Kidney360Pub Date : 2026-09-29DOI: 10.34067/KID.0000001385
Jonathan Marquez, Abbey A Scott, Lukas Kruidenier, Penny Chow, Jennifer C Hayek, Anita E Beck, Margaret P Adam, James T Bennett, Ian A Glass, Katrina M Dipple, Tara L Wenger, Elizabeth D Nguyen, Alexandra C Keefe
{"title":"Rapid Genome and Exome Sequencing as a First-Line Diagnostic Tool for Hospitalized Pediatric Kidney Disease Patients.","authors":"Jonathan Marquez, Abbey A Scott, Lukas Kruidenier, Penny Chow, Jennifer C Hayek, Anita E Beck, Margaret P Adam, James T Bennett, Ian A Glass, Katrina M Dipple, Tara L Wenger, Elizabeth D Nguyen, Alexandra C Keefe","doi":"10.34067/KID.0000001385","DOIUrl":"https://doi.org/10.34067/KID.0000001385","url":null,"abstract":"<p><strong>Background: </strong>Previous efforts have demonstrated the utility of exome sequencing approaches in improving diagnosis and management of kidney diseases with underlying genetic etiologies. Rapid clinical genome sequencing is increasingly used as a first line clinical diagnostic modality in the inpatient setting, yet its utility for individuals with kidney disease has not been examined.</p><p><strong>Methods: </strong>We conducted a retrospective analysis of pediatric inpatients with structural kidney abnormalities, pathological microscopic kidney abnormalities, and/or laboratory evidence of kidney disease who underwent rapid clinical genome or exome sequencing while hospitalized at a single tertiary pediatric center over a 42-month period. Diagnostic yield and the impact of genetic diagnoses on inpatient clinical management were assessed.</p><p><strong>Results: </strong>We identified 77 pediatric patients who met the study criteria, ranging in age from 1 day to 17 years at time of testing. Genetic variants considered explanatory or likely explanatory of the patient's phenotype were identified in 47% (36/77) of cases. Results spanned monogenic disorders caused by single nucleotide variants to multi-gene disorders ranging from large deletions or duplications, with explanatory findings across three defined categories (macroscopic, microscopic, and other). Among individuals given a genetic diagnosis, 92% (33/36) had results that were clinically actionable beyond disease-specific guidance, resulting in modifications to clinical management including targeted laboratory evaluations, imaging studies, subspecialty referrals, and initiation of gene-targeted therapies.</p><p><strong>Conclusions: </strong>Rapid exome or genome sequencing for pediatric inpatients with kidney disease yielded a diagnosis in 47% of cases, with high rates of actional clinical impact during the initial hospital admission.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kidney360Pub Date : 2026-09-28DOI: 10.34067/KID.0000001371
Muhammad Ibrahim Khan, Jielu Hao Robichaud, Humayra Afrin, Fouad T Chebib, Peter C Harris, Navin R Gupta
{"title":"The Polycystic Kidney Disease Cyst Transcriptome Defined by Integrating Spatial, Single Nuclear, and Bulk Transcriptomics.","authors":"Muhammad Ibrahim Khan, Jielu Hao Robichaud, Humayra Afrin, Fouad T Chebib, Peter C Harris, Navin R Gupta","doi":"10.34067/KID.0000001371","DOIUrl":"https://doi.org/10.34067/KID.0000001371","url":null,"abstract":"<p><strong>Background: </strong>Autosomal dominant polycystic kidney disease (ADPKD) has been transcriptionally profiled at single cellular resolution, yet dissociation eliminated cyst-defining morphology to preclude a retrograde analysis of the cyst transcriptome. Transcriptional profiling of dissected ADPKD cysts has demonstrated size-based transcriptional heterogeneity, impossible to define in prior single cell analysis, but sampling was neither single cell nor comprehensive to limit downstream transcriptional analysis.</p><p><strong>Methods: </strong>10X Genomics Visium spatial transcriptomics of an autosomal dominant polycystic kidney disease patient sample morphologically recognizes cysts to spatially characterize their ligand-receptor engagement, the signaling pathways of cystic transformation, and candidate cystic anchor genes that are specific and sensitive for cystic epithelia. Anchor gene validation in single nuclear RNA sequencing and cyst bulk RNA sequencing enhanced resolution, extended to cysts of variable size, and corroborated across ADPKD samples, prior to confirmatory confocal microscopy for protein-level localization.