Pub Date : 2025-05-22DOI: 10.1038/s41581-025-00967-w
M. Arfan Ikram
Ageing populations worldwide face increasing challenges of multimorbidity (that is, the co-occurrence of two or more chronic conditions). The combination of chronic kidney disease (CKD) and dementia occurs more frequently than it would by simple coincidence, owing to several underlying biological and clinical mechanisms. Population-based cohort studies are an important epidemiological tool and have contributed to improved understanding of these mechanisms. These mechanisms include uniquely shared haemodynamic features of vasculature, overlapping risk factor profiles, and direct neurotoxic effects of accumulating waste products due to poor kidney function. The effect of these pathways is suggested to differ across gender, relevant demographic subgroups, and populations from low- to middle-income countries. Yet, given their study design, population-based cohort studies also inherently face several methodological challenges. These challenges pertain to the use of biomarkers that do not always fully capture the structure and function of the kidney or the brain; bidirectionality across the pathways under study; and practical issues of proper causal inference in light of incomplete distinction between confounders, mediators and effect modifiers. This Review describes our current understanding of the link between CKD and dementia, with a focus on knowledge synthesized from population-based cohort studies. Methodological challenges and possible solutions will be described and directions for future research areas will be outlined. This Review provides an overview of the epidemiological link between chronic kidney disease and dementia. It describes current knowledge of underlying mechanisms, methodological challenges and potential solutions, and implications for clinical practice and future research.
{"title":"Chronic kidney disease and dementia: an epidemiological perspective","authors":"M. Arfan Ikram","doi":"10.1038/s41581-025-00967-w","DOIUrl":"10.1038/s41581-025-00967-w","url":null,"abstract":"Ageing populations worldwide face increasing challenges of multimorbidity (that is, the co-occurrence of two or more chronic conditions). The combination of chronic kidney disease (CKD) and dementia occurs more frequently than it would by simple coincidence, owing to several underlying biological and clinical mechanisms. Population-based cohort studies are an important epidemiological tool and have contributed to improved understanding of these mechanisms. These mechanisms include uniquely shared haemodynamic features of vasculature, overlapping risk factor profiles, and direct neurotoxic effects of accumulating waste products due to poor kidney function. The effect of these pathways is suggested to differ across gender, relevant demographic subgroups, and populations from low- to middle-income countries. Yet, given their study design, population-based cohort studies also inherently face several methodological challenges. These challenges pertain to the use of biomarkers that do not always fully capture the structure and function of the kidney or the brain; bidirectionality across the pathways under study; and practical issues of proper causal inference in light of incomplete distinction between confounders, mediators and effect modifiers. This Review describes our current understanding of the link between CKD and dementia, with a focus on knowledge synthesized from population-based cohort studies. Methodological challenges and possible solutions will be described and directions for future research areas will be outlined. This Review provides an overview of the epidemiological link between chronic kidney disease and dementia. It describes current knowledge of underlying mechanisms, methodological challenges and potential solutions, and implications for clinical practice and future research.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 8","pages":"525-535"},"PeriodicalIF":39.8,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113643","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 : 2025-05-08DOI: 10.1038/s41581-025-00965-y
John F. Bertram, Luise A. Cullen-McEwen, Vinicius Andrade-Oliveira, Niels Olsen Saraiva Câmara
Podocytes are key components of the glomerular filtration barrier — a specialized structure that is responsible for the filtration of blood by the kidneys. They therefore exist in a unique microenvironment exposed to mechanical force and the myriad molecules that cross the filtration barrier. To survive and thrive, podocytes must continually sense and respond to their ever-changing microenvironment. Sensing is achieved by interactions with the surrounding extracellular matrix and neighbouring cells, through a variety of pathways, to sense changes in environmental factors such as nutrient levels including glucose and lipids, oxygen levels, pH and pressure. The response mechanisms similarly involve a range of processes, including signalling pathways and the actions of specific organelles that initiate and regulate appropriate responses, including alterations in cell metabolism, immune regulation and changes in podocyte structure and cognate functions. These functions ultimately affect glomerular and kidney health. Imbalances in these processes can lead to inflammation, podocyte loss and glomerular disease. Podocytes reside in a unique microenvironment where they are exposed to mechanical force and a variety of molecules that cross the filtration barrier. This Review describes the various mechanisms by which podocytes sense and respond to their complex environment and how these processes affect glomerular and kidney health.
