Pub Date : 2025-08-29DOI: 10.1038/s41581-025-01002-8
Ellen F. Carney
{"title":"Accumulation of pathogenic mitochondrial DNA mutations in the kidney","authors":"Ellen F. Carney","doi":"10.1038/s41581-025-01002-8","DOIUrl":"10.1038/s41581-025-01002-8","url":null,"abstract":"","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 10","pages":"649-649"},"PeriodicalIF":39.8,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144915394","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 : 2025-08-26DOI: 10.1038/s41581-025-01001-9
Susan J. Allison
{"title":"Regulation of autophagy by a tRNA-derived fragment","authors":"Susan J. Allison","doi":"10.1038/s41581-025-01001-9","DOIUrl":"10.1038/s41581-025-01001-9","url":null,"abstract":"","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 10","pages":"649-649"},"PeriodicalIF":39.8,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899103","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 : 2025-08-19DOI: 10.1038/s41581-025-00998-3
Paula A. Marioli
Renálida is an organizational model that transforms healthcare coverage into genuine access. In contexts where older adults are excluded from effective care, Renálida offers early and sustained attention through connection, science and meaning. This is an invitation to trust: change is possible when clinical practice is humanized and purposefully organized.
{"title":"A strength-based community: transforming renal care through connection and meaning","authors":"Paula A. Marioli","doi":"10.1038/s41581-025-00998-3","DOIUrl":"10.1038/s41581-025-00998-3","url":null,"abstract":"Renálida is an organizational model that transforms healthcare coverage into genuine access. In contexts where older adults are excluded from effective care, Renálida offers early and sustained attention through connection, science and meaning. This is an invitation to trust: change is possible when clinical practice is humanized and purposefully organized.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 10","pages":"648-648"},"PeriodicalIF":39.8,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144883263","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 : 2025-08-11DOI: 10.1038/s41581-025-00990-x
Matteo Bargagli, Martin Scoglio, Sarah A. Howles, Daniel G. Fuster
Nephrolithiasis is the most common health condition affecting the kidney and urinary tract and constitutes a major global health-care problem. The prevalence of nephrolithiasis has increased substantially over the past five decades, irrespective of age, sex or ethnicity. Kidney stones cause substantial morbidity, reduced quality of life and enormous health-care expenditure, largely due to their frequent recurrence. Furthermore, nephrolithiasis is now recognized as a systemic condition associated with increased risks of chronic kidney disease, cardiovascular disease, metabolic syndrome and low bone mass. Nephrolithiasis exhibits marked pathophysiological heterogeneity. Dietary and environmental exposures interact with genetic predisposition to shape individual disease risk. Calcium oxalate stones are most prevalent, commonly driven by hypercalciuria, hyperoxaluria, hypocitraturia and low urine volume, whereas the formation of uric acid and calcium phosphate stones is commonly linked to urinary pH. A comprehensive clinical evaluation can uncover underlying metabolic abnormalities, distinguish idiopathic, secondary and Mendelian forms of nephrolithiasis, identify systemic disease associations and guide therapy. Recurrence prevention requires individualized strategies that combine dietary and pharmacological interventions. For established stones, surgical management is effective, with ureteroscopy and percutaneous nephrolithotomy achieving high stone-free rates. Despite its considerable clinical and societal burden, nephrolithiasis remains under-recognized, underserved and under-researched. Greater awareness and investments in research, innovation and education are urgently needed. This Review discusses the pathophysiology of kidney stone formation and examines the contribution of urinary risk factors and genetic variants. The authors also consider current approaches to the management of nephrolithiasis, including the role of metabolic evaluation and interventions for prevention of kidney stone recurrence.