</p><p><strong>Results: </strong>The polycystic kidney disease interactome may be enriched for vscular endothelial growth inhibitor-mediated hypoxia, fibrotic extracellular matrix, and proinflammatory transforming growth factor-β (TGF-β), tumor necrosis factor, and interferon-γ signaling. Enhanced ligand-receptor engagement between cysts and fibroblasts suggests Osteopontin and Macrophage migration inhibitory factor signals emanate from cysts and TWEAK, Tenascin-C, and Pleiotrophin signals into cysts. Cystic principal cells, standardized to non-cystic counterparts, implicates Hippo (YAP/TAZ), transforming growth factor-β (TGF-β/SMAD3), and mammalian target of rapamycin (mTORC2/SGK1) signaling in cystic transformation, while pathway analysis newly implicates nicotinic acetylcholine, cadherin, toll-like, and cholecystokinin receptor signaling. Top DEGs of cystic principal cells, interrogated for their specificity for cysts and their consistency across individual samples of single cell and cyst bulk RNA-seq, prioritizes musculin as a cystic anchor gene.</p><p><strong>Conclusions: </strong>Spatial transcriptomics morphologically and transcriptionally characterizes the polycystic kidney disease transcriptome. Ligand-receptor, pathway, and reactome analyses may provide clinically-relevant disease associations that inform mechanistic studies in animal and organoid models. Integrating spatial, single nuclear, and cyst bulk RNA-seq spatially recognizes cysts at single cell resolution, while accounting for size-based heterogeneity of cysts.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149075182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Online Kidney Transplant Information in the United States: A National Readability Analysis of Transplant Center Websites.","authors":"Olena Holub, Divya Randhawa, Rebecca Allen, Aditya S Pawar, Keren Ladin, Devin Eckhoff, Alexei Nakonechnyi","doi":"10.34067/KID.0000001401","DOIUrl":"https://doi.org/10.34067/KID.0000001401","url":null,"abstract":"<p><strong>Background: </strong>Clear information is essential for patients navigating kidney transplantation, yet patient-facing materials may be difficult to understand. Patient education guidelines recommend reading levels near a sixth-grade level to support comprehension across diverse populations. This study evaluated readability of patient-directed content on United States kidney transplant center websites.</p><p><strong>Methods: </strong>Patient-facing webpages from United States kidney transplant programs were identified using a previously assembled national dataset. Website text was extracted and processed to isolate patient-directed educational content, excluding non-English pages and pages with fewer than five sentences. Readability was assessed using validated indices, including the Flesch-Kincaid Grade Level, Simple Measure of Gobbledygook (SMOG), Gunning Fog Index, and a pretrained transformer-based readability model. Summary statistics characterized reading difficulty and proportion of webpages exceeding recommended levels.</p><p><strong>Results: </strong>A total of 92,461 English-language webpages from 194 transplant center websites were included. Median readability exceeded recommended levels across measures. At the webpage level, the median SMOG score was 14.69 (interquartile range, 13.01-16.63); >99% of webpages exceeded the recommended sixth-grade level, 98% exceeded tenth-grade level, 86% exceeded twelfth-grade level, and 61% exceeded fourteenth-grade level. Among the 144 eligible hosts, the median SMOG score was 14.92 (interquartile range, 14.11-15.45). Similar patterns were observed across the Flesch-Kincaid Grade Level, Gunning Fog Index, and transformer-based readability model, demonstrating consistent findings across methods.</p><p><strong>Conclusions: </strong>Patient-facing kidney transplant center websites were written at reading levels substantially exceeding recommended standards. This widespread, modifiable barrier in transplant center communication may limit patients' ability to understand transplant-related information.