{"title":"The intelligent podocyte: sensing and responding to a complex microenvironment","authors":"John F. Bertram, Luise A. Cullen-McEwen, Vinicius Andrade-Oliveira, Niels Olsen Saraiva Câmara","doi":"10.1038/s41581-025-00965-y","DOIUrl":"10.1038/s41581-025-00965-y","url":null,"abstract":"Podocytes are key components of the glomerular filtration barrier — a specialized structure that is responsible for the filtration of blood by the kidneys. They therefore exist in a unique microenvironment exposed to mechanical force and the myriad molecules that cross the filtration barrier. To survive and thrive, podocytes must continually sense and respond to their ever-changing microenvironment. Sensing is achieved by interactions with the surrounding extracellular matrix and neighbouring cells, through a variety of pathways, to sense changes in environmental factors such as nutrient levels including glucose and lipids, oxygen levels, pH and pressure. The response mechanisms similarly involve a range of processes, including signalling pathways and the actions of specific organelles that initiate and regulate appropriate responses, including alterations in cell metabolism, immune regulation and changes in podocyte structure and cognate functions. These functions ultimately affect glomerular and kidney health. Imbalances in these processes can lead to inflammation, podocyte loss and glomerular disease. Podocytes reside in a unique microenvironment where they are exposed to mechanical force and a variety of molecules that cross the filtration barrier. This Review describes the various mechanisms by which podocytes sense and respond to their complex environment and how these processes affect glomerular and kidney health.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 7","pages":"503-516"},"PeriodicalIF":39.8,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143920372","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 : 2025-05-06DOI: 10.1038/s41581-025-00966-x
Ellen F. Carney
{"title":"The effects of sex hormone therapy on kidney function","authors":"Ellen F. Carney","doi":"10.1038/s41581-025-00966-x","DOIUrl":"10.1038/s41581-025-00966-x","url":null,"abstract":"","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 6","pages":"365-365"},"PeriodicalIF":39.8,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143909974","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 : 2025-04-29DOI: 10.1038/s41581-025-00961-2
Surabhi R. Madhvapathy, Soongwon Cho, Elisa Gessaroli, Eleonora Forte, Yirui Xiong, Lorenzo Gallon, John A. Rogers
Established clinical practices for monitoring kidney health and disease — including biopsy and serum biomarker analysis — suffer from practical limitations in monitoring frequency and lack adequate sensitivity for early disease detection. Engineering advances in biosensors have led to the development of wearable and implantable systems for monitoring of kidney health. Non-invasive microfluidic systems have demonstrated utility in the detection of kidney-relevant biomarkers, such as creatinine, urea and electrolytes in peripheral body fluids such as sweat, interstitial fluid, tears and saliva. Implantable systems may aid the identification of early transplant rejection through analysis of organ temperature and perfusion, and enable real-time assessment of inflammation through the use of thermal sensors. These technologies enable continuous, real-time monitoring of kidney health, offering complementary information to standard clinical procedures to alert physicians of changes in kidney health for early intervention. In this Review, we explore devices for monitoring renal biomarkers in peripheral biofluids and discuss developments in implantable sensors for the direct measurement of the local, biophysical properties of kidney tissue. We also describe potential clinical applications, including monitoring of chronic kidney disease, acute kidney injury and allograft health. Advances in biosensor technology have the potential to enable continuous, non-invasive monitoring of kidney health through wearable and implantable systems. Non-invasive microfluidic systems have demonstrated utility in the detection of kidney-relevant biomarkers in peripheral body fluids such as sweat, interstitial fluid, tears and saliva, whereas implantable systems permit the direct measurement of biophysical tissue properties including tissue oxygenation, perfusion and temperature.