{"title":"Kidney stone disease: risk factors, pathophysiology and management","authors":"Matteo Bargagli, Martin Scoglio, Sarah A. Howles, Daniel G. Fuster","doi":"10.1038/s41581-025-00990-x","DOIUrl":"10.1038/s41581-025-00990-x","url":null,"abstract":"Nephrolithiasis is the most common health condition affecting the kidney and urinary tract and constitutes a major global health-care problem. The prevalence of nephrolithiasis has increased substantially over the past five decades, irrespective of age, sex or ethnicity. Kidney stones cause substantial morbidity, reduced quality of life and enormous health-care expenditure, largely due to their frequent recurrence. Furthermore, nephrolithiasis is now recognized as a systemic condition associated with increased risks of chronic kidney disease, cardiovascular disease, metabolic syndrome and low bone mass. Nephrolithiasis exhibits marked pathophysiological heterogeneity. Dietary and environmental exposures interact with genetic predisposition to shape individual disease risk. Calcium oxalate stones are most prevalent, commonly driven by hypercalciuria, hyperoxaluria, hypocitraturia and low urine volume, whereas the formation of uric acid and calcium phosphate stones is commonly linked to urinary pH. A comprehensive clinical evaluation can uncover underlying metabolic abnormalities, distinguish idiopathic, secondary and Mendelian forms of nephrolithiasis, identify systemic disease associations and guide therapy. Recurrence prevention requires individualized strategies that combine dietary and pharmacological interventions. For established stones, surgical management is effective, with ureteroscopy and percutaneous nephrolithotomy achieving high stone-free rates. Despite its considerable clinical and societal burden, nephrolithiasis remains under-recognized, underserved and under-researched. Greater awareness and investments in research, innovation and education are urgently needed. This Review discusses the pathophysiology of kidney stone formation and examines the contribution of urinary risk factors and genetic variants. The authors also consider current approaches to the management of nephrolithiasis, including the role of metabolic evaluation and interventions for prevention of kidney stone recurrence.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 11","pages":"794-808"},"PeriodicalIF":39.8,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812845","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 : 2025-08-08DOI: 10.1038/s41581-025-00995-6
Kar Hui Ng
{"title":"A call for funds and training for kidney genomics programmes","authors":"Kar Hui Ng","doi":"10.1038/s41581-025-00995-6","DOIUrl":"10.1038/s41581-025-00995-6","url":null,"abstract":"","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 10","pages":"647-647"},"PeriodicalIF":39.8,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144797103","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 : 2025-08-05DOI: 10.1038/s41581-025-00994-7
Hiroshi Nishi, Masaomi Nangaku
Anaemia is a frequent complication of chronic kidney disease (CKD) that is associated with reduced quality of life and adverse clinical outcomes. A new analysis suggests that the global burden of anaemia in CKD will rise substantially in the next 25 years.
{"title":"The increasing burden of mild and moderate anaemia in CKD","authors":"Hiroshi Nishi, Masaomi Nangaku","doi":"10.1038/s41581-025-00994-7","DOIUrl":"10.1038/s41581-025-00994-7","url":null,"abstract":"Anaemia is a frequent complication of chronic kidney disease (CKD) that is associated with reduced quality of life and adverse clinical outcomes. A new analysis suggests that the global burden of anaemia in CKD will rise substantially in the next 25 years.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 10","pages":"651-652"},"PeriodicalIF":39.8,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144786815","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 : 2025-07-31DOI: 10.1038/s41581-025-00989-4
Yu Ah Hong (, ), Reiko Inagi (, )
The endoplasmic reticulum (ER) is a key organelle involved in a wide range of intracellular biological processes, including Ca2+ homeostasis; lipid metabolism; proteostasis through protein synthesis, folding and processing of secretory and transmembrane proteins; and signal transduction. The ER forms extensive physical interactions with various intracellular organelles through the membrane contact sites, enabling direct exchange of ions and lipids without vesicular transport. At mitochondria-associated membranes, ER–mitochondria communication governs calcium transfer, lipid synthesis, mitochondrial dynamics, the unfolded protein response and inflammation, all of which are essential for maintaining cellular homeostasis. The ER also interacts with the Golgi apparatus, endosomes and plasma membrane to facilitate transfer of calcium and lipids. Disruption of ER–organelle communication contributes to the development and progression of various kidney diseases, including diabetic kidney disease, acute kidney injury and polycystic kidney disease. Accordingly, ER–organelle communication has emerged as a promising therapeutic target. Pharmacological agents such as SGLT2 inhibitors, AMPK activators, mTOR inhibitors and RAAS blockers have been shown to restore ER–mitochondria communication and alleviate kidney injury in experimental models. Advancing our understanding of ER–organelle crosstalk may offer new mechanistic insights and contribute to the optimization of current treatment strategies for kidney disease. Here, the authors discuss communication between the ER and other intracellular organelles under physiological and pathological conditions. They highlight the potential role of this crosstalk in the pathogenesis of kidney diseases and discuss potential therapeutic strategies aimed at modulating this crosstalk.
