American Journal of Nephrology最新文献

{"title":"Electrolytes Abnormalities in Cancer Patients.","authors":"Arash Rashidi, Nada Youssef, Biruh Workeneh, Alex Carsel, Victoria Gutgarts, Sheron Latcha","doi":"10.1159/000544877","DOIUrl":"https://doi.org/10.1159/000544877","url":null,"abstract":"<p><strong>Background: </strong>Electrolyte disorders are common in cancer patients and have significant impacts on treatment outcomes and quality of life. The frequency, severity, complexity and etiology of fluid and electrolyte disorders is different among cancer patients when compared to the general population.</p><p><strong>Summary: </strong>This review describes the key electrolyte imbalances and pathogenesis, including sodium disorders, potassium disorders, and abnormalities in magnesium, calcium, and phosphorus levels, within the context of cancer therapies. Cancer specific therapies reviewed surgical and radiologic therapies, cellular therapies, use of checkpoint inhibitors and traditional cytotoxic chemotherapy that can result in specific patterns of electrolyte derangements.</p><p><strong>Key message: </strong>The objective of this article is to highlight clinical presentations and to discuss management of some cancer specific electrolyte disturbances. This article underscores the importance of regular electrolyte monitoring and timely intervention in managing cancer patients.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1-20"},"PeriodicalIF":4.3,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143497967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Five-Year Time Profiles of Clearances of Different Uremic Solutes in Incident Peritoneal Dialysis Patients.","authors":"Ji Ji, Min Lu, Shulan Guo, Bo Xiang, Weiwei Wu, Yang Li, Xiaoyan Jiao, Jun Ji, Xiaoqiang Ding, Xiaofang Yu","doi":"10.1159/000543622","DOIUrl":"10.1159/000543622","url":null,"abstract":"<p><strong>Introduction: </strong>Different uremic solutes have varying degrees of clearances owing to different chemical properties and the pathological and physiological changes in the kidneys and peritoneum.</p><p><strong>Methods: </strong>The 5-year time profiles of renal, peritoneal, and total clearances of creatinine, urea nitrogen (UN), uric acid (UA), trimethylamine <sc>n</sc>-oxide (TMAO), phosphate, beta-2-microglobulin (β2-MG), interleukin-6 (IL-6), indoxyl sulfate (IS), and p-cresol sulfate (PCS) were investigated in 64 peritoneal dialysis (PD) patients. The patients were divided into an early start and a late start group according to baseline estimated glomerular filtration rate to investigate the effect of dialysis initiation timing on uremic solutes clearances. Patients were also divided into incremental peritoneal dialysis (IPD) and full-dose PD groups to investigate the impact of PD strategy on uremic solutes clearances.</p><p><strong>Results: </strong>Peritoneal clearances of creatinine, UN, UA, and phosphate increased over time, while the peritoneal clearance of IL-6 showed a downward trend. The peritoneal clearances of TMAO, β2-MG, IS, and PCS did not change significantly. Patients in early start group showed a lower level of variation and a higher average of renal clearances. IPD patients had a higher level of total clearances of uremic solutes than full-dose PD patients in the first 3 years after PD initiation.</p><p><strong>Conclusion: </strong>In a long-term follow-up period, the peritoneal clearance of water-soluble small solutes increased over time, but that of protein-bound toxins and middle molecules did not. Initiating PD when residual kidney function remains at a relatively high level and performing IPD may better improve the efficiency of PD and help preserve the renal clearances of uremic solutes.