Pub Date : 2024-02-01DOI: 10.1038/s41581-024-00816-2
Monica Wang
{"title":"Macrophages clean out the tubules","authors":"Monica Wang","doi":"10.1038/s41581-024-00816-2","DOIUrl":"10.1038/s41581-024-00816-2","url":null,"abstract":"","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":null,"pages":null},"PeriodicalIF":41.5,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139660050","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 : 2024-01-30DOI: 10.1038/s41581-024-00813-5
Susan J. Allison
{"title":"Design of a renal-sparing antifungal","authors":"Susan J. Allison","doi":"10.1038/s41581-024-00813-5","DOIUrl":"10.1038/s41581-024-00813-5","url":null,"abstract":"","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":null,"pages":null},"PeriodicalIF":41.5,"publicationDate":"2024-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139642571","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 : 2024-01-30DOI: 10.1038/s41581-024-00814-4
Ellen F. Carney
{"title":"Effects of SGLT2 inhibitors on the metabolic environment and uraemic toxins","authors":"Ellen F. Carney","doi":"10.1038/s41581-024-00814-4","DOIUrl":"10.1038/s41581-024-00814-4","url":null,"abstract":"","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":null,"pages":null},"PeriodicalIF":41.5,"publicationDate":"2024-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139642572","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 : 2024-01-29DOI: 10.1038/s41581-024-00812-6
Susan E. Quaggin, Benjamin Magod
Improved understanding of the interrelated nature of cardiovascular, kidney and metabolic (CKM) health, the development of novel risk prediction equations, and the availability of powerful new therapies provide an opportunity to change the course of CKM health. Achieving such change at a population level will require additional advances to deliver equitable interdisciplinary care.
{"title":"A united vision for cardiovascular–kidney–metabolic health","authors":"Susan E. Quaggin, Benjamin Magod","doi":"10.1038/s41581-024-00812-6","DOIUrl":"10.1038/s41581-024-00812-6","url":null,"abstract":"Improved understanding of the interrelated nature of cardiovascular, kidney and metabolic (CKM) health, the development of novel risk prediction equations, and the availability of powerful new therapies provide an opportunity to change the course of CKM health. Achieving such change at a population level will require additional advances to deliver equitable interdisciplinary care.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":null,"pages":null},"PeriodicalIF":41.5,"publicationDate":"2024-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139573502","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 : 2024-01-29DOI: 10.1038/s41581-024-00808-2
Dina Greenberg, Norman D. Rosenblum, Marcello Tonelli
Hearing loss affects nearly 1.6 billion people and is the third-leading cause of disability worldwide. Chronic kidney disease (CKD) is also a common condition that is associated with adverse clinical outcomes and high health-care costs. From a developmental perspective, the structures responsible for hearing have a common morphogenetic origin with the kidney, and genetic abnormalities that cause familial forms of hearing loss can also lead to kidney disease. On a cellular level, normal kidney and cochlea function both depend on cilial activities at the apical surface, and kidney tubular cells and sensory epithelial cells of the inner ear use similar transport mechanisms to modify luminal fluid. The two organs also share the same collagen IV basement membrane network. Thus, strong developmental and physiological links exist between hearing and kidney function. These theoretical considerations are supported by epidemiological data demonstrating that CKD is associated with a graded and independent excess risk of sensorineural hearing loss. In addition to developmental and physiological links between kidney and cochlear function, hearing loss in patients with CKD may be driven by specific medications or treatments, including haemodialysis. The associations between these two common conditions are not commonly appreciated, yet have important implications for research and clinical practice. Chronic kidney disease is associated with a graded and independent excess risk of sensorineural hearing loss. This Review describes how disruption of shared signalling pathways that are important for the development of both the ear and the kidney and/or the presence of clinical drivers, such as specific medications or treatments, may underlie these associations.