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149075237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Symptom Burden and Clinical Clues in Gitelman Syndrome and Pseudo-Gitelman Syndrome.","authors":"Yuta Inoki, Tomoko Horinouchi, Atsushi Kondo, Asahi Yamamoto, Shuhei Aoyama, Yuka Kimura, Hiroaki Hanafusa, Tomohiko Yamamura, Nana Sakakibara, China Nagano, Shingo Ishimori, Kandai Nozu","doi":"10.34067/KID.0000001384","DOIUrl":"https://doi.org/10.34067/KID.0000001384","url":null,"abstract":"<p><strong>Background: </strong>Gitelman syndrome and pseudo-Gitelman syndrome share overlapping biochemical abnormalities, complicating clinical differentiation and genetic testing allocation. While Gitelman syndrome impairs health-related quality of life (QOL), the comparable burden in pseudo-Gitelman syndrome remains unclear. We compared QOL burden and symptom profiles between individuals with genetically confirmed Gitelman syndrome and those classified as pseudo-Gitelman syndrome.</p><p><strong>Methods: </strong>We evaluated 128 participants aged ≥10 years referred for genetic testing due to suspected Gitelman syndrome (hypokalemia and metabolic alkalosis). Participants were divided into a Gitelman syndrome subgroup (genetically confirmed biallelic SLC12A3 variants; n=66) and a pseudo-Gitelman syndrome subgroup (no disease-causing variants; n=62). Seventy controls were frequency-matched to Gitelman syndrome by age and sex. QOL and clinical manifestations were assessed using a structured 21-item questionnaire covering taste, urinary, muscle, and nonspecific symptom domains. To limit false-positive findings from multiple comparisons, P values were adjusted using the Benjamini-Hochberg procedure; the resulting adjusted P values (q values) <0.05 were considered statistically significant.</p><p><strong>Results: </strong>Total QOL scores indicated significant and comparable impairment in both the Gitelman syndrome and pseudo-Gitelman syndrome subgroups versus controls (both q <0.001), with no significant difference between the affected groups (q = 0.33). Despite similar overall burdens, specific clinical features differed between the groups. Nocturnal enuresis scores were higher in Gitelman syndrome group than in pseudo-Gitelman syndrome group and controls (both q < 0.001); 50% of Gitelman syndrome participants reported persistence at least until elementary school entry. The taste-related domain was higher in Gitelman syndrome group than in pseudo-Gitelman syndrome group (q = 0.01), but no individual taste item differed after correction.</p><p><strong>Conclusions: </strong>Individuals with pseudo-Gitelman syndrome experienced QOL impairment comparable to those with genetically confirmed Gitelman syndrome. However, the severity and duration of nocturnal enuresis and overall taste-related symptom burden were prominent descriptive features of Gitelman syndrome. Systematic symptom assessment may contribute to a more comprehensive clinical characterization of individuals with suspected Gitelman syndrome.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149030834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kidney360Pub Date : 2026-09-23DOI: 10.34067/KID.0000001323
Lucinda Wynter, Brendan Smyth, John Saunders, Carmen Moroney, Lilijana Gorringe, Kylie Turner, Sreeram Venugopal, Leyla Aouad, Lisa Tientstra, Rowena Monteverde, Amy Kang, George Mangos, Shaundeep Sen, Melanie Wyld, Sarah Norris, Steve Chadban
{"title":"Prevalence of Undertreated CKD among Hospital Inpatients: A Prospective Cross-Sectional Study.","authors":"Lucinda Wynter, Brendan Smyth, John Saunders, Carmen Moroney, Lilijana Gorringe, Kylie Turner, Sreeram Venugopal, Leyla Aouad, Lisa Tientstra, Rowena Monteverde, Amy Kang, George Mangos, Shaundeep Sen, Melanie Wyld, Sarah Norris, Steve Chadban","doi":"10.34067/KID.0000001323","DOIUrl":"https://doi.org/10.34067/KID.0000001323","url":null,"abstract":"<p><strong>Background: </strong>CKD affects 14% of adults in Australia and is frequently under-recognised or diagnosed in late stages when opportunities to prevent progression to kidney failure have been missed. Existing early identification programs target primary care or specific high-risk populations. Hospitalisation may present an opportunity to identify undertreated CKD. We hypothesise that there is a high prevalence of undertreated stage 3b-5 CKD among patients admitted to teaching hospitals in Sydney, Australia.