{"title":"Implantable bioelectronics and wearable sensors for kidney health and disease","authors":"Surabhi R. Madhvapathy, Soongwon Cho, Elisa Gessaroli, Eleonora Forte, Yirui Xiong, Lorenzo Gallon, John A. Rogers","doi":"10.1038/s41581-025-00961-2","DOIUrl":"10.1038/s41581-025-00961-2","url":null,"abstract":"Established clinical practices for monitoring kidney health and disease — including biopsy and serum biomarker analysis — suffer from practical limitations in monitoring frequency and lack adequate sensitivity for early disease detection. Engineering advances in biosensors have led to the development of wearable and implantable systems for monitoring of kidney health. Non-invasive microfluidic systems have demonstrated utility in the detection of kidney-relevant biomarkers, such as creatinine, urea and electrolytes in peripheral body fluids such as sweat, interstitial fluid, tears and saliva. Implantable systems may aid the identification of early transplant rejection through analysis of organ temperature and perfusion, and enable real-time assessment of inflammation through the use of thermal sensors. These technologies enable continuous, real-time monitoring of kidney health, offering complementary information to standard clinical procedures to alert physicians of changes in kidney health for early intervention. In this Review, we explore devices for monitoring renal biomarkers in peripheral biofluids and discuss developments in implantable sensors for the direct measurement of the local, biophysical properties of kidney tissue. We also describe potential clinical applications, including monitoring of chronic kidney disease, acute kidney injury and allograft health. Advances in biosensor technology have the potential to enable continuous, non-invasive monitoring of kidney health through wearable and implantable systems. Non-invasive microfluidic systems have demonstrated utility in the detection of kidney-relevant biomarkers in peripheral body fluids such as sweat, interstitial fluid, tears and saliva, whereas implantable systems permit the direct measurement of biophysical tissue properties including tissue oxygenation, perfusion and temperature.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 7","pages":"443-463"},"PeriodicalIF":39.8,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143889436","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 : 2025-04-25DOI: 10.1038/s41581-025-00963-0
Giovambattista Capasso, Casper F. M. Franssen, Alessandra F. Perna, Ziad A. Massy, Robert I. Menzies, Carmine Zoccali, Alessandro Tessitore, Maiken Nedergaard, Mark D. Okusa, Alberto Ortiz, Carsten A. Wagner, Robert J. Unwin
Cognitive impairment is highly prevalent among individuals with chronic kidney disease (CKD). Despite its high prevalence, the contributing factors and mechanisms underlying brain–kidney dysfunction in CKD remain poorly understood. However, advances in neuroscience, including novel imaging techniques and cognitive assessment methods, have begun to clarify this complex relationship. Several factors contribute directly to cognitive decline in people with CKD, including accumulation of uraemic toxins, microvascular damage, malnutrition, chronic inflammation and disruptions in key neuroprotective pathways, such as those involving Klotho and the glymphatic system. These factors are also linked to the accelerated ageing observed in people with CKD, a key contributor to cognitive decline. However, most studies on cognition in people with CKD have been cross-sectional and associative, offering limited insight into causation. Research advances, such as studies on the effect of uraemic toxins on the blood–brain barrier and the role of the endothelial glycocalyx in vascular damage, offer promising new directions. Emerging data from longitudinal cohort studies are also enhancing our understanding of these processes, with potential implications for both the treatment of CKD-related cognitive decline and the broader issue of cognitive dysfunction in ageing populations. Here, we examine key mechanisms linking CKD to cognitive decline and consider potential therapeutic interventions. The prevalence of cognitive dysfunction among people with chronic kidney disease (CKD) is disproportionately high compared with that in the general population. This Review examines current evidence on key drivers of cognitive impairment in people with CKD, and highlights gaps in knowledge and potential therapeutic targets.