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1-12"},"PeriodicalIF":4.3,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143497969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adjunctive Active Vitamin D Decreases Kidney Function during Treatment of Secondary Hyperparathyroidism with Extended-Release Calcifediol in Non-Dialysis Chronic Kidney Disease in a Randomized Trial.","authors":"Akhtar Ashfaq, John Choe, Stephen A Strugnell, Nilay Patel, Stuart M Sprague, Keith C Norris, Edgar Lerma, P Martin Petkovich, Charles W Bishop","doi":"10.1159/000544086","DOIUrl":"10.1159/000544086","url":null,"abstract":"<p><strong>Introduction: </strong>Sustained 30% reductions of intact parathyroid hormone (iPTH) with extended-release calcifediol (ERC) are associated with slower decline in estimated glomerular filtration rate (eGFR) in non-dialysis chronic kidney disease (ND-CKD) patients with secondary hyperparathyroidism (SHPT). Such iPTH reductions usually require elevation of serum total 25-hydroxyvitamin D (25D) to ≥50 ng/mL, but achieving these reductions can be limited by the ERC dose ceiling (60 μg/day), raising the question of whether adjunctive active vitamin D (adj AVD) might be appropriate to further reduce iPTH.</p><p><strong>Methods: </strong>This randomized controlled trial (RCT) examined whether adj AVD could safely increase iPTH reductions achieved with ERC and further reduce the rate of eGFR decline in 78 ND-CKD adults treated with ERC for 38 weeks. Participants had mean age of 66 years, body mass index of 35 kg/m2, were 41% female, 63% white, 36% black, 19% Hispanic. At ERC initiation, participants had plasma iPTH 85-<500 pg/mL, eGFR 15-<60 mL/min/1.73 m2, serum 25D 10-<30 ng/mL, corrected serum calcium (Ca) 8.4-<9.8 mg/dL, serum phosphorus (P) 2.0-<5.0 mg/dL, and absence of macroalbuminuria (>3 g/g creatinine). At baseline (BL; week 38), participants had plasma iPTH >70 pg/mL and serum Ca <9.8 mg/dL and were randomized 3:1:1:1 to daily ERC (60 μg) for 14 additional weeks with (n = 40) or without (n = 38) adj daily oral calcitriol (0.25 μg), doxercalciferol (0.5 μg), or paricalcitol (1.0 μg). Measurements of eGFR, iPTH, 25D, Ca, P, and fibroblast growth factor 23 (FGF23) were obtained at BL and through end of treatment (EOT).</p><p><strong>Results: </strong>No significant intergroup differences were observed at BL. Mean 25D at BL was 65 ng/mL and rose 14 ng/mL by EOT in both groups (p < 0.001). Mean BL iPTH was 137 pg/mL and fell by a further 35.4% (p < 0.001) with adj AVD therapy versus 2.2% without. Mean Ca, P, and FGF23 increased with adj AVD by 0.40 mg/dL (p < 0.001), 0.27 mg/dL (p < 0.01), and 49.1 pg/mL (155%; p < 0.001), respectively, but remained unchanged with ERC alone. Mean BL eGFR was 25.4 mL/min/1.73 m2 and fell by 11.8% (p < 0.05) with adj AVD versus 3.0% without.</p><p><strong>Conclusion: </strong>Adj AVD at these doses enabled 35% more iPTH reduction in ND-CKD patients with mild to moderate SHPT on long-term ERC treatment but increased mean serum Ca and P by 0.40 and 0.27 mg/dL, respectively, FGF23 by more than 2-fold, and eGFR decline by 4-fold, suggesting that adding AVD to ERC has untoward effects that override the nephrosparing impact of iPTH reductions with ERC treatment alone. Corroboration is warranted with a larger, longer RCT.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1-10"},"PeriodicalIF":4.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fibroblast Growth Factor 23, Endogenous Erythropoietin, Erythropoiesis-Stimulating Agents, and Erythropoietin Resistance in Hemodialysis Patients.","authors":"Naoto Hamano, Hirotaka Komaba, Hisae Tanaka, Hiroo Takahashi, Yuichiro Takahashi, Toru Hyodo, Miho Hida, Takao Suga, Takehiko Wada, Takatoshi Kakuta, Masafumi Fukagawa","doi":"10.1159/000543506","DOIUrl":"https://doi.org/10.1159/000543506","url":null,"abstract":"<p><strong>Introduction: </strong>Recent experimental studies have reported that fibroblast growth factor 23 (FGF23) inhibits erythropoiesis by suppressing erythropoietin (EPO) production and downregulating the EPO receptor. Conversely, either endogenous or exogenous EPO has been shown to stimulate FGF23 production. However, little is known about the relationships between FGF23, erythropoiesis-stimulating agent (ESA) treatment, ESA resistance, and endogenous EPO in hemodialysis patients.</p><p><strong>Methods: </strong>We analyzed cross-sectional data from a cohort of 654 maintenance hemodialysis patients. We examined the associations of intact or C-terminal FGF23 with ESA treatment, ESA resistance index (ERI), hemoglobin, C-reactive protein, and endogenous EPO levels using linear regression models. EPO was measured only in patients not receiving ESAs.