{"title":"Proteomic CKD Prediction in Type 2 Diabetes: Underexplored Limitations and Translational Gaps.","authors":"Shiuan-Chih Chen,Yuan-Ti Lee","doi":"10.1681/asn.0000000991","DOIUrl":"https://doi.org/10.1681/asn.0000000991","url":null,"abstract":"","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":"275 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146005086","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}
Jennifer H Yo,Yuanhang Yang,Aurora Caldinelli,Morgan E Grams,Kate Bramham,Giorgina B Piccoli,Juan-Jesús Carrero,Anna Sara Oberg
BACKGROUNDPreeclampsia, a systemic hypertensive disorder of pregnancy, has been associated with the risk of kidney failure, an outcome that may take decades to develop. However, its association with early kidney disease, which could be targeted for intervention, remains underexplored. Here we quantified the risk of chronic kidney disease (CKD), defined by laboratory markers of kidney damage, in women who had a pregnancy complicated by preeclampsia versus a pregnancy without preeclampsia.METHODSPopulation-based cohort study in Stockholm, Sweden, using inverse probability of treatment weights to minimize confounding. All nulliparous women who had at least one pregnancy ending in live or stillbirth between January 1, 2006, and December 31, 2020 were identified, excluding pre-existing hypertension, diabetes or CKD. Primary outcomes were (1) albuminuria defined by urine albumin to creatinine ratio >300mg/g; (2) estimated Glomerular Filtration Rate (eGFR)<60ml/min/1.73m2; and (3) composite of albuminuria>300mg/g and/or eGFR<60ml/min/1.73m2.RESULTSThe study included 171,693 pregnancies (170 192 women: mean [SD] age, 29[5] years), of whom 10,538 (6%) had at least one pregnancy complicated by preeclampsia. During median follow up of 7.0 years (IQR, 3.3-10.5), albuminuria >300mg/g occurred after 775 pregnancies (0.5%), eGFR <60ml/min/1.73m2 occurred after 248 pregnancies (0.1%), and the composite outcome occurred after 985 pregnancies (0.6%). Incidence rates per 1,000 person-years were higher after preeclampsia vs no preeclampsia for albuminuria>300mg/g (1.53 vs 0.57), eGFR<60ml/min/1.73m2 (0.52 vs 0.18), and the composite outcome (2.00 vs 0.73). Weighted hazard ratios were 2.53 (95% CI, 2.04-3.13) for albuminuria>300mg/g, 2.18 (95% CI, 1.49-3.19) for eGFR<60 mL/min/1.73 m2, and 2.43 (95% CI, 2.01-2.95) for the composite outcome. In the first postpartum year, 2080 (20%) and 1043 (10%) of women with preeclampsia had serum creatinine or urine albumin testing, respectively.CONCLUSIONSPreeclampsia is associated with higher risk of laboratory signs of early kidney damage. There were low rates of postpartum kidney function monitoring.
{"title":"Laboratory Signs of CKD after Preeclampsia.","authors":"Jennifer H Yo,Yuanhang Yang,Aurora Caldinelli,Morgan E Grams,Kate Bramham,Giorgina B Piccoli,Juan-Jesús Carrero,Anna Sara Oberg","doi":"10.1681/asn.0000001001","DOIUrl":"https://doi.org/10.1681/asn.0000001001","url":null,"abstract":"BACKGROUNDPreeclampsia, a systemic hypertensive disorder of pregnancy, has been associated with the risk of kidney failure, an outcome that may take decades to develop. However, its association with early kidney disease, which could be targeted for intervention, remains underexplored. Here we quantified the risk of chronic kidney disease (CKD), defined by laboratory markers of kidney damage, in women who had a pregnancy complicated by preeclampsia versus a pregnancy without preeclampsia.METHODSPopulation-based cohort study in Stockholm, Sweden, using inverse probability of treatment weights to minimize confounding. All nulliparous women who had at least one pregnancy ending in live or stillbirth between January 1, 2006, and December 31, 2020 were identified, excluding pre-existing hypertension, diabetes or CKD. Primary outcomes were (1) albuminuria defined by urine albumin to creatinine ratio >300mg/g; (2) estimated Glomerular Filtration Rate (eGFR)<60ml/min/1.73m2; and (3) composite of albuminuria>300mg/g and/or