Pub Date : 2024-08-23DOI: 10.1016/j.kint.2024.08.012
Chee Kay Cheung, Jonathan Barratt, Richard Lafayette, Adrian Liew, Yusuke Suzuki, Vladimír Tesař, Hernán Trimarchi, Muh Geot Wong, Hong Zhang, Dana V Rizk
A PRoliferation Inducing Ligand (APRIL) is a key member of the tumor necrosis factor (TNF)-superfamily of cytokines, and plays a central role in B cell survival, proliferation and immunoglobulin class switching. Recently, there has been increasing interest in the role of APRIL and the related cytokine B cell activating factor (BAFF) in several glomerular diseases, due to their importance in the above processes. The therapeutic inhibition of APRIL represents a potentially attractive immunomodulatory approach, that may abrogate deleterious host immune responses in autoimmune diseases while leaving other important functions of humoral immunity intact, such as memory B cell function and responses to vaccination, in contrast to B cell depleting strategies. In this review, we describe the physiological roles of APRIL in B cell development and their relevance to glomerular diseases, and outline emerging clinical trial data studying APRIL inhibition, with a focus on IgA nephropathy where the clinical development of APRIL inhibitors is in its most advanced stage.
增殖诱导配体(APRIL)是肿瘤坏死因子(TNF)超家族细胞因子的一个重要成员,在 B 细胞存活、增殖和免疫球蛋白类别转换中起着核心作用。最近,由于 APRIL 和相关细胞因子 B 细胞活化因子(BAFF)在上述过程中的重要作用,人们越来越关注它们在几种肾小球疾病中的作用。治疗性抑制 APRIL 代表了一种具有潜在吸引力的免疫调节方法,它可以消除自身免疫性疾病中有害的宿主免疫反应,同时保持体液免疫的其他重要功能完好无损,如记忆 B 细胞功能和疫苗接种反应,与 B 细胞耗竭策略形成鲜明对比。在这篇综述中,我们描述了APRIL在B细胞发育中的生理作用及其与肾小球疾病的相关性,并概述了研究APRIL抑制剂的新临床试验数据,重点是IgA肾病,APRIL抑制剂的临床开发正处于最后期阶段。
{"title":"Targeting APRIL in the treatment of glomerular diseases.","authors":"Chee Kay Cheung, Jonathan Barratt, Richard Lafayette, Adrian Liew, Yusuke Suzuki, Vladimír Tesař, Hernán Trimarchi, Muh Geot Wong, Hong Zhang, Dana V Rizk","doi":"10.1016/j.kint.2024.08.012","DOIUrl":"https://doi.org/10.1016/j.kint.2024.08.012","url":null,"abstract":"<p><p>A PRoliferation Inducing Ligand (APRIL) is a key member of the tumor necrosis factor (TNF)-superfamily of cytokines, and plays a central role in B cell survival, proliferation and immunoglobulin class switching. Recently, there has been increasing interest in the role of APRIL and the related cytokine B cell activating factor (BAFF) in several glomerular diseases, due to their importance in the above processes. The therapeutic inhibition of APRIL represents a potentially attractive immunomodulatory approach, that may abrogate deleterious host immune responses in autoimmune diseases while leaving other important functions of humoral immunity intact, such as memory B cell function and responses to vaccination, in contrast to B cell depleting strategies. In this review, we describe the physiological roles of APRIL in B cell development and their relevance to glomerular diseases, and outline emerging clinical trial data studying APRIL inhibition, with a focus on IgA nephropathy where the clinical development of APRIL inhibitors is in its most advanced stage.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055925","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 : 2024-08-22DOI: 10.1016/j.kint.2024.07.030
Michelle Willicombe, David J Roberts
HLA sensitisation remains an impediment to successful solid organ transplantation, whether it be chances of receiving a transplant offer or subsequent transplant longevity. Current treatments targeting HLA antibodies lack long term effectiveness, therefore preventing HLA sensitisation should remain a priority in all potential waitlist candidates and transplant recipients. Recent advances in the management of anaemia in patients with chronic kidney disease may reduce the need for red cell transfusions. However, data from several anaemia intervention studies of novel therapeutic agents have shown that a need for transfusion will remain. It has also been increasingly recognised that blood transfusions following kidney transplantation, especially in the peri-operative period, are common. Routine data on transfusion incidence, indications and outcomes, is not captured by most kidney and transplant registries across the globe. This restricts the evidence to inform both clinicians and patients on the clinical effects of transfusion, which have been considered both an allogeneic stimulus and to be immunomodulatory. This review aims to provide an update on what is currently known about transfusion-induced HLA sensitisation in waitlist candidates and transplant recipients, summarises where evidence is lacking and demonstrates the distinct need for patient blood management guidelines in the field of kidney transplantation.