</p><p><strong>Results: </strong>A total of 458 patients (70%) were treated with ESAs. The median EPO concentration in non-ESA users was 7.8 (interquartile range, 5.3-14.4) mIU/mL. The median levels of intact and C-terminal FGF23 were 1,598 (interquartile range, 548-4,586) pg/mL and 38.7 (interquartile range, 14.0-127.6) pmol/L, respectively, in non-ESA users and 1,955 (interquartile range, 573-5,264) pg/mL and 41.4 (interquartile range, 13.9-116.8) pmol/L, respectively, in ESA users. After adjustment for potential confounders, higher ESA dose was associated with higher FGF23 levels measured by both intact and C-terminal assays. Higher C-terminal FGF23 was also associated with higher ERI, lower hemoglobin, and higher endogenous EPO, but no such associations were observed for intact FGF23 levels.</p><p><strong>Conclusions: </strong>Both intact and C-terminal FGF23 showed similar associations with ESA dose, but they showed different patterns of association with other parameters related to anemia. Further research is needed to elucidate the mechanisms underlying these different associations.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1-9"},"PeriodicalIF":4.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143466494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunotherapy and Cellular Therapies for Cancers in Kidney Transplant Patients.","authors":"Massini Merzkani, Rose Mary Attieh, Kenar D Jhaveri, Naoka Murakami","doi":"10.1159/000544826","DOIUrl":"10.1159/000544826","url":null,"abstract":"<p><strong>Background: </strong>Kidney transplant is the treatment of choice for end-stage kidney disease, with longer survival and better quality of life posttransplant. However, long-term immunosuppression comes with an increased risk of cancer and infection. Cancer is one of the leading causes of death after kidney transplant. While novel cancer therapies become available, transplant recipients are usually excluded from clinical trials.</p><p><strong>Summary: </strong>In this review, we summarize the updated knowledge on immunosuppression management in kidney transplant recipients treated with immune checkpoint inhibitors (ICIs), bispecific T-cell engager therapy, and chimeric antigen receptor (CAR)-T-cell therapies.</p><p><strong>Key messages: </strong>Transplant nephrologists should be empowered to participate in the decision-making of cancer treatment together with patients, care partners, and oncologists, by managing immunosuppression.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1-14"},"PeriodicalIF":4.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143466542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Supplement-Induced Acute Kidney Injury Reproduced in Kidney Organoids.","authors":"Hiroyuki Nakanoh, Kenji Tsuji, Kazuhiko Fukushima, Soichiro Haraguchi, Shinji Kitamura, Jun Wada","doi":"10.1159/000544795","DOIUrl":"10.1159/000544795","url":null,"abstract":"<p><strong>Introduction: </strong>Acute kidney injury associated with the consumption of Beni-koji CholesteHelp supplements, which contain red yeast rice (Beni-Koji), has become a significant public health concern in Japan. While renal biopsy findings from several case reports have suggested tubular damage, no definitive causal relationship has been established, and the underlying mechanisms of kidney injury remain poorly understood. The complexity of identifying toxic substances in supplements containing various bioactive compounds makes conventional investigative approaches both time-consuming and challenging. This highlights an urgent need to establish a reliable platform for assessing organ-specific toxicity in such supplements. In this study, we utilized a kidney organoid model derived from adult rat kidney stem cells (KS cells) to assess the potential tubular toxicity of these supplements.</p><p><strong>Methods: </strong>KS cell clusters were cultured in three-dimensional system supplemented with growth factors to promote kidney organoids. The organoids were subsequently exposed to Beni-koji CholesteHelp supplements or cisplatin, followed by histological and molecular analyses to evaluate structural impacts.