听力损失影响着近 16 亿人，是全球第三大致残原因。慢性肾脏病（CKD）也是一种常见疾病，与不良的临床结果和高昂的医疗费用有关。从发育的角度来看，负责听力的结构与肾脏有着共同的形态发生起源，导致家族性听力损失的基因异常也可能导致肾脏疾病。在细胞层面上，肾脏和耳蜗的正常功能都依赖于纤毛在顶端表面的活动，肾小管细胞和内耳的感觉上皮细胞使用类似的运输机制来改变管腔液体。这两个器官还具有相同的胶原蛋白 IV 基底膜网络。因此，听力和肾功能之间存在着密切的发育和生理联系。流行病学数据证明，慢性肾功能衰竭与感音神经性听力损失的分级和独立超额风险有关，这为这些理论考虑提供了支持。除了肾脏和耳蜗功能之间的发育和生理联系外，慢性肾功能衰竭患者的听力损失可能是由特定药物或治疗（包括血液透析）引起的。这两种常见疾病之间的关联并未得到普遍重视，但却对研究和临床实践具有重要意义。
{"title":"The multifaceted links between hearing loss and chronic kidney disease","authors":"Dina Greenberg, Norman D. Rosenblum, Marcello Tonelli","doi":"10.1038/s41581-024-00808-2","DOIUrl":"10.1038/s41581-024-00808-2","url":null,"abstract":"Hearing loss affects nearly 1.6 billion people and is the third-leading cause of disability worldwide. Chronic kidney disease (CKD) is also a common condition that is associated with adverse clinical outcomes and high health-care costs. From a developmental perspective, the structures responsible for hearing have a common morphogenetic origin with the kidney, and genetic abnormalities that cause familial forms of hearing loss can also lead to kidney disease. On a cellular level, normal kidney and cochlea function both depend on cilial activities at the apical surface, and kidney tubular cells and sensory epithelial cells of the inner ear use similar transport mechanisms to modify luminal fluid. The two organs also share the same collagen IV basement membrane network. Thus, strong developmental and physiological links exist between hearing and kidney function. These theoretical considerations are supported by epidemiological data demonstrating that CKD is associated with a graded and independent excess risk of sensorineural hearing loss. In addition to developmental and physiological links between kidney and cochlear function, hearing loss in patients with CKD may be driven by specific medications or treatments, including haemodialysis. The associations between these two common conditions are not commonly appreciated, yet have important implications for research and clinical practice. Chronic kidney disease is associated with a graded and independent excess risk of sensorineural hearing loss. This Review describes how disruption of shared signalling pathways that are important for the development of both the ear and the kidney and/or the presence of clinical drivers, such as specific medications or treatments, may underlie these associations.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":null,"pages":null},"PeriodicalIF":41.5,"publicationDate":"2024-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139573495","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 : 2024-01-25DOI: 10.1038/s41581-023-00801-1
Nina E. Diana, Saraladevi Naicker
The HIV epidemic has devastated millions of people globally, with approximately 40 million deaths since its start. The availability of antiretroviral therapy (ART) has transformed the prognosis of millions of individuals infected with HIV such that a diagnosis of HIV infection no longer automatically confers death. However, morbidity and mortality remain substantial among people living with HIV. HIV can directly infect the kidney to cause HIV-associated nephropathy (HIVAN) — a disease characterized by podocyte and tubular damage and associated with an increased risk of kidney failure. The reports of HIVAN occurring primarily in those of African ancestry led to the discovery of its association with APOL1 risk alleles. The advent of ART has led to a substantial decrease in the prevalence of HIVAN; however, reports have emerged of an increase in the prevalence of other kidney pathology, such as focal segmental glomerulosclerosis and pathological conditions associated with co-morbidities of ageing, such as hypertension and diabetes mellitus. Early initiation of ART also results in a longer cumulative exposure to medications, increasing the likelihood of nephrotoxicity. A substantial body of literature supports the use of kidney transplantation in people living with HIV, demonstrating significant survival benefits compared with that of people undergoing chronic dialysis, and similar long-term allograft and patient survival compared with that of HIV-negative kidney transplant recipients. The availability of antiretroviral therapy has led to a transformation in the spectrum of kidney diseases associated with HIV infection. This Review describes the changing pattern of kidney diseases associated with HIV infection, their risk factors, methods of evaluating kidney function in patients with HIV and current therapeutic approaches.