{"title":"Endoplasmic reticulum-mediated organelle crosstalk in kidney disease","authors":"Yu Ah Hong \u0000 (, ), Reiko Inagi \u0000 (, )","doi":"10.1038/s41581-025-00989-4","DOIUrl":"10.1038/s41581-025-00989-4","url":null,"abstract":"The endoplasmic reticulum (ER) is a key organelle involved in a wide range of intracellular biological processes, including Ca2+ homeostasis; lipid metabolism; proteostasis through protein synthesis, folding and processing of secretory and transmembrane proteins; and signal transduction. The ER forms extensive physical interactions with various intracellular organelles through the membrane contact sites, enabling direct exchange of ions and lipids without vesicular transport. At mitochondria-associated membranes, ER–mitochondria communication governs calcium transfer, lipid synthesis, mitochondrial dynamics, the unfolded protein response and inflammation, all of which are essential for maintaining cellular homeostasis. The ER also interacts with the Golgi apparatus, endosomes and plasma membrane to facilitate transfer of calcium and lipids. Disruption of ER–organelle communication contributes to the development and progression of various kidney diseases, including diabetic kidney disease, acute kidney injury and polycystic kidney disease. Accordingly, ER–organelle communication has emerged as a promising therapeutic target. Pharmacological agents such as SGLT2 inhibitors, AMPK activators, mTOR inhibitors and RAAS blockers have been shown to restore ER–mitochondria communication and alleviate kidney injury in experimental models. Advancing our understanding of ER–organelle crosstalk may offer new mechanistic insights and contribute to the optimization of current treatment strategies for kidney disease. Here, the authors discuss communication between the ER and other intracellular organelles under physiological and pathological conditions. They highlight the potential role of this crosstalk in the pathogenesis of kidney diseases and discuss potential therapeutic strategies aimed at modulating this crosstalk.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 11","pages":"736-755"},"PeriodicalIF":39.8,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144756080","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 : 2025-07-31DOI: 10.1038/s41581-025-00982-x
Dawiyat Massoudi, Jeffrey H. Miner, Douglas B. Gould
Collagen IV is a basement membrane component that is encoded by six genes in mammals (COL4Α1–COL4A6). The α-chains encoded by these genes assemble into three known heterotrimers — collagen α1α1α2(IV), α3α4α5(IV) and α5α5α6(IV) — that provide structure and act as multifunctional signalling platforms. The ancestral collagen superfamily members collagen alpha-1(IV) chain (COL4Α1) and collagen alpha-2(IV) chain (COL4Α2) are present throughout the animal kingdom and in all developing and most mature mammalian tissues. Consistent with this broad distribution, variants in COL4A1 and COL4A2 cause a congenital multisystem disorder called Gould syndrome (GS), which is characterized by cerebral, ocular, muscular and kidney defects. The main clinical consequences involve the cerebral vasculature (porencephaly, small-vessel disease, leukoencephalopathy and intracerebral haemorrhage). However, the full clinical spectrum, including the organs affected and acquired phenotypes such as vascular dementia, is still being defined. By contrast, variants in COL4A3, COL4A4 or COL4A5 cause Alport syndrome (AS), a disorder of variable severity that affects the kidney, ear and eye. AS nephropathies often progress from haematuria to proteinuria, renal impairment and kidney failure. The auditory features include sensorineural hearing loss, whereas the ocular features comprise corneal dystrophy, lenticonus, dot-and-fleck retinopathy and maculopathy. Although GS and AS have little clinical resemblance, the high conservation of the genes and proteins suggests common elements of underlying pathophysiology. Conventional therapies that modify haemodynamics have lengthened the time to kidney failure for patients living with AS. However, no curative or mechanism-based interventions exist for GS. Gene-editing approaches hold promise for both disorders. In this Review, the authors focus on the role of collagen IV in Gould syndrome and Alport syndrome. They discuss the molecular and phenotypic similarities and differences between these syndromes, as well as potential targeted therapeutic strategies.