{"title":"TRANSFUSION-INDUCED HLA SENSITISATION IN WAITLIST PATIENTS AND KIDNEY TRANSPLANT RECIPIENTS.","authors":"Michelle Willicombe, David J Roberts","doi":"10.1016/j.kint.2024.07.030","DOIUrl":"https://doi.org/10.1016/j.kint.2024.07.030","url":null,"abstract":"<p><p>HLA sensitisation remains an impediment to successful solid organ transplantation, whether it be chances of receiving a transplant offer or subsequent transplant longevity. Current treatments targeting HLA antibodies lack long term effectiveness, therefore preventing HLA sensitisation should remain a priority in all potential waitlist candidates and transplant recipients. Recent advances in the management of anaemia in patients with chronic kidney disease may reduce the need for red cell transfusions. However, data from several anaemia intervention studies of novel therapeutic agents have shown that a need for transfusion will remain. It has also been increasingly recognised that blood transfusions following kidney transplantation, especially in the peri-operative period, are common. Routine data on transfusion incidence, indications and outcomes, is not captured by most kidney and transplant registries across the globe. This restricts the evidence to inform both clinicians and patients on the clinical effects of transfusion, which have been considered both an allogeneic stimulus and to be immunomodulatory. This review aims to provide an update on what is currently known about transfusion-induced HLA sensitisation in waitlist candidates and transplant recipients, summarises where evidence is lacking and demonstrates the distinct need for patient blood management guidelines in the field of kidney transplantation.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055927","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 : 2024-08-22DOI: 10.1016/j.kint.2024.07.026
Esilida Sula Karreci, Sonako Jacas, Olivia Donovan, Diana Pintye, Nicholas Wiley, Zsuzsanna K Zsengeller, Johannes Schlondorff, Seth L Alper, David J Friedman, Martin R Pollak
Apolipoprotein L1 (APOL1) variants G1 and G2 contribute to the excess risk of kidney disease in individuals of recent African ancestry. Since disease mechanisms and optimal treatments remain controversial, we study the effect of current standard-of-care drugs in mouse models of APOL1 kidney disease. Experiments were performed in APOL1 BAC-transgenic mice, which develop proteinuria and glomerulosclerosis following injection with a pCpG-free IFNɤ plasmid. Proteinuric, plasmid injected G1/G1 and G2/G2 mice were randomized to drug treatment or no treatment. Lisinopril, dapagliflozin, and hydralazine were administered in drinking water starting day seven. The urine albumin/creatinine ratio was measured twice weekly, and the kidneys examined histologically with the focal segmental glomerulosclerosis score computed from periodic acid-Shiff-stained sections. The angiotensin converting enzyme inhibitor lisinopril, at standard dose, reduced proteinuria by approximately 90-fold and reduced glomerulosclerosis in the APOL1 G1/G1 BAC-transgenic mice. These effects were independent of blood pressure. Dapagliflozin did not alter disease progression in either G1/G1 or G2/G2 mice. Proteinuria reduction and glomerulosclerosis in G2/G2 BAC-transgenic mice required lisinopril doses two times higher than were effective in G1/G1 mice but achieved a much smaller benefit. Therefore, in these BAC-transgenic mouse models of APOL1 disease, the anti-proteinuric and anti-glomerulosclerotic effects of standard dose lisinopril were markedly effective in G1/G1 compared with G2/G2 APOL1 mice. Comparable reduction in blood pressure by hydralazine treatment provided no such protection. Neither G1/G1 or G2/G2 mice showed improvement with the sodium-glucose cotransporter-2 inhibition dapagliflozin. Thus, it remains to be determined if similar differences in ACE inhibitor responsiveness are observed in patients.