eGFR<60ml/min/1.73m2.RESULTSThe study included 171,693 pregnancies (170 192 women: mean [SD] age, 29[5] years), of whom 10,538 (6%) had at least one pregnancy complicated by preeclampsia. During median follow up of 7.0 years (IQR, 3.3-10.5), albuminuria >300mg/g occurred after 775 pregnancies (0.5%), eGFR <60ml/min/1.73m2 occurred after 248 pregnancies (0.1%), and the composite outcome occurred after 985 pregnancies (0.6%). Incidence rates per 1,000 person-years were higher after preeclampsia vs no preeclampsia for albuminuria>300mg/g (1.53 vs 0.57), eGFR<60ml/min/1.73m2 (0.52 vs 0.18), and the composite outcome (2.00 vs 0.73). Weighted hazard ratios were 2.53 (95% CI, 2.04-3.13) for albuminuria>300mg/g, 2.18 (95% CI, 1.49-3.19) for eGFR<60 mL/min/1.73 m2, and 2.43 (95% CI, 2.01-2.95) for the composite outcome. In the first postpartum year, 2080 (20%) and 1043 (10%) of women with preeclampsia had serum creatinine or urine albumin testing, respectively.CONCLUSIONSPreeclampsia is associated with higher risk of laboratory signs of early kidney damage. There were low rates of postpartum kidney function monitoring.","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":"66 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146015136","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 : 2026-01-01Epub Date: 2025-09-02DOI: 10.1681/ASN.0000000881
Ayodeji O Oteyola, Bailey Chan, Amado A Quintar, Dario F Riascos-Bernal, Michael J Ross, Nicholas E S Sibinga, Wei Chen
{"title":"Emerging Role of FAT Atypical Cadherin 1 in Kidney Function and Disease.","authors":"Ayodeji O Oteyola, Bailey Chan, Amado A Quintar, Dario F Riascos-Bernal, Michael J Ross, Nicholas E S Sibinga, Wei Chen","doi":"10.1681/ASN.0000000881","DOIUrl":"10.1681/ASN.0000000881","url":null,"abstract":"","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":"186-189"},"PeriodicalIF":9.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12513539/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144958713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-07-25DOI: 10.1681/ASN.0000000810
Yoshiki Tanaka, Ayumu Nakashima, Naoki Ishiuchi, Kisho Miyasako, Keisuke Morimoto, Maria Yoshida, Kensuke Sasaki, Satoshi Maeda, Go Matsuda, Takao Masaki
{"title":"Overexpression of Thrombomodulin in Adipose-Derived Mesenchymal Stem Cells Reduces Thrombogenic Risk and Enhances Therapeutic Efficacy.","authors":"Yoshiki Tanaka, Ayumu Nakashima, Naoki Ishiuchi, Kisho Miyasako, Keisuke Morimoto, Maria Yoshida, Kensuke Sasaki, Satoshi Maeda, Go Matsuda, Takao Masaki","doi":"10.1681/ASN.0000000810","DOIUrl":"10.1681/ASN.0000000810","url":null,"abstract":"","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":"85-100"},"PeriodicalIF":9.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12807147/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144715095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-10-07DOI: 10.1681/ASN.0000000908
Dillan Prasad, Austin Drysch, Deep Upadhyay, Eric G Neilson
Aldosterone escape refers to the spontaneous and compensatory diuresis that occurs in primary aldosteronism to correct and rebalance fluid homeostasis during conditions of sodium retention. Although widely observed in humans and animals, the precise mechanisms underpinning aldosterone escape remain unclear. The escape phenomenon is clinically relevant as primary aldosteronism affects nearly one in ten hypertensive adults and is associated with a two-fold higher risk of stroke and atrial fibrillation. Studying the phenomenon provides additional insights into the intricate physiology of renal sodium handling that may inform future development of novel therapeutics. This review is a modern account of the complex interplay of renal hemodynamics, hormonal signaling, paracrine modulation, and tubular adaptations underlying aldosterone escape. By re-examining classical and emerging mechanisms, including the With-No-Lysine (WNK) kinase system as a potassium-sensitive distal homeostasis mechanism, we suggest a general framework for this remarkable phenomenon.