{"title":"Drivers and mechanisms of cognitive decline in chronic kidney disease","authors":"Giovambattista Capasso, Casper F. M. Franssen, Alessandra F. Perna, Ziad A. Massy, Robert I. Menzies, Carmine Zoccali, Alessandro Tessitore, Maiken Nedergaard, Mark D. Okusa, Alberto Ortiz, Carsten A. Wagner, Robert J. Unwin","doi":"10.1038/s41581-025-00963-0","DOIUrl":"10.1038/s41581-025-00963-0","url":null,"abstract":"Cognitive impairment is highly prevalent among individuals with chronic kidney disease (CKD). Despite its high prevalence, the contributing factors and mechanisms underlying brain–kidney dysfunction in CKD remain poorly understood. However, advances in neuroscience, including novel imaging techniques and cognitive assessment methods, have begun to clarify this complex relationship. Several factors contribute directly to cognitive decline in people with CKD, including accumulation of uraemic toxins, microvascular damage, malnutrition, chronic inflammation and disruptions in key neuroprotective pathways, such as those involving Klotho and the glymphatic system. These factors are also linked to the accelerated ageing observed in people with CKD, a key contributor to cognitive decline. However, most studies on cognition in people with CKD have been cross-sectional and associative, offering limited insight into causation. Research advances, such as studies on the effect of uraemic toxins on the blood–brain barrier and the role of the endothelial glycocalyx in vascular damage, offer promising new directions. Emerging data from longitudinal cohort studies are also enhancing our understanding of these processes, with potential implications for both the treatment of CKD-related cognitive decline and the broader issue of cognitive dysfunction in ageing populations. Here, we examine key mechanisms linking CKD to cognitive decline and consider potential therapeutic interventions. The prevalence of cognitive dysfunction among people with chronic kidney disease (CKD) is disproportionately high compared with that in the general population. This Review examines current evidence on key drivers of cognitive impairment in people with CKD, and highlights gaps in knowledge and potential therapeutic targets.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 8","pages":"536-552"},"PeriodicalIF":39.8,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143872227","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 : 2025-04-24DOI: 10.1038/s41581-025-00960-3
Chris W. McIntyre, Arsh Jain
People with chronic kidney disease who require maintenance dialysis characteristically experience accelerated and aggravated cognitive decline compared with those with advanced kidney disease who are not receiving this form of kidney replacement therapy. This effect is inadequately appreciated, but of crucial importance to patients, their carers and the health-care systems that support them. Although many of the comorbid conditions prevalent in this patient population have the potential to affect brain structure and function, an evolving body of evidence indicates that the dialysis therapy itself has a central role in the pathophysiology of progressive cognitive impairment. Both haemodialysis and peritoneal dialysis are associated with structural and functional changes in the brain that can lead to characteristic short-term symptoms, such as headache, confusion, delirium and brain fog, as well as long-term reductions in cognitive functional ability. Here, we explore the mechanisms, both established and putative, underlying these effects and consider approaches to addressing this issue with both single and complex therapeutic interventions. Treatment with dialysis in people with kidney failure has been implicated in accelerated cognitive impairment. Here, the authors consider how dialysis treatment — haemodialysis and peritoneal dialysis — can promote cerebral injury and might exacerbate chronic kidney disease-associated brain alterations and cognitive decline.