{"title":"Differing sensitivities to angiotensin converting enzyme inhibition of kidney disease mediated by APOL1 high-risk variants G1 and G2.","authors":"Esilida Sula Karreci, Sonako Jacas, Olivia Donovan, Diana Pintye, Nicholas Wiley, Zsuzsanna K Zsengeller, Johannes Schlondorff, Seth L Alper, David J Friedman, Martin R Pollak","doi":"10.1016/j.kint.2024.07.026","DOIUrl":"https://doi.org/10.1016/j.kint.2024.07.026","url":null,"abstract":"<p><p>Apolipoprotein L1 (APOL1) variants G1 and G2 contribute to the excess risk of kidney disease in individuals of recent African ancestry. Since disease mechanisms and optimal treatments remain controversial, we study the effect of current standard-of-care drugs in mouse models of APOL1 kidney disease. Experiments were performed in APOL1 BAC-transgenic mice, which develop proteinuria and glomerulosclerosis following injection with a pCpG-free IFNɤ plasmid. Proteinuric, plasmid injected G1/G1 and G2/G2 mice were randomized to drug treatment or no treatment. Lisinopril, dapagliflozin, and hydralazine were administered in drinking water starting day seven. The urine albumin/creatinine ratio was measured twice weekly, and the kidneys examined histologically with the focal segmental glomerulosclerosis score computed from periodic acid-Shiff-stained sections. The angiotensin converting enzyme inhibitor lisinopril, at standard dose, reduced proteinuria by approximately 90-fold and reduced glomerulosclerosis in the APOL1 G1/G1 BAC-transgenic mice. These effects were independent of blood pressure. Dapagliflozin did not alter disease progression in either G1/G1 or G2/G2 mice. Proteinuria reduction and glomerulosclerosis in G2/G2 BAC-transgenic mice required lisinopril doses two times higher than were effective in G1/G1 mice but achieved a much smaller benefit. Therefore, in these BAC-transgenic mouse models of APOL1 disease, the anti-proteinuric and anti-glomerulosclerotic effects of standard dose lisinopril were markedly effective in G1/G1 compared with G2/G2 APOL1 mice. Comparable reduction in blood pressure by hydralazine treatment provided no such protection. Neither G1/G1 or G2/G2 mice showed improvement with the sodium-glucose cotransporter-2 inhibition dapagliflozin. Thus, it remains to be determined if similar differences in ACE inhibitor responsiveness are observed in patients.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055923","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 : 2024-08-22DOI: 10.1016/j.kint.2024.07.025
Thibaut Vaulet, Maarten Naesens
{"title":"Stronger together: the power of cross-organ data sets for improved allograft study outcomes.","authors":"Thibaut Vaulet, Maarten Naesens","doi":"10.1016/j.kint.2024.07.025","DOIUrl":"https://doi.org/10.1016/j.kint.2024.07.025","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142140386","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 : 2024-08-22DOI: 10.1016/j.kint.2024.07.028
Lianqin Sun, Lishan Liu, Juanjuan Jiang, Kang Liu, Jingfeng Zhu, Lin Wu, Xiaohan Lu, Zhimin Huang, Yanggang Yuan, Steven D Crowley, Huijuan Mao, Changying Xing, Jiafa Ren
The transcription factor Twist1 plays a vital role in normal development in many tissue systems and continues to be important throughout life. However, inappropriate Twist1 activity has been associated with kidney injury and fibrosis, though the underlying mechanisms involved remain incomplete. Here, we explored the role of Twist1 in regulating fibroblast behaviors and the development kidney fibrosis. Initially Twist1 protein and activity was found to be markedly increased within interstitial myofibroblasts in fibrotic kidneys in both humans and rodents. Treatment of rat kidney interstitial fibroblasts with transforming growth factor-β1 (a profibrotic factor) also induced Twist1 expression in vitro. Gain- and loss-of-function experiments supported that Twist1 signaling was responsible for transforming growth factor-β1-induced fibroblast activation and fetal bovine serum-induced fibroblast proliferation. Mechanistically, Twist1 protein promoted kidney fibroblast activation by driving the expression of downstream signaling proteins, Prrx1 and Tnc. Twist1 directly enhanced binding to the promoter of Prrx1 but not TNC, whereas the promoter of TNC was directly bound by Prrx1. Finally, mice with fibroblast-specific deletion of Twist1 exhibited less Prrx1 and TNC protein abundance, interstitial extracellular matrix deposition and kidney inflammation in both the unilateral ureteral obstruction and ischemic-reperfusion injury-induced-kidney fibrotic models. Inhibition of Twist1 signaling with Harmine, a β-carboline alkaloid, improved extracellular matrix deposition in both injury models. Thus, our results suggest that Twist1 signaling promotes the activation and proliferation of kidney fibroblasts, contributing to the development of interstitial fibrosis, offering a potential therapeutic target for chronic kidney disease.
