Pub Date : 2026-01-21DOI: 10.1016/j.kint.2026.01.003
Georg W. Sendtner, Julia Miranda, Pia Naumann, Maximilian Weiss, Pelin Güls, Ernst Molitor, Uta Scheidt, Axel Schmidt, Kerstin U. Ludwig, Annika Hilger, Ulrich Dobrindt, Thomas Mayrhofer, Christian Kurts, Florian Wagenlehner, Olga Shevshuk, Sibylle von Vietinghoff
{"title":"Sodium glucose transporter 2 inhibition maintains kidney antibacterial response by decreasing complement C1q","authors":"Georg W. Sendtner, Julia Miranda, Pia Naumann, Maximilian Weiss, Pelin Güls, Ernst Molitor, Uta Scheidt, Axel Schmidt, Kerstin U. Ludwig, Annika Hilger, Ulrich Dobrindt, Thomas Mayrhofer, Christian Kurts, Florian Wagenlehner, Olga Shevshuk, Sibylle von Vietinghoff","doi":"10.1016/j.kint.2026.01.003","DOIUrl":"https://doi.org/10.1016/j.kint.2026.01.003","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"6 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146014624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-21DOI: 10.1016/j.kint.2025.11.007
Vicente E. Torres
Autosomal dominant polycystic kidney disease has some effects on cholesterol metabolism and cardiovascular disease that are shared with other chronic kidney diseases and others that are distinctive and directly caused by disruption of polycystins. The pravastatin clinical trial by Gitomer et al. does not support treatment with statins for the only purpose of delaying disease progression. Emergence of novel lipid-lowering therapies presents new therapeutic opportunities but also risks. Recent studies suggest that cholesterol is important for traffic to and function of polycystins in primary cilia.
{"title":"The many faces of cholesterol in autosomal dominant polycystic kidney disease","authors":"Vicente E. Torres","doi":"10.1016/j.kint.2025.11.007","DOIUrl":"10.1016/j.kint.2025.11.007","url":null,"abstract":"<div><div>Autosomal dominant polycystic kidney disease has some effects on cholesterol metabolism and cardiovascular disease that are shared with other chronic kidney diseases and others that are distinctive and directly caused by disruption of polycystins. The pravastatin clinical trial by Gitomer <em>et al.</em> does not support treatment with statins for the only purpose of delaying disease progression. Emergence of novel lipid-lowering therapies presents new therapeutic opportunities but also risks. Recent studies suggest that cholesterol is important for traffic to and function of polycystins in primary cilia.</div></div>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"109 2","pages":"Pages 269-272"},"PeriodicalIF":12.6,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146001692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-21DOI: 10.1016/j.kint.2025.07.042
Shuang-Shuang Fu , Zheng-Xiang Tian
{"title":"Pericatheter vascular calcification in a long-term hemodialysis patient","authors":"Shuang-Shuang Fu , Zheng-Xiang Tian","doi":"10.1016/j.kint.2025.07.042","DOIUrl":"10.1016/j.kint.2025.07.042","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"109 2","pages":"Page 401"},"PeriodicalIF":12.6,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146001686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-20DOI: 10.1016/j.kint.2025.12.024
Mark Canney,Sana Shan,Lee Er,Laurent Billot,Jialin Han,Muh Geot Wong,Helen Monaghan,Michelle Hladunewich,Lai Seong Hooi,Vivek Jha,Jicheng Lv,Vlado Perkovic,Hong Zhang,Daniel C Cattran,Sean J Barbour,
INTRODUCTIONCorticosteroids are effective for treating IgA nephropathy but have important adverse effects. In this secondary analysis of the TESTING cohort, we generated a model to predicts, for an individual patient, the probability that they will respond to corticosteroids.METHODSTime to the primary outcome (40% reduction in eGFR, kidney failure or death due to kidney disease) was evaluated in a Cox proportional hazards model including all potential treatment modifiers as main effects. Selected variables were forced into a model with treatment exposure and interaction terms between treatment and each included variable. The predicted four-year absolute risk of the primary outcome was generated for every patient individually under separate scenarios of being treated with methylprednisolone or placebo. The difference between the two scenarios was the predicted individual treatment effect on absolute risk reduction (ARR). Model performance was assessed using discrimination plots, restricted mean survival time (RMST) and the C-statistic for benefit.RESULTSDuring a median of 43 months follow-up, 176 of 483 participants experienced the primary outcome. Selected treatment modifiers were eGFR, age, proteinuria, renin-angiotensin-aldosterone-system blockade dose, ethnicity, time from biopsy to enrollment, systolic blood pressure, sex, body mass index, and MEST-C T-score and C-score. Compared to the average ARR associated with methylprednisolone (16.1%), the predicted individual-level ARR was highly variable (-10% to 40%). Patients with predicted ARR over 10% had greater observed benefit from methylprednisolone (ARR 24%) versus those with predicted ARR 10% or less (observed ARR -5%). A policy of treating only patients with higher anticipated benefit had a longer RMST than using random treatment allocation (1,194 v 1,028 days). The C-statistic for benefit was 0.63 (95% confidence interval 0.56-0.70). The frequency of adverse events was similar across tertiles of ARR.CONCLUSIONWe have generated a model that can predict individual patient response to methylprednisolone so that corticosteroids can be targeted to those most likely to benefit.