{"title":"Dialysis and cognitive impairment","authors":"Chris W. McIntyre, Arsh Jain","doi":"10.1038/s41581-025-00960-3","DOIUrl":"10.1038/s41581-025-00960-3","url":null,"abstract":"People with chronic kidney disease who require maintenance dialysis characteristically experience accelerated and aggravated cognitive decline compared with those with advanced kidney disease who are not receiving this form of kidney replacement therapy. This effect is inadequately appreciated, but of crucial importance to patients, their carers and the health-care systems that support them. Although many of the comorbid conditions prevalent in this patient population have the potential to affect brain structure and function, an evolving body of evidence indicates that the dialysis therapy itself has a central role in the pathophysiology of progressive cognitive impairment. Both haemodialysis and peritoneal dialysis are associated with structural and functional changes in the brain that can lead to characteristic short-term symptoms, such as headache, confusion, delirium and brain fog, as well as long-term reductions in cognitive functional ability. Here, we explore the mechanisms, both established and putative, underlying these effects and consider approaches to addressing this issue with both single and complex therapeutic interventions. Treatment with dialysis in people with kidney failure has been implicated in accelerated cognitive impairment. Here, the authors consider how dialysis treatment — haemodialysis and peritoneal dialysis — can promote cerebral injury and might exacerbate chronic kidney disease-associated brain alterations and cognitive decline.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 8","pages":"553-564"},"PeriodicalIF":39.8,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143866383","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 : 2025-04-23DOI: 10.1038/s41581-025-00956-z
Thoralf Niendorf, Thomas Gladytz, Kathleen Cantow, Jason M. Millward, Sonia Waiczies, Erdmann Seeliger
Renal hypoxia has a key role in the pathophysiology of many kidney diseases. MRI provides surrogate markers of oxygenation, offering a critical opportunity to detect renal hypoxia. However, studies that have assessed the diagnostic performance of oxygenation MRI for kidney disorders have provided inconsistent results because MRI metrics do not fully capture the complexity of renal oxygenation. Most oxygenation MRI studies are descriptive in nature and fail to detail the pathophysiological importance of the imaging findings. These limitations have restricted the clinical application of oxygenation MRI and the full potential of this technology to facilitate early diagnosis, risk prediction and treatment monitoring of kidney disease has not yet been realized. Understanding of the relationship between renal tissue oxygenation and MRI metrics, which is affected by kidney size, tubular volume fraction and renal blood volume fraction, and measurement of these factors using novel MR methods is imperative for correct physiological interpretation of renal MR oximetry findings. Next steps to enable the clinical adoption of MR oximetry should involve multidisciplinary collaboration to address standardization of acquisition and data analysis protocols and establish reference values of MRI metrics. MRI is a powerful technology for assessment of renal oxygenation. This Review highlights important considerations for the physiological interpretation of renal oxygenation changes measured by MR oximetry and discusses use of this technology in research as well as potential clinical applications.
{"title":"Magnetic resonance imaging of renal oxygenation","authors":"Thoralf Niendorf, Thomas Gladytz, Kathleen Cantow, Jason M. Millward, Sonia Waiczies, Erdmann Seeliger","doi":"10.1038/s41581-025-00956-z","DOIUrl":"10.1038/s41581-025-00956-z","url":null,"abstract":"Renal hypoxia has a key role in the pathophysiology of many kidney diseases. MRI provides surrogate markers of oxygenation, offering a critical opportunity to detect renal hypoxia. However, studies that have assessed the diagnostic performance of oxygenation MRI for kidney disorders have provided inconsistent results because MRI metrics do not fully capture the complexity of renal oxygenation. Most oxygenation MRI studies are descriptive in nature and fail to detail the pathophysiological importance of the imaging findings. These limitations have restricted the clinical application of oxygenation MRI and the full potential of this technology to facilitate early diagnosis, risk prediction and treatment monitoring of kidney disease has not yet been realized. Understanding of the relationship between renal tissue oxygenation and MRI metrics, which is affected by kidney size, tubular volume fraction and renal blood volume fraction, and measurement of these factors using novel MR methods is imperative for correct physiological interpretation of renal MR oximetry findings. Next steps to enable the clinical adoption of MR oximetry should involve multidisciplinary collaboration to address standardization of acquisition and data analysis protocols and establish reference values of MRI metrics. MRI is a powerful technology for assessment of renal oxygenation. This Review highlights important considerations for the physiological interpretation of renal oxygenation changes measured by MR oximetry and discusses use of this technology in research as well as potential clinical applications.