</p><p><strong>Methods: </strong>We prospectively identified all adult patients with an eGFR < 45ml/min/1.73m2 admitted to hospital under a non-nephrology service, in six metropolitan hospitals from two health districts of Sydney, Australia, between March 2024-Feb 2025 inclusive. To identify those mostly likely to benefit from guideline directed medical therapy (GDMT) for CKD, we excluded those >80 years of age, pregnant, diagnosed with dementia, nursing home residents, who had a life-expectancy less than 2 years, or who had acute kidney injury. We extracted demographic, co-morbidity and medication data from the electronic medical record.</p><p><strong>Results: </strong>Among 77,447 patients, 11,243 (14.5%) had an eGFR < 45ml/min/1.73m2 on admission. After exclusions, 956 patients (1.2%) were included in the study. Median age was 75 years (IQR: 70,78), and participants had multiple co-morbidities including hypertension (78.1%), diabetes (40.7%), obesity (46.8%), coronary artery disease (34.6%) and heart failure (22.1%). CKD was documented in 24.2% and 5.8% had a urine albumin:creatinine (UACR) result available. Medications on admission included SGLT2 inhibitors (18.5%), renin-angiotensin blockers (52.1%), and statins (63.2%).</p><p><strong>Conclusions: </strong>Hospital admission represents a unique opportunity to identify undiagnosed and/or undertreated patients with mid to late-stage CKD. Interventions designed to detect and better manage this population warrant further investigation.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149030829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kidney360Pub Date : 2026-09-22DOI: 10.34067/KID.0000001413
Michael Kolland, Nikolaus Schreiber, Jascha A Amenitsch, Simon Aberger, Bernhard Tomek, Kathrin Eller, Alexander H Kirsch
{"title":"Biopsy-Proven Versus Clinically-Suspected Acute Interstitial Nephritis: A Comparative Analysis.","authors":"Michael Kolland, Nikolaus Schreiber, Jascha A Amenitsch, Simon Aberger, Bernhard Tomek, Kathrin Eller, Alexander H Kirsch","doi":"10.34067/KID.0000001413","DOIUrl":"https://doi.org/10.34067/KID.0000001413","url":null,"abstract":"","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149025263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kidney360Pub Date : 2026-09-22DOI: 10.34067/KID.0000001362
Stephen M Korbet, Joni K Evans, William L Whittier
{"title":"Percutaneous Renal Biopsy of Native Kidneys in Adults: A Single Center 40-Year Experience.","authors":"Stephen M Korbet, Joni K Evans, William L Whittier","doi":"10.34067/KID.0000001362","DOIUrl":"https://doi.org/10.34067/KID.0000001362","url":null,"abstract":"<p><strong>Background: </strong>Percutaneous renal biopsy of native kidneys is essential in the diagnosis and management of renal disease. We report one of the largest single center experiences on the success and safety of the procedure.</p><p><strong>Methods: </strong>From 6/1983 to 12/2022, 1384 adults underwent percutaneous renal biopsy using real-time ultrasound guidance using predominantly automated 14- and 16-gauge needles. A complication was defined by the need for an intervention (transfusion, radiologic or surgical procedure) or death. Multivariate analysis using logistic regression was performed to determine which features were predictive of attaining >20 total glomeruli and a complication or need for a transfusion post renal biopsy.</p><p><strong>Results: </strong>Adequate tissue for diagnosis was obtained in 99% of biopsies. Significantly more glomeruli were obtained using the 14- vs 16-gauge automated needle (32±14 vs 27±12, P <0.001) with 81% vs 74% having >20 glomeruli (P 0.01). There was no difference in complication rate (7.0 vs 8.0%, P 0.6) or transfusion requirement (5.6 vs 5.7%, P 1.0) for the 14- vs 16-gauge automated needle. By multivariate analysis the features predictive of >20 total glomeruli per biopsy were the use of a 14- v. 16-gauge automated needle and obtaining >3 cores. By multivariate analysis, baseline features predictive of a complication were female gender (Adjusted Odds Ratio (OR) 2.1), systolic blood pressure >130 mmHg and >175 mmHg (OR 1.8 and 6.4, respectfully) and Hgb <10.5 g/dL OR 3.5).</p><p><strong>Conclusions: </strong>Percutaneous renal biopsy of native kidneys using real-time ultrasound remains a successful and safe procedure. The use of a 14-gauge automated needle not only provides a more glomeruli but is equally as safe as a 16-gauge automated needle.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149025275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kidney360Pub Date : 2026-09-22DOI: 10.34067/KID.0000001347
