Advances in kidney disease and health最新文献

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Evaluation and Long-Term Follow-Up of Living Kidney Donors 活体肾脏捐献者的评估和长期随访
Advances in kidney disease and health Pub Date : 2024-09-01 DOI: 10.1053/j.akdh.2024.04.003
{"title":"Evaluation and Long-Term Follow-Up of Living Kidney Donors","authors":"","doi":"10.1053/j.akdh.2024.04.003","DOIUrl":"10.1053/j.akdh.2024.04.003","url":null,"abstract":"<div><p>The evaluation of living kidney donor candidates is a complex and lengthy process. Donor candidates face geographic and socioeconomic barriers to completing donor evaluation. Inequities in access to living donations persist. With a growing demand for kidney transplants and a shortage of living donors, transplant centers are more permissive of accepting less-than-ideal donor candidates. Donors have an increased lifetime risk of kidney failure, but the absolute risk increase is small. Efforts are needed to support donor candidates to complete donor nephrectomy safely and efficiently and receive optimal follow-up care to prevent risk factors for kidney disease and detect complications early. In this article, the authors address key elements of donor kidney evaluation, including current living donation policy requirements and transplant center practices. The authors present a simplified comprehensive practical approach to help guide providers in completing donor evaluation and follow-up care with best outcomes possible.</p></div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2949813924000739/pdfft?md5=95256588bf60e85ca91544b9c6c1f540&pid=1-s2.0-S2949813924000739-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142122449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Non-Immunoglobulin Amyloidosis-Mediated Kidney Disease: Emerging Understanding of Underdiagnosed Entities 非免疫球蛋白淀粉样变性肾病:对诊断不足实体的新认识。
Advances in kidney disease and health Pub Date : 2024-07-01 DOI: 10.1053/j.akdh.2024.02.001
{"title":"Non-Immunoglobulin Amyloidosis-Mediated Kidney Disease: Emerging Understanding of Underdiagnosed Entities","authors":"","doi":"10.1053/j.akdh.2024.02.001","DOIUrl":"10.1053/j.akdh.2024.02.001","url":null,"abstract":"<div><p>Amyloidosis is a complex group of rare disorders characterized by the deposition of misfolded proteins in the extracellular space of various tissues and organs, leading to progressive organ dysfunction. The kidneys constitute a very common site affected, most notably by immunoglobulin-mediated (light chain, heavy chain, and light and heavy chain amyloidosis), but other types that include serum amyloid A (AA) amyloidosis and leukocyte chemotactic factor 2 amyloidosis, along with mutant proteins in several hereditary forms of amyloidosis such as transthyretin, fibrinogen α-chain, gelsolin, lysozyme, and apolipoproteins AI/AII/AIV/CII/CIII amyloidosis have been incriminated as well. The clinical presentation is variable and can range from minimal proteinuria for leukocyte chemotactic factor 2 amyloidosis to a full-blown nephrotic syndrome for AA amyloidosis. Clinical correlation, genetic analysis, and adequate tissue typing through a kidney biopsy are essential to make the correct diagnosis, especially when a family history of amyloidosis is absent. Except for AA and transthyretin amyloidosis, the treatment is usually purely supportive. Kidney transplantation is an acceptable form of treatment for end-stage kidney disease in all types of non-Ig-mediated renal amyloidosis.</p></div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141861789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Membranous Nephropathy: Updates on Management 膜性肾病:管理更新。
Advances in kidney disease and health Pub Date : 2024-07-01 DOI: 10.1053/j.akdh.2024.04.004
{"title":"Membranous Nephropathy: Updates on Management","authors":"","doi":"10.1053/j.akdh.2024.04.004","DOIUrl":"10.1053/j.akdh.2024.04.004","url":null,"abstract":"<div><p>Membranous nephropathy is a major etiology of nephrotic syndrome in adults and less frequently in children. Circulating antibodies to intrinsic podocyte antigens, such as M-type phospholipase A2 receptor, or to extrinsic proteins accumulate beneath the podocyte to cause damage via complement activation and/or other mechanisms. The availability of clinical testing for autoantibodies to M-type phospholipase A2 receptor has allowed noninvasive diagnosis of this form of membranous nephropathy and a means to monitor immunologic activity to guide immunosuppressive therapy. Treatment of membranous nephropathy includes optimal supportive care with renin-angiotensin-system blockers, lipid-lowering agents, diuretics, lifestyle changes, and additional immunosuppressive therapy in patients with an increased risk of progression to kidney failure. Rituximab has been recognized as a first-line immunosuppressive therapy for most membranous nephropathy patients with an increased risk of progressive disease, except those with life-threatening nephrotic syndrome or rapidly deteriorating kidney function from membranous nephropathy. This article discusses the major and minor antigens described in membranous nephropathy, the natural history of the disease, and guidelines for clinical management and immunosuppressive treatment.</p></div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141861787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