{"title":"The changing landscape of HIV-associated kidney disease","authors":"Nina E. Diana, Saraladevi Naicker","doi":"10.1038/s41581-023-00801-1","DOIUrl":"10.1038/s41581-023-00801-1","url":null,"abstract":"The HIV epidemic has devastated millions of people globally, with approximately 40 million deaths since its start. The availability of antiretroviral therapy (ART) has transformed the prognosis of millions of individuals infected with HIV such that a diagnosis of HIV infection no longer automatically confers death. However, morbidity and mortality remain substantial among people living with HIV. HIV can directly infect the kidney to cause HIV-associated nephropathy (HIVAN) — a disease characterized by podocyte and tubular damage and associated with an increased risk of kidney failure. The reports of HIVAN occurring primarily in those of African ancestry led to the discovery of its association with APOL1 risk alleles. The advent of ART has led to a substantial decrease in the prevalence of HIVAN; however, reports have emerged of an increase in the prevalence of other kidney pathology, such as focal segmental glomerulosclerosis and pathological conditions associated with co-morbidities of ageing, such as hypertension and diabetes mellitus. Early initiation of ART also results in a longer cumulative exposure to medications, increasing the likelihood of nephrotoxicity. A substantial body of literature supports the use of kidney transplantation in people living with HIV, demonstrating significant survival benefits compared with that of people undergoing chronic dialysis, and similar long-term allograft and patient survival compared with that of HIV-negative kidney transplant recipients. The availability of antiretroviral therapy has led to a transformation in the spectrum of kidney diseases associated with HIV infection. This Review describes the changing pattern of kidney diseases associated with HIV infection, their risk factors, methods of evaluating kidney function in patients with HIV and current therapeutic approaches.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":null,"pages":null},"PeriodicalIF":41.5,"publicationDate":"2024-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139550793","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 : 2024-01-22DOI: 10.1038/s41581-023-00800-2
Nathan J. Coffey, M. Celeste Simon
Kidney cancer is the seventh leading cause of cancer in the world, and its incidence is on the rise. Renal cell carcinoma (RCC) is the most common form and is a heterogeneous disease comprising three major subtypes that vary in their histology, clinical course and driver mutations. These subtypes include clear cell RCC, papillary RCC and chromophobe RCC. Molecular analyses of hereditary and sporadic forms of RCC have revealed that this complex and deadly disease is characterized by metabolic pathway alterations in cancer cells that lead to deregulated oxygen and nutrient sensing, as well as impaired tricarboxylic acid cycle activity. These metabolic changes facilitate tumour growth and survival. Specifically, studies of the metabolic features of RCC have led to the discovery of oncometabolites — fumarate and succinate — that can promote tumorigenesis, moonlighting functions of enzymes, and substrate auxotrophy owing to the disruption of pathways that enable the production of arginine and cholesterol. These metabolic alterations within RCC can be exploited to identify new therapeutic targets and interventions, in combination with novel approaches that minimize the systemic toxicity of metabolic inhibitors and reduce the risk of drug resistance owing to metabolic plasticity. Renal cell carcinoma is a metabolic disease linked to a variety of alterations in genes that regulate cellular metabolism. Here, the authors examine cell-intrinsic metabolic alterations in hereditary and sporadic renal cell carcinoma, and how they can be exploited to develop novel therapeutic interventions.