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 7","pages":"483-502"},"PeriodicalIF":39.8,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143862195","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 : 2025-04-22DOI: 10.1038/s41581-025-00958-x
Xiao-ming Meng, Li Wang, David J. Nikolic-Paterson, Hui-Yao Lan
Acute kidney injury (AKI) and chronic kidney disease (CKD) are inter-related clinical and pathophysiological disorders. Cells of the innate immune system, such as granulocytes and macrophages, can induce AKI through the secretion of pro-inflammatory mediators such as cytokines, chemokines and enzymes, and the release of extracellular traps. In addition, macrophages and dendritic cells can drive the progression of CKD through a wide range of pro-inflammatory and pro-fibrotic mechanisms, and by regulation of the adaptive immune response. However, innate immune cells can also promote kidney repair after acute injury. These actions highlight the multifaceted nature of the way by which innate immune cells respond to signals within the kidney microenvironment, including interaction with the complement and coagulation cascades, cells of the adaptive immune system, intrinsic renal cells and infiltrating mesenchymal cells. The factors and mechanisms that underpin the ability of innate immune cells to contribute to renal injury or repair and to drive the progression of CKD are of great interest for understanding disease processes and for developing new therapeutic approaches to limit AKI and the AKI-to-CKD transition. Here, the authors describe the mechanisms by which innate immune cells contribute to acute kidney injury, the transition from acute kidney injury to chronic kidney disease, and the progression of chronic kidney disease. They also discuss potential therapeutic strategies that target the innate immune system.
{"title":"Innate immune cells in acute and chronic kidney disease","authors":"Xiao-ming Meng, Li Wang, David J. Nikolic-Paterson, Hui-Yao Lan","doi":"10.1038/s41581-025-00958-x","DOIUrl":"10.1038/s41581-025-00958-x","url":null,"abstract":"Acute kidney injury (AKI) and chronic kidney disease (CKD) are inter-related clinical and pathophysiological disorders. Cells of the innate immune system, such as granulocytes and macrophages, can induce AKI through the secretion of pro-inflammatory mediators such as cytokines, chemokines and enzymes, and the release of extracellular traps. In addition, macrophages and dendritic cells can drive the progression of CKD through a wide range of pro-inflammatory and pro-fibrotic mechanisms, and by regulation of the adaptive immune response. However, innate immune cells can also promote kidney repair after acute injury. These actions highlight the multifaceted nature of the way by which innate immune cells respond to signals within the kidney microenvironment, including interaction with the complement and coagulation cascades, cells of the adaptive immune system, intrinsic renal cells and infiltrating mesenchymal cells. The factors and mechanisms that underpin the ability of innate immune cells to contribute to renal injury or repair and to drive the progression of CKD are of great interest for understanding disease processes and for developing new therapeutic approaches to limit AKI and the AKI-to-CKD transition. Here, the authors describe the mechanisms by which innate immune cells contribute to acute kidney injury, the transition from acute kidney injury to chronic kidney disease, and the progression of chronic kidney disease. They also discuss potential therapeutic strategies that target the innate immune system.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 7","pages":"464-482"},"PeriodicalIF":39.8,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143857820","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 : 2025-04-22DOI: 10.1038/s41581-025-00964-z
Susan J. Allison
{"title":"GalNAc-T14-associated defects in B cell homing in IgA nephropathy","authors":"Susan J. Allison","doi":"10.1038/s41581-025-00964-z","DOIUrl":"10.1038/s41581-025-00964-z","url":null,"abstract":"","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 6","pages":"365-365"},"PeriodicalIF":39.8,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143857819","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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