An Update on Viral Infection-Associated Collapsing Glomerulopathy 病毒感染相关塌陷性肾小球病的最新进展。
Advances in kidney disease and health Pub Date : 2024-07-01 DOI: 10.1053/j.akdh.2023.12.007
{"title":"An Update on Viral Infection-Associated Collapsing Glomerulopathy","authors":"","doi":"10.1053/j.akdh.2023.12.007","DOIUrl":"10.1053/j.akdh.2023.12.007","url":null,"abstract":"<div><p>The COVID-19 era has been a reminder to clinicians around the world of the important role that viral infections play in promoting glomerular disease. Several viral infections including human immunodeficiency virus (HIV), severe acute respiratory syndrome coronavirus 2, Epstein-Barr virus, cytomegalovirus, and parvovirus B19 can cause podocyte injury and present with a collapsing glomerulopathy (CG) variant of focal segmental glomerulosclerosis or minimal change disease. CG associated with COVID-19 has been termed COVID-19-associated nephropathy due to its striking resemblance to HIV-associated nephropathy. Host susceptibility is a major determinant of viral infection-associated CG, and the presence of two <em>APOL1</em> risk variants explains most of the racial predilection to viral-associated CG observed in individuals of African ancestry. Interactions between <em>APOL1</em> risk variants, viral genes, and the systemic inflammatory response to viral infection all contribute to kidney injury. This review will summarize our current knowledge of viral infection-associated CG, focusing primarily on the clinical presentation, histological features, mechanisms, and disease course of HIV-associated nephropathy and COVID-19-associated nephropathy.</p></div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141861831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Minimal Change Disease 最小变化疾病。
Advances in kidney disease and health Pub Date : 2024-07-01 DOI: 10.1053/j.akdh.2024.02.002
{"title":"Minimal Change Disease","authors":"","doi":"10.1053/j.akdh.2024.02.002","DOIUrl":"10.1053/j.akdh.2024.02.002","url":null,"abstract":"<div><p>Minimal change disease represents a common cause of nephrotic syndrome in both pediatric and adult patients. Although much remains to be discovered, there have been significant recent advancements in our understanding of the pathophysiology of minimal change disease, including the discovery of antinephrin antibodies as a marker for diagnosis of disease. Here we will review what is known about the pathophysiology, treatment, and prognosis of minimal change disease and the differences between pediatric and adult patients. Recent advances in our understanding of the mechanisms of disease will be noted. We will discuss how this may change the treatment of minimal change disease going forward and what remains to be studied.</p></div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141861788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Updates on the Diagnosis and Management of Fibrillary Glomerulonephritis 纤维性肾小球肾炎诊断和治疗的最新进展。
Advances in kidney disease and health Pub Date : 2024-07-01 DOI: 10.1053/j.akdh.2024.03.006
{"title":"Updates on the Diagnosis and Management of Fibrillary Glomerulonephritis","authors":"","doi":"10.1053/j.akdh.2024.03.006","DOIUrl":"10.1053/j.akdh.2024.03.006","url":null,"abstract":"<div><p>Fibrillary glomerulonephritis (FGN) is a rare kidney disease typically affecting individuals in middle age, frequently presenting with advanced renal failure, proteinuria, and hypertension. FGN can be associated with autoimmune diseases, hepatitis C infection, and malignancies. Its exact pathogenesis remains elusive, and the exact role of DnaJ homolog subfamily B member 9 is yet to be determined. On renal biopsy, FGN exhibits distinctive Congo-red-negative, nonbranching fibrils, approximately 20 nm in diameter. DnaJ homolog subfamily B member 9 immunohistochemical staining has become a gold standard for diagnosis. Atypical variants exist, including congophilic, monotypic, and crescentic FGN, highlighting the disease's heterogeneity. Treatment with immunosuppression, including rituximab, has shown variable success, with no standard therapy established. FGN often leads to end-stage kidney disease, with a median progression time of 2-4 years postdiagnosis. Kidney transplantation is a viable option for FGN-related end-stage kidney disease, but recurrence in transplanted kidneys is not rare.</p></div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141861792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Collapsing Glomerulopathy 崩解性肾小球病