{"title":"A secondary analysis of the TESTING trial predicted individual patient response to corticosteroid treatment in IgA nephropathy.","authors":"Mark Canney,Sana Shan,Lee Er,Laurent Billot,Jialin Han,Muh Geot Wong,Helen Monaghan,Michelle Hladunewich,Lai Seong Hooi,Vivek Jha,Jicheng Lv,Vlado Perkovic,Hong Zhang,Daniel C Cattran,Sean J Barbour, ","doi":"10.1016/j.kint.2025.12.024","DOIUrl":"https://doi.org/10.1016/j.kint.2025.12.024","url":null,"abstract":"INTRODUCTIONCorticosteroids are effective for treating IgA nephropathy but have important adverse effects. In this secondary analysis of the TESTING cohort, we generated a model to predicts, for an individual patient, the probability that they will respond to corticosteroids.METHODSTime to the primary outcome (40% reduction in eGFR, kidney failure or death due to kidney disease) was evaluated in a Cox proportional hazards model including all potential treatment modifiers as main effects. Selected variables were forced into a model with treatment exposure and interaction terms between treatment and each included variable. The predicted four-year absolute risk of the primary outcome was generated for every patient individually under separate scenarios of being treated with methylprednisolone or placebo. The difference between the two scenarios was the predicted individual treatment effect on absolute risk reduction (ARR). Model performance was assessed using discrimination plots, restricted mean survival time (RMST) and the C-statistic for benefit.RESULTSDuring a median of 43 months follow-up, 176 of 483 participants experienced the primary outcome. Selected treatment modifiers were eGFR, age, proteinuria, renin-angiotensin-aldosterone-system blockade dose, ethnicity, time from biopsy to enrollment, systolic blood pressure, sex, body mass index, and MEST-C T-score and C-score. Compared to the average ARR associated with methylprednisolone (16.1%), the predicted individual-level ARR was highly variable (-10% to 40%). Patients with predicted ARR over 10% had greater observed benefit from methylprednisolone (ARR 24%) versus those with predicted ARR 10% or less (observed ARR -5%). A policy of treating only patients with higher anticipated benefit had a longer RMST than using random treatment allocation (1,194 v 1,028 days). The C-statistic for benefit was 0.63 (95% confidence interval 0.56-0.70). The frequency of adverse events was similar across tertiles of ARR.CONCLUSIONWe have generated a model that can predict individual patient response to methylprednisolone so that corticosteroids can be targeted to those most likely to benefit.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"19 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146021290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-20DOI: 10.1016/j.kint.2025.12.025
Carolina S Wagner,Rosilene M Elias,Thomas L Nickolas,Aline Martin,Marta Martinez-Calle,Ivone B Oliveira,Ana C Coelho,Luciene M Dos Reis,Vanda Jorgetti,Valentin David,Rosa M A Moysés
INTRODUCTIONChronic kidney disease (CKD)-associated osteoporosis is highly prevalent and increases the risk of fractures. Current therapy aims to preserve normal bone turnover, by maintaining parathyroid hormone (PTH) at relatively adequate levels. However, these patients continue to experience fractures.METHODSTo assess potential adverse effects of PTH on bone, we examined bone histology and osteocytic gene and protein expression in 76 patients receiving hemodialysis compared to that of 33 control individuals.RESULTSUsing bulk bone tissue RNAseq, we observed that CKD is associated with enhanced inflammatory signaling, increased cell death, impaired osteoblastic differentiation, and reduced bone mass, consistent with low osteocyte count and increased apoptosis. Patients with elevated PTH levels showed an attenuation of these alterations, but exhibited increased expression of genes related to fibrosis, matrix apposition, and bone remodeling, leading to increased cortical porosity.CONCLUSIONSCKD induces inflammation and cell death in bone. However, elevated PTH levels exhibited dual effects that were both protective and detrimental to bone tissue quality and strength. Our findings suggest that combining anabolic agents with relatively low PTH levels may be a potential approach to improve bone quality in CKD. This hypothesis warrants further investigation in future studies.