</p><p><strong>Results: </strong>Established organoids had the kidney-like structures including tubular-like structures and glomerulus-like structures at the tips of multiple tubules. Treatment with Beni-koji CholesteHelp supplements induced significant tubular damage in the organoids, characterized by epithelial cell thinning, structural disruption, and increase in cleaved-caspase 3-positive apoptotic tubular cells, similar to the organoids treated with cisplatin.</p><p><strong>Conclusion: </strong>These findings provide the first evidence suggesting that certain toxicants in specific batches of Beni-koji CholesteHelp supplements cause direct renal tubular injury. This KS cell-based organoid system represents a cost-effective, reproducible, and technically simple platform for nephrotoxicity screening.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1-9"},"PeriodicalIF":4.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143466508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum.","authors":"","doi":"10.1159/000543485","DOIUrl":"https://doi.org/10.1159/000543485","url":null,"abstract":"","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1"},"PeriodicalIF":4.3,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143412847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DOT1L regulates cellular senescence during the progression from acute kidney injury to chronic kidney disease via the micro-222-5p/WNT9B signaling pathway.","authors":"Congcong Yao, Wei Wei, Guoyu Wu, Yan Zhang, Keke Sun, Zhiyuan Liu, Yushanjiang Abudureheman, Heng Wu, Qi Lv, Ayinuer Paredong, Songtao Shou, Heng Jin","doi":"10.1159/000544694","DOIUrl":"https://doi.org/10.1159/000544694","url":null,"abstract":"<p><strong>Background: </strong>Acute kidney injury (AKI) is a common clinical condition where cellular senescence plays a crucial role in its progression. Previous studies have suggested that DOT1L plays a pivotal role in cellular senescence, yet its specific mechanisms in regulating AKI cellular senescence remain unclear.</p><p><strong>Methods: </strong>This study utilized a glycerol-induced in vivo AKI model and employed the DOT1L-specific inhibitor EPZ004777 (EPZ) to suppress DOT1L function. Aging staining, PAS staining, and Masson staining were employed to assess renal aging, injury, and interstitial fibrosis. In vitro experiments utilized doxorubicin-treated human kidney tubular epithelial (HK-2) cells to establish an AKI cellular senescence model. EPZ was used to inhibit DOT1L, evaluating its impact on cellular senescence. High-throughput miRNA sequencing was performed to analyze differential expression of miRNAs downstream of DOT1L, and DOT1L overexpression and dual luciferase reporter gene experiments were conducted to explore interactions among DOT1L, miR-222-5p, and WNT9B.</p><p><strong>Results: </strong>The results demonstrated that in vivo inhibition of DOT1L significantly reduced cellular senescence and improved renal tubular injury and interstitial fibrosis. In the doxorubicin -induced HK-2 cell model, DOT1L inhibition markedly decreased cellular senescence and lowered mRNA and protein levels of senescence markers, while alleviating cell cycle arrest. DOT1L inhibition notably upregulated miR-222-5p expression and suppressed WNT9B expression, with opposite effects observed with DOT1L overexpression.</p><p><strong>Conclusion: </strong>DOT1L regulates cellular senescence through the miR-222-5p/WNT9B pathway in AKI. These findings suggest that DOT1L may serve as a potential therapeutic target to mitigate the progression of AKI to chronic kidney disease.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1-20"},"PeriodicalIF":4.3,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143405051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Value of Diffusion Kurtosis Imaging to Assess Liver and Kidney Recovery after Mesenchymal Stem Cell Intervention in CCl4-Induced Cirrhotic Rats.","authors":"Jiaming Qin, Shuangshuang Xie, Yongquan Yu, Cheng Zhang, Yumeng Zhao, Dan Tong, Zhandong Hu, Jinxia Zhu, Wen Shen","doi":"10.1159/000544056","DOIUrl":"10.1159/000544056","url":null,"abstract":"<p><strong>Introduction: </strong>The aim of the study was to investigate the potential of diffusion kurtosis imaging (DKI) in monitoring the improvement of liver and kidney injury in cirrhotic rats after bone marrow-derived mesenchymal stem cell (BMSCs) treatment.