{"title":"Transcription factor Twist1 drives fibroblast activation to promote kidney fibrosis via signaling proteins Prrx1/TNC3.","authors":"Lianqin Sun, Lishan Liu, Juanjuan Jiang, Kang Liu, Jingfeng Zhu, Lin Wu, Xiaohan Lu, Zhimin Huang, Yanggang Yuan, Steven D Crowley, Huijuan Mao, Changying Xing, Jiafa Ren","doi":"10.1016/j.kint.2024.07.028","DOIUrl":"10.1016/j.kint.2024.07.028","url":null,"abstract":"<p><p>The transcription factor Twist1 plays a vital role in normal development in many tissue systems and continues to be important throughout life. However, inappropriate Twist1 activity has been associated with kidney injury and fibrosis, though the underlying mechanisms involved remain incomplete. Here, we explored the role of Twist1 in regulating fibroblast behaviors and the development kidney fibrosis. Initially Twist1 protein and activity was found to be markedly increased within interstitial myofibroblasts in fibrotic kidneys in both humans and rodents. Treatment of rat kidney interstitial fibroblasts with transforming growth factor-β1 (a profibrotic factor) also induced Twist1 expression in vitro. Gain- and loss-of-function experiments supported that Twist1 signaling was responsible for transforming growth factor-β1-induced fibroblast activation and fetal bovine serum-induced fibroblast proliferation. Mechanistically, Twist1 protein promoted kidney fibroblast activation by driving the expression of downstream signaling proteins, Prrx1 and Tnc. Twist1 directly enhanced binding to the promoter of Prrx1 but not TNC, whereas the promoter of TNC was directly bound by Prrx1. Finally, mice with fibroblast-specific deletion of Twist1 exhibited less Prrx1 and TNC protein abundance, interstitial extracellular matrix deposition and kidney inflammation in both the unilateral ureteral obstruction and ischemic-reperfusion injury-induced-kidney fibrotic models. Inhibition of Twist1 signaling with Harmine, a β-carboline alkaloid, improved extracellular matrix deposition in both injury models. Thus, our results suggest that Twist1 signaling promotes the activation and proliferation of kidney fibroblasts, contributing to the development of interstitial fibrosis, offering a potential therapeutic target for chronic kidney disease.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055926","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 : 2024-08-22DOI: 10.1016/j.kint.2024.08.009
Sanjeev Sethi, Benjamin Madden, Marta Casal Moura, Samih H Nasr, Mariam P Alexander, Hanna Debiec, Nate Torrel, LouAnn Gross, Vivian Negron, Ulrich Specks, Fernando C Fervenza, Mark Haas, Pierre Ronco, Ibrahim Batal
{"title":"FAT1 is a target antigen in a subset of de novo allograft membranous nephropathy associated with antibody mediated rejection.","authors":"Sanjeev Sethi, Benjamin Madden, Marta Casal Moura, Samih H Nasr, Mariam P Alexander, Hanna Debiec, Nate Torrel, LouAnn Gross, Vivian Negron, Ulrich Specks, Fernando C Fervenza, Mark Haas, Pierre Ronco, Ibrahim Batal","doi":"10.1016/j.kint.2024.08.009","DOIUrl":"https://doi.org/10.1016/j.kint.2024.08.009","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055924","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 : 2024-08-20DOI: 10.1016/j.kint.2024.06.019
Yamamoto et al. developed an exciting technical advance to examine intracellular adenosine triphosphate levels with single-cell resolution in intact living kidney tissue, including in tubular and vascular segments that lie deep under the kidney surface. The work is a significant advance on prior in vivo biosensor studies, and it allows for mechanistic investigation of alterations in cell metabolism, kidney disease pathobiology, and the effects of drug treatments on energy sources in different kidney cell types.