{"title":"Collagen IV in Gould syndrome and Alport syndrome","authors":"Dawiyat Massoudi, Jeffrey H. Miner, Douglas B. Gould","doi":"10.1038/s41581-025-00982-x","DOIUrl":"10.1038/s41581-025-00982-x","url":null,"abstract":"Collagen IV is a basement membrane component that is encoded by six genes in mammals (COL4Α1–COL4A6). The α-chains encoded by these genes assemble into three known heterotrimers — collagen α1α1α2(IV), α3α4α5(IV) and α5α5α6(IV) — that provide structure and act as multifunctional signalling platforms. The ancestral collagen superfamily members collagen alpha-1(IV) chain (COL4Α1) and collagen alpha-2(IV) chain (COL4Α2) are present throughout the animal kingdom and in all developing and most mature mammalian tissues. Consistent with this broad distribution, variants in COL4A1 and COL4A2 cause a congenital multisystem disorder called Gould syndrome (GS), which is characterized by cerebral, ocular, muscular and kidney defects. The main clinical consequences involve the cerebral vasculature (porencephaly, small-vessel disease, leukoencephalopathy and intracerebral haemorrhage). However, the full clinical spectrum, including the organs affected and acquired phenotypes such as vascular dementia, is still being defined. By contrast, variants in COL4A3, COL4A4 or COL4A5 cause Alport syndrome (AS), a disorder of variable severity that affects the kidney, ear and eye. AS nephropathies often progress from haematuria to proteinuria, renal impairment and kidney failure. The auditory features include sensorineural hearing loss, whereas the ocular features comprise corneal dystrophy, lenticonus, dot-and-fleck retinopathy and maculopathy. Although GS and AS have little clinical resemblance, the high conservation of the genes and proteins suggests common elements of underlying pathophysiology. Conventional therapies that modify haemodynamics have lengthened the time to kidney failure for patients living with AS. However, no curative or mechanism-based interventions exist for GS. Gene-editing approaches hold promise for both disorders. In this Review, the authors focus on the role of collagen IV in Gould syndrome and Alport syndrome. They discuss the molecular and phenotypic similarities and differences between these syndromes, as well as potential targeted therapeutic strategies.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 11","pages":"778-793"},"PeriodicalIF":39.8,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144747080","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 : 2025-07-29DOI: 10.1038/s41581-025-00985-8
Alexandria N. Fusco, Leif Oxburgh, Thomas J. Carroll
The kidney is one of the most complex organs in the body. It is made up of thousands of patterned epithelial and endothelial tubules that work together to maintain body chemistry. Precise spatial integration of these different cell types is essential for the organ to function optimally. A complex and heterogeneous network of cells collectively referred to as ‘stroma’ lies between the epithelial and endothelial tubules. A growing body of evidence suggests that the stroma mediates communication between the epithelia and endothelia, and functions to support a variety of processes during kidney development and in the adult kidney, with implications for disease. However, stromal cells remain far less well defined than the epithelia and endothelia, and we understand only a fraction of their functions, leading some to refer to the stroma as the ‘dark matter’ of the kidney. In this Review, we discuss the developmental origins of the stroma and describe current understanding of its roles in the growth and patterning of the renal epithelia and endothelia, and in the maintenance and repair of the adult organ. Finally, we highlight critical questions that remain unanswered and the resources that will be required to answer them so that we can fully understand the function of these enigmatic cells. Available evidence suggests that the kidney stroma mediates cell communication and supports a variety of processes during kidney development and in the adult kidney. This Review describes the developmental origins of the stroma and current understanding of its roles in the growth and patterning of renal epithelia and endothelia, and in the maintenance and repair of the adult organ.
{"title":"The kidney stroma in development and disease","authors":"Alexandria N. Fusco, Leif Oxburgh, Thomas J. Carroll","doi":"10.1038/s41581-025-00985-8","DOIUrl":"10.1038/s41581-025-00985-8","url":null,"abstract":"The kidney is one of the most complex organs in the body. It is made up of thousands of patterned epithelial and endothelial tubules that work together to maintain body chemistry. Precise spatial integration of these different cell types is essential for the organ to function optimally. A complex and heterogeneous network of cells collectively referred to as ‘stroma’ lies between the epithelial and endothelial tubules. A growing body of evidence suggests that the stroma mediates communication between the epithelia and endothelia, and functions to support a variety of processes during kidney development and in the adult kidney, with implications for disease. However, stromal cells remain far less well defined than the epithelia and endothelia, and we understand only a fraction of their functions, leading some to refer to the stroma as the ‘dark matter’ of the kidney. In this Review, we discuss the developmental origins of the stroma and describe current understanding of its roles in the growth and patterning of the renal epithelia and endothelia, and in the maintenance and repair of the adult organ. Finally, we highlight critical questions that remain unanswered and the resources that will be required to answer them so that we can fully understand the function of these enigmatic cells. Available evidence suggests that the kidney stroma mediates cell communication and supports a variety of processes during kidney development and in the adult kidney. This Review describes the developmental origins of the stroma and current understanding of its roles in the growth and patterning of renal epithelia and endothelia, and in the maintenance and repair of the adult organ.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 11","pages":"756-777"},"PeriodicalIF":39.8,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144737178","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 : 2025-07-28DOI: 10.1038/s41581-025-00988-5