Abeda Jamadar, Lauren G Douma, Robin L Maser, Michelle L Gumz, Reena Rao
{"title":"Pkd1 Deficiency Causes Intrinsic Renal Circadian Clock Dysfunction.","authors":"Abeda Jamadar, Lauren G Douma, Robin L Maser, Michelle L Gumz, Reena Rao","doi":"10.34067/KID.0000001347","DOIUrl":"10.34067/KID.0000001347","url":null,"abstract":"<p><strong>Background: </strong>Circadian rhythms are governed by cell-autonomous molecular clocks that regulate organ function and homeostasis. We previously showed that disruption of the renal circadian clock accelerates cyst growth in a mouse model of autosomal dominant polycystic kidney disease (ADPKD). Whether ADPKD is associated with intrinsic renal circadian clock dysfunction, and whether such dysfunction is directly attributable to loss of the PKD1 gene, remain unknown.</p><p><strong>Methods: </strong>We examined circadian regulation across organismal, organ and cellular levels using slow (Pkd1RC/RC) and rapidly (Pkd1-KO) progressing ADPKD mouse models, along with Pkd1 deficient proximal tubular and inner medullary collecting duct cells. Diurnal water intake and urine output were assessed longitudinally. Time-course analyses of core clock gene expression in mouse kidneys and synchronized renal epithelial cells, together with real-time Per2luciferase (PER2::LUC) bioluminescence imaging of kidney explants, were performed.</p><p><strong>Results: </strong>Pkd1RC/RC mice showed progressive disruption of diurnal rhythms in water intake and urine output, paralleling cystic burden. Cystic kidneys exhibited dampened, desynchronized oscillations of core circadian clock genes and PER2::LUC bioluminescence. These abnormalities were more pronounced in Pkd1-KO mice. Furthermore, Pkd1 loss blunted clock gene oscillations in synchronized renal epithelial cells in vitro, indicating cell-autonomous circadian clock dysfunction.</p><p><strong>Conclusions: </strong>Pkd1 deficiency contributes to intrinsic renal circadian clock dysfunction independent of systemic cues, although additional studies will be required to distinguish direct effects of Pkd1 loss from secondary consequences of cystic remodeling in vivo.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149025201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kidney360Pub Date : 2026-09-21DOI: 10.34067/KID.0000001405
Joel Neugarten, Ladan Golestaneh
{"title":"CKD Progression to ESKD in Women.","authors":"Joel Neugarten, Ladan Golestaneh","doi":"10.34067/KID.0000001405","DOIUrl":"https://doi.org/10.34067/KID.0000001405","url":null,"abstract":"<p><p>Despite the passage of nearly three decades since it was first suggested that sex may influence the course of CKD, the role that sex plays in promoting renal disease progression remains controversial. Arguably, large observational studies have established that women show less rapid progression of CKD than men, however, it remains to be established to what extent biologic versus cultural, lifestyle and socio-economic factors contribute to sexual dimorphism in renal disease progression. Complex interactions exist between biologic and non-biologic factors, making it difficult to elucidate the precise role that each play in mediating the effects of sex on renal disease progression. Despite these caveats, the authors believe that available data support the conclusion that sexual dimorphism in renal disease progression is primarily attributable to direct actions of sex hormones on cellular processes that influence renal injury and repair.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149017189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}