</p><p><strong>Methods: </strong>Thirty rats were induced with liver cirrhosis via subcutaneous injection of carbon tetrachloride. Six rats were randomly selected for DKI scanning and subsequently euthanized for biochemical and histological analysis. The remaining 24 rats were randomly divided into a BMSC group (n = 12) and a control group (n = 12). In the BMSC group, six rats underwent dynamic DKI scans and were sacrificed after 13, 14, 15, and 16 weeks, while the other 6 rats were sacrificed after being scanned in the 14th week. The control group followed the same protocol as the BMSC group. Additionally, six normal rats were euthanized after undergoing DKI scanning to provide baseline data. Liver and kidney DKI parameters, biochemical markers, liver fibers, kidney hematoxylin and eosin (HE) score, and alpha smooth muscle actin (α-SMA) were analyzed.</p><p><strong>Results: </strong>Compared to baseline, there was a significant increase in liver fibers and kidney HE scores by week 12. At weeks 13, 14, 15, and 16, the mean kurtosis (MK) of the liver in the BMSC group was significantly lower than that at week 12 and in the control group. At week 16, the mean diffusion in the BMSC group was significantly higher than that at week 12 and in the control group. The apparent diffusivity coefficient (ADC) values in the BMSC group were higher than those at week 12 and in the control group at weeks 13, 14, and 16. All regions of kidney showed decreased MK values from weeks 14-16 compared to week 12 and the control group. Liver fiber was moderately or highly correlated with all DKI parameters. MK and ADC of the renal cortex and outer stripe of the outer medulla showed moderate correlation with HE scores and α-SMA.</p><p><strong>Conclusion: </strong>DKI can serve as a non-invasive means to effectively monitor the process of liver and kidney injury improvement in cirrhotic rats treated with BMSCs.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1-15"},"PeriodicalIF":4.3,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143397762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gender Differences in Kidney Failure incidence in Australia: a Registry study.","authors":"Belinda C Stallard, Stephen P McDonald","doi":"10.1159/000543663","DOIUrl":"https://doi.org/10.1159/000543663","url":null,"abstract":"<p><p>Introduction Previous studies have shown that there is a higher incidence of men initiating kidney replacement therapy (KRT) in comparison to women. However, the contribution of gender disparity may well differ among the different types of kidney disease, and over time. Utilising a nationwide Registry, we examined disease- and gender-specific trends in incident kidney failure required KRT. Methods Registry-based analysis of all incident patients commencing KRT in Australia using data from the Australia and New Zealand Dialysis and Transplant (ANZDATA) Registry. All patients who initiated dialysis in Australia from January 1971 to 31 December 2021 were included. Confidence intervals around rates were calculated and compared using Poisson distributions. Results During the study period a total of 31834 women and 47718 men were recorded in ANZDATA to have commenced KRT in Australia, a male to female ratio of 1.51 [1.49-1.53]. The male to female ratio increased over time from 1.05 [0.83-1.34] in 1971 to 1.78 [1.66-1.92] in 2021. There was a progressive increase in the male:female ratio with age; for those starting in 2017-21 this rose from 1.37 [95% CI 1.26-1.50] among 25-44 years olds to 4.38 [2.47-5.53] among those ≥85 years at KRT start. Conclusions Men had a significantly higher rate of starting KRT in Australia compared with women, and this difference is increasing over time. This disparity also varied between types of primary kidney disease but was higher among older age groups. It is still seen for causes (such as polycystic kidney disease) that have equal gender disease distribution, suggesting differences in propensity to commence KRT as well as differences in underlying disease processes.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1-20"},"PeriodicalIF":4.3,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143121861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}