Patricia P. Bloom, Wendy S. Garrett, Kristina L. Penniston, Mari-Karoliina H. Winkler, Stanley L. Hazen, Jose Agudelo, Mangesh Suryavanshi, Ahmed Babiker, Dylan Dodd, Michael A. Fischbach, Kerwyn Casey Huang, Curtis Huttenhower, Bina Joe, Kamyar Kalantar-Zadeh, Rob Knight, Aaron W. Miller, Hamid Rabb, Anvesha Srivastava, W. H. Wilson Tang, Peter J. Turnbaugh, Alan W. Walker, Nicola Wilck, Jiaojiao Xu, Tao Yang (, ), Jonathan Himmelfarb, Matthew R. Redinbo, Gary D. Wu, Michael H. Woodworth, A. Lenore Ackerman, Sebastian Winter, Markus M. Rinschen, Hatim A. Hassan, Annabel Biruete, Amanda H. Anderson, Jennifer L. Pluznick
More than 850 million individuals worldwide, accounting for 10–15% of the adult population, are estimated to have chronic kidney disease. Each of these individuals is host to tens of trillions of microorganisms that are collectively referred to as microbiota — a dynamic ecosystem that both influences host health and is itself influenced by changes in the host. Available evidence supports the existence of functional connections between resident microorganisms and kidney health that are altered in the context of specific kidney diseases, including acute kidney injury, chronic kidney disease and renal stone disease. Moreover, promising data from preclinical studies suggest that targeting of gut microbial pathways may provide new therapeutic opportunities for the treatment of kidney disease. This Roadmap describes current understanding of the mechanisms by which microorganisms regulate host organ function, the effects of kidney disease on the gut microbiome, and how these insights may contribute to the development of microbe-targeted therapeutics. We highlight key knowledge gaps that remain to be addressed and strategies for addressing these, outlining both the promise and the potential pitfalls of leveraging our understanding of the gut microbiota to better understand and treat kidney disease. Available evidence supports the existence of functional connections between resident microorganisms and the kidney that are altered in the context of specific kidney diseases. This Roadmap article describes current understanding of the mechanisms by which microorganisms regulate host organ function, highlighting key knowledge gaps that remain to be addressed and opportunities for future research.
{"title":"Microbiota and kidney disease: the road ahead","authors":"Patricia P. Bloom, Wendy S. Garrett, Kristina L. Penniston, Mari-Karoliina H. Winkler, Stanley L. Hazen, Jose Agudelo, Mangesh Suryavanshi, Ahmed Babiker, Dylan Dodd, Michael A. Fischbach, Kerwyn Casey Huang, Curtis Huttenhower, Bina Joe, Kamyar Kalantar-Zadeh, Rob Knight, Aaron W. Miller, Hamid Rabb, Anvesha Srivastava, W. H. Wilson Tang, Peter J. Turnbaugh, Alan W. Walker, Nicola Wilck, Jiaojiao Xu, Tao Yang \u0000 (, ), Jonathan Himmelfarb, Matthew R. Redinbo, Gary D. Wu, Michael H. Woodworth, A. Lenore Ackerman, Sebastian Winter, Markus M. Rinschen, Hatim A. Hassan, Annabel Biruete, Amanda H. Anderson, Jennifer L. Pluznick","doi":"10.1038/s41581-025-00988-5","DOIUrl":"10.1038/s41581-025-00988-5","url":null,"abstract":"More than 850 million individuals worldwide, accounting for 10–15% of the adult population, are estimated to have chronic kidney disease. Each of these individuals is host to tens of trillions of microorganisms that are collectively referred to as microbiota — a dynamic ecosystem that both influences host health and is itself influenced by changes in the host. Available evidence supports the existence of functional connections between resident microorganisms and kidney health that are altered in the context of specific kidney diseases, including acute kidney injury, chronic kidney disease and renal stone disease. Moreover, promising data from preclinical studies suggest that targeting of gut microbial pathways may provide new therapeutic opportunities for the treatment of kidney disease. This Roadmap describes current understanding of the mechanisms by which microorganisms regulate host organ function, the effects of kidney disease on the gut microbiome, and how these insights may contribute to the development of microbe-targeted therapeutics. We highlight key knowledge gaps that remain to be addressed and strategies for addressing these, outlining both the promise and the potential pitfalls of leveraging our understanding of the gut microbiota to better understand and treat kidney disease. Available evidence supports the existence of functional connections between resident microorganisms and the kidney that are altered in the context of specific kidney diseases. This Roadmap article describes current understanding of the mechanisms by which microorganisms regulate host organ function, highlighting key knowledge gaps that remain to be addressed and opportunities for future research.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 10","pages":"702-716"},"PeriodicalIF":39.8,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144719393","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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