{"title":"Metabolic alterations in hereditary and sporadic renal cell carcinoma","authors":"Nathan J. Coffey, M. Celeste Simon","doi":"10.1038/s41581-023-00800-2","DOIUrl":"10.1038/s41581-023-00800-2","url":null,"abstract":"Kidney cancer is the seventh leading cause of cancer in the world, and its incidence is on the rise. Renal cell carcinoma (RCC) is the most common form and is a heterogeneous disease comprising three major subtypes that vary in their histology, clinical course and driver mutations. These subtypes include clear cell RCC, papillary RCC and chromophobe RCC. Molecular analyses of hereditary and sporadic forms of RCC have revealed that this complex and deadly disease is characterized by metabolic pathway alterations in cancer cells that lead to deregulated oxygen and nutrient sensing, as well as impaired tricarboxylic acid cycle activity. These metabolic changes facilitate tumour growth and survival. Specifically, studies of the metabolic features of RCC have led to the discovery of oncometabolites — fumarate and succinate — that can promote tumorigenesis, moonlighting functions of enzymes, and substrate auxotrophy owing to the disruption of pathways that enable the production of arginine and cholesterol. These metabolic alterations within RCC can be exploited to identify new therapeutic targets and interventions, in combination with novel approaches that minimize the systemic toxicity of metabolic inhibitors and reduce the risk of drug resistance owing to metabolic plasticity. Renal cell carcinoma is a metabolic disease linked to a variety of alterations in genes that regulate cellular metabolism. Here, the authors examine cell-intrinsic metabolic alterations in hereditary and sporadic renal cell carcinoma, and how they can be exploited to develop novel therapeutic interventions.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":null,"pages":null},"PeriodicalIF":41.5,"publicationDate":"2024-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139510890","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 : 2024-01-22DOI: 10.1038/s41581-024-00810-8
Miranda Scanlon
All patients with kidney disease have the right to have a say in their own clinical care, the provision of health services and research into kidney disease. Patient empowerment and advocacy, especially for those whose views are seldom heard, can be enhanced by working together in communities.
{"title":"Amplifying the voices of patients with kidney disease","authors":"Miranda Scanlon","doi":"10.1038/s41581-024-00810-8","DOIUrl":"10.1038/s41581-024-00810-8","url":null,"abstract":"All patients with kidney disease have the right to have a say in their own clinical care, the provision of health services and research into kidney disease. Patient empowerment and advocacy, especially for those whose views are seldom heard, can be enhanced by working together in communities.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":null,"pages":null},"PeriodicalIF":41.5,"publicationDate":"2024-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139510802","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 : 2024-01-18DOI: 10.1038/s41581-024-00811-7
Ricardo Silvariño, Laura Solá
Treatment of chronic kidney disease requires a comprehensive approach including universal access to early diagnosis and to medications that can slow disease progression. Such equitable access is not only an ethical requirement but can also reduce the financial and human costs of advancing kidney and cardiovascular disease.
{"title":"Health policy for universal, sustainable and equitable kidney care","authors":"Ricardo Silvariño, Laura Solá","doi":"10.1038/s41581-024-00811-7","DOIUrl":"10.1038/s41581-024-00811-7","url":null,"abstract":"Treatment of chronic kidney disease requires a comprehensive approach including universal access to early diagnosis and to medications that can slow disease progression. Such equitable access is not only an ethical requirement but can also reduce the financial and human costs of advancing kidney and cardiovascular disease.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":null,"pages":null},"PeriodicalIF":41.5,"publicationDate":"2024-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139489569","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 : 2024-01-11DOI: 10.1038/s41581-024-00807-3
Adeera Levin
Overcoming barriers to deliver high-quality care requires an assessment of the contribution of each barrier within a local context. Tools to identify early disease, knowledge of best therapies, access to care providers and medications, and an accountable and integrated health-care system are essential elements of quality care. Education of patients, providers and policy makers in conjunction with advocacy efforts and national policy frameworks are required to deliver high-quality care worldwide.
{"title":"Overcoming barriers to deliver high quality kidney care","authors":"Adeera Levin","doi":"10.1038/s41581-024-00807-3","DOIUrl":"10.1038/s41581-024-00807-3","url":null,"abstract":"Overcoming barriers to deliver high-quality care requires an assessment of the contribution of each barrier within a local context. Tools to identify early disease, knowledge of best therapies, access to care providers and medications, and an accountable and integrated health-care system are essential elements of quality care. Education of patients, providers and policy makers in conjunction with advocacy efforts and national policy frameworks are required to deliver high-quality care worldwide.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":null,"pages":null},"PeriodicalIF":41.5,"publicationDate":"2024-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139420100","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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