{"title":"See the power in kidney cells with ATP biosensor","authors":"","doi":"10.1016/j.kint.2024.06.019","DOIUrl":"10.1016/j.kint.2024.06.019","url":null,"abstract":"<div><p>Yamamoto <em>et al.</em> developed an exciting technical advance to examine intracellular adenosine triphosphate levels with single-cell resolution in intact living kidney tissue, including in tubular and vascular segments that lie deep under the kidney surface. The work is a significant advance on prior <em>in vivo</em> biosensor studies, and it allows for mechanistic investigation of alterations in cell metabolism, kidney disease pathobiology, and the effects of drug treatments on energy sources in different kidney cell types.</p></div>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142012474","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 : 2024-08-20DOI: 10.1016/j.kint.2024.05.013
{"title":"The Case | Obstructive acute renal failure due to acute uric acid nephrolithiasis","authors":"","doi":"10.1016/j.kint.2024.05.013","DOIUrl":"10.1016/j.kint.2024.05.013","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142012575","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 : 2024-08-20DOI: 10.1016/j.kint.2024.07.001
Identifying people at risk for progressive chronic kidney disease and connecting them with recommended care is crucial for providing timely and optimal treatment. The ASSIST-CKD (A programme to Spread eGFR [estimated glomerular filtration rate] graph Surveillance for the early identification, Support and Treatment of people with progressive CKD [chronic kidney disease]) trial evaluated the effect of graphical eGFR reporting to primary care physicians on late presentation to a nephrologist in the United Kingdom. Trial data were obtained from the UK Renal Registry. Although the results were neutral, the data generated from the ASSIST-CKD trial are informative and provide useful estimates of the intervention effect. The trial also provides valuable insights into the challenges of implementing complex interventions in busy health care environments, which can be used to guide the designs of future interventions.
{"title":"Improving the management of chronic kidney disease in primary care by enhancing laboratory reports with additional information and follow-up procedures","authors":"","doi":"10.1016/j.kint.2024.07.001","DOIUrl":"10.1016/j.kint.2024.07.001","url":null,"abstract":"<div><p>Identifying people at risk for progressive chronic kidney disease and connecting them with recommended care is crucial for providing timely and optimal treatment. The ASSIST-CKD (A programme to Spread eGFR [estimated glomerular filtration rate] graph Surveillance for the early identification, Support and Treatment of people with progressive CKD [chronic kidney disease]) trial evaluated the effect of graphical eGFR reporting to primary care physicians on late presentation to a nephrologist in the United Kingdom. Trial data were obtained from the UK Renal Registry. Although the results were neutral, the data generated from the ASSIST-CKD trial are informative and provide useful estimates of the intervention effect. The trial also provides valuable insights into the challenges of implementing complex interventions in busy health care environments, which can be used to guide the designs of future interventions.</p></div>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142012512","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}