25, iron) were examined using multivariate linear regression analysis and multivariate repeated measures analysis.</p><p><strong>Results: </strong>At baseline, a high MCV (≥ 100 fL) was significantly related to low TIBC and low muscle mass. Multiple regression analysis showed that MCV was associated with low TIBC. On multivariate repeated measures analysis, MCV was associated with a sustained low TIBC, and proportion of PEW and ERI were associated with a sustained high MCV.</p><p><strong>Conclusion: </strong>High MCV was associated with low TIBC. Furthermore, a sustained high MCV suggested ESA hypo-responsiveness and tendency to iron use disorder and may be a useful marker of PEW.</p>","PeriodicalId":10349,"journal":{"name":"Clinical and Experimental Nephrology","volume":" ","pages":"1350-1358"},"PeriodicalIF":2.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13518378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148142906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transforming hemodialysis care: a tripartite collaboration model among medical staff, AI agents, and robots.","authors":"Ryunosuke Noda, Tsutomu Sakurada, Daisuke Ichikawa, Yugo Shibagaki","doi":"10.1007/s10157-026-02903-z","DOIUrl":"10.1007/s10157-026-02903-z","url":null,"abstract":"<p><p>Hemodialysis demand is rising as populations age and the chronic kidney disease burden increases, yet dialysis units face persistent workforce constraints and substantial increases in cognitive and physical workloads, making workload reduction an urgent priority. We propose a tripartite collaboration model in which medical staff, artificial intelligence agents, and robots redesign hemodialysis workflows at the task level. Artificial intelligence agents support non-physical work through three coordinated modules: \"Eye\" integrates and visualizes multimodal data from dialysis machines, electronic health records, laboratories, and home or wearable monitoring to highlight early signals of deterioration; \"Brain\" uses machine learning to predict complications such as intradialytic hypotension and to support optimization of dry-weight estimation, anemia and chronic kidney disease-mineral and bone disorder management, and prescription trade-offs through scenario simulation; and \"Language\", based on large language models, drafts structured session summaries and plain-language explanations anchored to verified data, with clinician review to mitigate hallucinations and omissions. Robots reduce physical workload through equipment preparation, transport, and environmental maintenance, and may extend to reproducible vascular access surveillance using robotic ultrasound and, in the longer term, assisted cannulation. Clinicians/medical staff remain accountable for goal setting, value-laden decisions, communication, and authorization of automated outputs and actions. We also summarize governance requirements-interoperability, human factors evaluation, privacy and cybersecurity, and staged deployment starting from low-risk, verifiable functions. By delegating routine cognitive and physical work while preserving human responsibility and relational care, the model may enable more proactive, patient-centered hemodialysis and support sustainable staffing and workload reduction.</p>","PeriodicalId":10349,"journal":{"name":"Clinical and Experimental Nephrology","volume":" ","pages":"1270-1281"},"PeriodicalIF":2.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148216777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}