{"title":"Uremia and parathyroid hormone have distinct effects on bone protein and gene expression.","authors":"Carolina S Wagner,Rosilene M Elias,Thomas L Nickolas,Aline Martin,Marta Martinez-Calle,Ivone B Oliveira,Ana C Coelho,Luciene M Dos Reis,Vanda Jorgetti,Valentin David,Rosa M A Moysés","doi":"10.1016/j.kint.2025.12.025","DOIUrl":"https://doi.org/10.1016/j.kint.2025.12.025","url":null,"abstract":"INTRODUCTIONChronic kidney disease (CKD)-associated osteoporosis is highly prevalent and increases the risk of fractures. Current therapy aims to preserve normal bone turnover, by maintaining parathyroid hormone (PTH) at relatively adequate levels. However, these patients continue to experience fractures.METHODSTo assess potential adverse effects of PTH on bone, we examined bone histology and osteocytic gene and protein expression in 76 patients receiving hemodialysis compared to that of 33 control individuals.RESULTSUsing bulk bone tissue RNAseq, we observed that CKD is associated with enhanced inflammatory signaling, increased cell death, impaired osteoblastic differentiation, and reduced bone mass, consistent with low osteocyte count and increased apoptosis. Patients with elevated PTH levels showed an attenuation of these alterations, but exhibited increased expression of genes related to fibrosis, matrix apposition, and bone remodeling, leading to increased cortical porosity.CONCLUSIONSCKD induces inflammation and cell death in bone. However, elevated PTH levels exhibited dual effects that were both protective and detrimental to bone tissue quality and strength. Our findings suggest that combining anabolic agents with relatively low PTH levels may be a potential approach to improve bone quality in CKD. This hypothesis warrants further investigation in future studies.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"6 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146021726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
INTRODUCTIONGalactose-deficient IgA1 (Gd-IgA1) plays a key role in IgA nephropathy (IgAN), but the location of the plasma cells responsible for its production remain unknown.METHODSTo locate Gd-IgA1-producing cells, we profiled intestinal and circulating immune cells from three independent cohorts totaling 99 IgAN cases and 121 healthy controls. The IgA phenotypes-including total IgA, Gd-IgA1, IgA-IgG complexes, secretory IgA, and polymeric IgA levels were measured in paired ileocecal and blood samples. Bulk RNA sequencing, cell deconvolution, and spatial profiling of biopsies identified Gd-IgA1-producing cells in ileocecal samples and blood. Functional studies employed anti-integrin α4β7 monoclonal antibodies in vitro and in a humanized IgAN mouse model.RESULTSWe found significantly elevated levels of ileocecal IgA enriched for polymeric and Gd-IgA1 O-glycoforms in patients with IgAN. In parallel, terminal ileal rather than ascending colon IgA+ B cells were increased. Most of these cells expressed Gd-IgA1 and displayed dysregulation of enzymes involved in O-glycosylation. Furthermore, circulating IgA+ B cells in IgAN exhibited gene expression signatures more closely resembling that of terminal ileum-derived IgA+ B cells, rather than those from ascending colon or tonsil. Integrin β7 was identified as a biomarker for cells of terminal ileal origin, and there was an increase in IgA+β7+ plasmablasts/plasma cells, correlating with disease severity. In a mouse model of IgAN, anti-α4β7 monoclonal antibody reduced β7+ cells and Gd-IgA1 levels in vitro and induced attrition of Peyer's patches, decreased circulating β7+ plasmablasts/plasma cells, and prevented mesangial IgA deposition.CONCLUSIONSOur study highlights the importance of dysregulated B cell responses in the terminal ileum in IgAN and suggests the α4β7-MAdCAM-1 axis as a potential therapeutic target.