{"title":"The Story of Aldosterone Escape.","authors":"Dillan Prasad, Austin Drysch, Deep Upadhyay, Eric G Neilson","doi":"10.1681/ASN.0000000908","DOIUrl":"10.1681/ASN.0000000908","url":null,"abstract":"<p><p>Aldosterone escape refers to the spontaneous and compensatory diuresis that occurs in primary aldosteronism to correct and rebalance fluid homeostasis during conditions of sodium retention. Although widely observed in humans and animals, the precise mechanisms underpinning aldosterone escape remain unclear. The escape phenomenon is clinically relevant as primary aldosteronism affects nearly one in ten hypertensive adults and is associated with a two-fold higher risk of stroke and atrial fibrillation. Studying the phenomenon provides additional insights into the intricate physiology of renal sodium handling that may inform future development of novel therapeutics. This review is a modern account of the complex interplay of renal hemodynamics, hormonal signaling, paracrine modulation, and tubular adaptations underlying aldosterone escape. By re-examining classical and emerging mechanisms, including the With-No-Lysine (WNK) kinase system as a potassium-sensitive distal homeostasis mechanism, we suggest a general framework for this remarkable phenomenon.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":"164-171"},"PeriodicalIF":9.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12807134/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-12-02DOI: 10.1681/ASN.0000000927
Alexander Teumer, Matthias Wuttke
{"title":"Genetic Architecture of Peritoneal Ultrafiltration: Lessons from the Bio-PD Study.","authors":"Alexander Teumer, Matthias Wuttke","doi":"10.1681/ASN.0000000927","DOIUrl":"10.1681/ASN.0000000927","url":null,"abstract":"","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":"37 1","pages":"4-5"},"PeriodicalIF":9.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12807139/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146010978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-11-17DOI: 10.1681/ASN.0000000934
Sigrid Lundberg, Senka Sendic
{"title":"Smoldering Segmental Sclerosis: A Potential Guide to Therapy in IgA Nephropathy.","authors":"Sigrid Lundberg, Senka Sendic","doi":"10.1681/ASN.0000000934","DOIUrl":"10.1681/ASN.0000000934","url":null,"abstract":"","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":"37 1","pages":"15-17"},"PeriodicalIF":9.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12807179/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146010914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-08-26DOI: 10.1681/ASN.0000000822
Adrian Rafael Murillo-de-Ozores, Lihe Chen, Shuo-Ming Ou, Euijung Park, Shaza Khan, Viswanathan Raghuram, Chin-Rang Yang, Chung-Lin Chou, Mark A Knepper
{"title":"CREB-Family Transcription Factors and Vasopressin-Mediated Regulation of Aqp2 Gene Transcription.","authors":"Adrian Rafael Murillo-de-Ozores, Lihe Chen, Shuo-Ming Ou, Euijung Park, Shaza Khan, Viswanathan Raghuram, Chin-Rang Yang, Chung-Lin Chou, Mark A Knepper","doi":"10.1681/ASN.0000000822","DOIUrl":"10.1681/ASN.0000000822","url":null,"abstract":"","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":"67-84"},"PeriodicalIF":9.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12807160/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144958699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-09-12DOI: 10.1681/ASN.0000000897
Michelle N Rheault
Alport syndrome is a progressive, hereditary disorder of basement membranes caused by variants in genes encoding the α 3, α 4, or α 5 chains of type IV collagen ( COL4A3, COL4A4 , and COL4A5 ) leading to glomerulopathy, kidney failure, hearing loss, and eye abnormalities. The absence or dysfunction of the α 3- α 4- α 5 (IV) heterotrimer triggers multiple compensatory and detrimental pathways within all layers of the glomerular filtration barrier. Developing a therapeutic strategy for patients with Alport syndrome depends on understanding these mechanisms of disease progression that are predominant at different times throughout the disease course. These strategies may include reconstitution of the α 3- α 4- α 5 (IV) network in the glomerular basement membrane, reducing biomechanical strain and glomerular hyperfiltration, chaperone therapy, blocking aberrant signaling between the glomerular basement membrane and podocytes, reducing endothelial cell injury, reducing inflammation, and blocking fibrosis pathways.
{"title":"Treatment Approaches for Alport Syndrome.","authors":"Michelle N Rheault","doi":"10.1681/ASN.0000000897","DOIUrl":"10.1681/ASN.0000000897","url":null,"abstract":"<p><p>Alport syndrome is a progressive, hereditary disorder of basement membranes caused by variants in genes encoding the α 3, α 4, or α 5 chains of type IV collagen ( COL4A3, COL4A4 , and COL4A5 ) leading to glomerulopathy, kidney failure, hearing loss, and eye abnormalities. The absence or dysfunction of the α 3- α 4- α 5 (IV) heterotrimer triggers multiple compensatory and detrimental pathways within all layers of the glomerular filtration barrier. Developing a therapeutic strategy for patients with Alport syndrome depends on understanding these mechanisms of disease progression that are predominant at different times throughout the disease course. These strategies may include reconstitution of the α 3- α 4- α 5 (IV) network in the glomerular basement membrane, reducing biomechanical strain and glomerular hyperfiltration, chaperone therapy, blocking aberrant signaling between the glomerular basement membrane and podocytes, reducing endothelial cell injury, reducing inflammation, and blocking fibrosis pathways.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":"172-179"},"PeriodicalIF":9.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12807154/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145054103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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