{"title":"Multi-omics analyses reveal the pathogenic role of terminal ileum-derived IgA+β7+ cells in IgA nephropathy.","authors":"Xingzi Liu,Lan Wang,Miaomiao Lin,Niya Jia,Guanyi Liu,Jiawen Peng,Jingyu Wang,Tong Xie,Shaoqing Dang,Jingyi Wu,Xujie Zhou,Lijun Liu,Sufang Shi,Jicheng Lv,Jonathan Barratt,Yuemiao Zhang,Hong Zhang","doi":"10.1016/j.kint.2025.12.026","DOIUrl":"https://doi.org/10.1016/j.kint.2025.12.026","url":null,"abstract":"INTRODUCTIONGalactose-deficient IgA1 (Gd-IgA1) plays a key role in IgA nephropathy (IgAN), but the location of the plasma cells responsible for its production remain unknown.METHODSTo locate Gd-IgA1-producing cells, we profiled intestinal and circulating immune cells from three independent cohorts totaling 99 IgAN cases and 121 healthy controls. The IgA phenotypes-including total IgA, Gd-IgA1, IgA-IgG complexes, secretory IgA, and polymeric IgA levels were measured in paired ileocecal and blood samples. Bulk RNA sequencing, cell deconvolution, and spatial profiling of biopsies identified Gd-IgA1-producing cells in ileocecal samples and blood. Functional studies employed anti-integrin α4β7 monoclonal antibodies in vitro and in a humanized IgAN mouse model.RESULTSWe found significantly elevated levels of ileocecal IgA enriched for polymeric and Gd-IgA1 O-glycoforms in patients with IgAN. In parallel, terminal ileal rather than ascending colon IgA+ B cells were increased. Most of these cells expressed Gd-IgA1 and displayed dysregulation of enzymes involved in O-glycosylation. Furthermore, circulating IgA+ B cells in IgAN exhibited gene expression signatures more closely resembling that of terminal ileum-derived IgA+ B cells, rather than those from ascending colon or tonsil. Integrin β7 was identified as a biomarker for cells of terminal ileal origin, and there was an increase in IgA+β7+ plasmablasts/plasma cells, correlating with disease severity. In a mouse model of IgAN, anti-α4β7 monoclonal antibody reduced β7+ cells and Gd-IgA1 levels in vitro and induced attrition of Peyer's patches, decreased circulating β7+ plasmablasts/plasma cells, and prevented mesangial IgA deposition.CONCLUSIONSOur study highlights the importance of dysregulated B cell responses in the terminal ileum in IgAN and suggests the α4β7-MAdCAM-1 axis as a potential therapeutic target.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"20 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146021725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chronic kidney disease (CKD) of undetermined aetiology (CKDu) is a major cause of mortality, impacts communities, health systems and national economies. Despite two-decades of descriptive and analytical research, the causes of CKDu epidemics remain unclear. In February 2025, at the World Congress of Nephrology, the International Society of Nephrology's International Consortium of CKDu investigators met to discuss the obstacles to determining the cause(s) of the epidemics. Several key themes were identified: Firstly, differences in CKDu burden between regions are poorly described, and this is complicated by inconsistent terminology. Secondly, some proposed primary causes of CKDu are also progression factors in CKD of all causes. It is unclear whether such factors can explain CKDu epidemics, partly because of the challenges around distinguishing disease onset from progression. Lastly, the need for alternatives to self-report in capturing exposures. This report describes the current state-of-the-field, these themes in more detail, and provides suggestions to optimise future research efforts.
{"title":"Taking the 'unknown' out of CKDu - Optimising approaches to uncover the cause(s) of epidemic-level kidney disease in low- and middle-income settings: A report from the ISN's International Consortium of CKDu collaborators (ISN i3C).","authors":"Ben Caplin,Shuchi Anand,Marvin González Quiroz,Magdalena Madero,Marie Michael,Sumit Mohan,Anna Strasma,Sundararaman Swaminathan,Sushrut Waikar,Eranga Wijewickrama, ","doi":"10.1016/j.kint.2025.12.027","DOIUrl":"https://doi.org/10.1016/j.kint.2025.12.027","url":null,"abstract":"Chronic kidney disease (CKD) of undetermined aetiology (CKDu) is a major cause of mortality, impacts communities, health systems and national economies. Despite two-decades of descriptive and analytical research, the causes of CKDu epidemics remain unclear. In February 2025, at the World Congress of Nephrology, the International Society of Nephrology's International Consortium of CKDu investigators met to discuss the obstacles to determining the cause(s) of the epidemics. Several key themes were identified: Firstly, differences in CKDu burden between regions are poorly described, and this is complicated by inconsistent terminology. Secondly, some proposed primary causes of CKDu are also progression factors in CKD of all causes. It is unclear whether such factors can explain CKDu epidemics, partly because of the challenges around distinguishing disease onset from progression. Lastly, the need for alternatives to self-report in capturing exposures. This report describes the current state-of-the-field, these themes in more detail, and provides suggestions to optimise future research efforts.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"8 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146021729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-16DOI: 10.1016/j.kint.2025.11.009
Yuanhang Yang,Antoine Creon,Andrew S Levey,Anne-Laure Faucon,Aurora Caldinelli,Marie Evans,Arvid Sjölander,Alberto Ortiz,Edouard L Fu,Juan Jesus Carrero
INTRODUCTIONThere are currently no established strategies for early identification and primary prevention of chronic kidney disease (CKD). Automatic reporting of estimated glomerular filtration rate (eGFR) allows opportunistic CKD screening. Here, we hypothesized that comparison with population-based eGFR distributions may further help identify individuals at elevated risk.METHODSA population-based observational cohort study including adults aged 40 to 100 years with routine serum/plasma creatinine tests (Stockholm CREAtinine Measurements project) between 2006 and 2021 was conducted. The cohort captured 1,179,501 unique individuals (80% of the population in the region) with 6,914,993 repeated annual eGFR measurements. After computing eGFR distributions by age and sex, cause-specific Cox regressions evaluated the associations between eGFR percentiles and risks of kidney failure with replacement therapy (KFRT) and death.RESULTSMedian eGFR (2009 CKD-EPI) was lower at higher age, from 104-106 ml/min per 1.73 m2 (men-women) at age 40 to 45-50 ml/min per 1.73 m2 at age 100. Exclusion of individuals with selected comorbid conditions or adjustment for the non-tested population had minimal impact on eGFR distributions. Compared to the central percentiles (47.5-52.5th), eGFR percentiles below the 25th were significantly associated with increased risk of KFRT, and both low and high eGFR percentiles were associated with increased mortality. Associations were consistent across age groups. Among 421,547 individuals with eGFR 60 ml/min per 1.73 m2 or more who were below the 25th percentile, only 24% underwent albuminuria/proteinuria testing in the adjacent year and could have benefited from additional diagnostic work-up.CONCLUSIONSOur study shows that eGFR values below the 25th percentile of the population distribution are associated with increased risks of kidney failure and death. Population-based eGFR charts may complement current automatic reporting systems and provide opportunities for early identification and primary prevention of CKD.
{"title":"Population-based estimated Glomerular Filtration Rate distributions and associated health outcomes provide opportunities for early identification of and primary prevention of chronic kidney disease.","authors":"Yuanhang Yang,Antoine Creon,Andrew S Levey,Anne-Laure Faucon,Aurora Caldinelli,Marie Evans,Arvid Sjölander,Alberto Ortiz,Edouard L Fu,Juan Jesus Carrero","doi":"10.1016/j.kint.2025.11.009","DOIUrl":"https://doi.org/10.1016/j.kint.2025.11.009","url":null,"abstract":"INTRODUCTIONThere are currently no established strategies for early identification and primary prevention of chronic kidney disease (CKD). Automatic reporting of estimated glomerular filtration rate (eGFR) allows opportunistic CKD screening. Here, we hypothesized that comparison with population-based eGFR distributions may further help identify individuals at elevated risk.METHODSA population-based observational cohort study including adults aged 40 to 100 years with routine serum/plasma creatinine tests (Stockholm CREAtinine Measurements project) between 2006 and 2021 was conducted. The cohort captured 1,179,501 unique individuals (80% of the population in the region) with 6,914,993 repeated annual eGFR measurements. After computing eGFR distributions by age and sex, cause-specific Cox regressions evaluated the associations between eGFR percentiles and risks of kidney failure with replacement therapy (KFRT) and death.RESULTSMedian eGFR (2009 CKD-EPI) was lower at higher age, from 104-106 ml/min per 1.73 m2 (men-women) at age 40 to 45-50 ml/min per 1.73 m2 at age 100. Exclusion of individuals with selected comorbid conditions or adjustment for the non-tested population had minimal impact on eGFR distributions. Compared to the central percentiles (47.5-52.5th), eGFR percentiles below the 25th were significantly associated with increased risk of KFRT, and both low and high eGFR percentiles were associated with increased mortality. Associations were consistent across age groups. Among 421,547 individuals with eGFR 60 ml/min per 1.73 m2 or more who were below the 25th percentile, only 24% underwent albuminuria/proteinuria testing in the adjacent year and could have benefited from additional diagnostic work-up.CONCLUSIONSOur study shows that eGFR values below the 25th percentile of the population distribution are associated with increased risks of kidney failure and death. Population-based eGFR charts may complement current automatic reporting systems and provide opportunities for early identification and primary prevention of CKD.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"124 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145986566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.kint.2025.09.024
Rukshana Shroff , Franz Schaefer
Dialysis is a life-sustaining treatment but comes with a very high burden of cardiovascular (CV) morbidity and mortality risk. CV events account for almost 30% of deaths in children receiving dialysis. Multiple risk factors for CV disease, both traditional and uremia-related, are present in children before they even start kidney replacement therapy and increase in prevalence and severity on dialysis. Peritoneal dialysis, as well as the conventional 3 times per week regimen of hemodialysis, offers only suboptimal clearance of uremic toxins and fluid removal. Intensified dialysis regimens, in the form of adding in convective clearance with hemodiafiltration or increasing dialysis time with longer or more frequent sessions in home hemodialysis, may offer some cardioprotective effect, but data in children are scarce. Importantly, several risk factors for CV damage are modifiable and their early diagnosis and management are crucial to mitigate CV damage. Intensified dialysis may attenuate the progression of subclinical CV disease, but no treatment to date has shown that the inexorable progression of CV disease can be reversed. Children on dialysis have a lifetime of kidney replacement therapy ahead of them, so our management must focus on early diagnosis and robust preventive strategies to give them the best chance of optimal CV health and survival. In this mini review, we discuss the key risk factors for CV disease and how to optimize CV outcomes in children receiving dialysis.
{"title":"Optimizing cardiovascular outcomes in pediatric dialysis","authors":"Rukshana Shroff , Franz Schaefer","doi":"10.1016/j.kint.2025.09.024","DOIUrl":"10.1016/j.kint.2025.09.024","url":null,"abstract":"<div><div>Dialysis is a life-sustaining treatment but comes with a very high burden of cardiovascular (CV) morbidity and mortality risk. CV events account for almost 30% of deaths in children receiving dialysis. Multiple risk factors for CV disease, both traditional and uremia-related, are present in children before they even start kidney replacement therapy and increase in prevalence and severity on dialysis. Peritoneal dialysis, as well as the conventional 3 times per week regimen of hemodialysis, offers only suboptimal clearance of uremic toxins and fluid removal. Intensified dialysis regimens, in the form of adding in convective clearance with hemodiafiltration or increasing dialysis time with longer or more frequent sessions in home hemodialysis, may offer some cardioprotective effect, but data in children are scarce. Importantly, several risk factors for CV damage are modifiable and their early diagnosis and management are crucial to mitigate CV damage. Intensified dialysis may attenuate the progression of subclinical CV disease, but no treatment to date has shown that the inexorable progression of CV disease can be reversed. Children on dialysis have a lifetime of kidney replacement therapy ahead of them, so our management must focus on early diagnosis and robust preventive strategies to give them the best chance of optimal CV health and survival. In this mini review, we discuss the key risk factors for CV disease and how to optimize CV outcomes in children receiving dialysis.</div></div>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"109 1","pages":"Pages 73-80"},"PeriodicalIF":12.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145382746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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