Advances in kidney disease and health Pub Date : 2024-07-01 DOI: 10.1053/j.akdh.2024.03.008
{"title":"Collapsing Glomerulopathy","authors":"","doi":"10.1053/j.akdh.2024.03.008","DOIUrl":"10.1053/j.akdh.2024.03.008","url":null,"abstract":"<div><p>Collapsing glomerulopathy (CG) is a pattern of kidney injury characterized by segmental or global collapse of the glomerular tuft associated with overlying epithelial cell hyperplasia. Although CG may be idiopathic, a wide range of etiologies have been identified that can lead to this pattern of injury. Recent advances have highlighted the role of inflammatory and interferon signaling pathways and upregulation of apolipoprotein L1 (APOL1) within podocytes in those carrying a high-risk APOL1 genotype. In this review, we describe the etiology, pathogenesis, pathology, and clinical course of CG, focusing on nonviral etiologies. We also describe current treatments and explore potential therapeutic options targeting interferon/APOL1 pathways in CG.</p></div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141861832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Genetic Causes of Nephrotic Syndrome and Focal and Segmental Glomerulosclerosis 肾病综合征以及局灶性和节段性肾小球硬化症的遗传原因。
Advances in kidney disease and health Pub Date : 2024-07-01 DOI: 10.1053/j.akdh.2024.04.001
{"title":"Genetic Causes of Nephrotic Syndrome and Focal and Segmental Glomerulosclerosis","authors":"","doi":"10.1053/j.akdh.2024.04.001","DOIUrl":"10.1053/j.akdh.2024.04.001","url":null,"abstract":"<div><p>The field of nephrology has a long-standing interest in deciphering the genetic basis of nephrotic syndrome (NS), motivated by the mechanistic insights it provides in chronic kidney disease. The initial era of genetic studies solidified NS and the focal segmental glomerulosclerosis lesion as podocyte disorders. The likelihood of identifying a single gene (called monogenic) cause is higher if certain factors are present such as positive family history. Obtaining a monogenic diagnosis enables reproductive counseling and screening of family members. Now, with a new era of genomic studies facilitated by technological advances and the emergence of large genetically characterized cohorts, more insights are apparent. This includes the phenotypic breadth associated with disease genes, as evidenced in Alport syndrome and congenital NS of the Finnish type. Moreover, the underlying genetic architecture is more complex than previously appreciated, as shown by genome-wide association studies, suggesting that variants in multiple genes collectively influence risk. Achieving molecularly informed diagnoses also holds substantial potential for personalizing medicine, including the development of targeted therapeutics. Illustrative examples include coenzyme Q<sub>10</sub> for <em>ADCK4</em>-associated NS and inaxaplin, a small molecule that inhibits apolipoprotein L1 channel activity, though larger studies are required to confirm benefit.</p></div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141861834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Nephrotic Syndrome: Have We Entered a New Era? 肾病综合征:我们是否进入了一个新时代?
Advances in kidney disease and health Pub Date : 2024-07-01 DOI: 10.1053/j.akdh.2024.05.004
{"title":"Nephrotic Syndrome: Have We Entered a New Era?","authors":"","doi":"10.1053/j.akdh.2024.05.004","DOIUrl":"10.1053/j.akdh.2024.05.004","url":null,"abstract":"","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2949813924001113/pdfft?md5=b0bf2b8b7011a70620f61a659db2c1e3&pid=1-s2.0-S2949813924001113-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141461152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Immunotactoid Glomerulopathy 免疫性肾小球疾病
Advances in kidney disease and health Pub Date : 2024-07-01 DOI: 10.1053/j.akdh.2024.03.003
{"title":"Immunotactoid Glomerulopathy","authors":"","doi":"10.1053/j.akdh.2024.03.003","DOIUrl":"10.1053/j.akdh.2024.03.003","url":null,"abstract":"<div><p>Immunotactoid glomerulopathy (ITG) is a rare glomerular disease that typically presents with proteinuria, hematuria, and kidney dysfunction. A kidney biopsy is essential to establish the diagnosis of ITG. ITG is characterized by glomerular electron-dense immunoglobulin deposits with hollow-cored microtubules. ITG is classified as either monoclonal or polyclonal based on immunofluorescence staining of the immunoglobulin deposits. Monoclonal ITG is associated with an underlying hematologic disorder in two-thirds of the cases, lymphoma and plasma cell dyscrasias being the most common. Polyclonal ITG is associated with autoimmune diseases but can be seen with hematologic disorders and chronic infections. Due to the preponderance of hematologic disorders in both monoclonal and polyclonal ITG, a thorough hematologic workup must be performed in all cases of ITG. In monoclonal ITG with a detectable clone, clone-directed therapy is administered to achieve hematologic remission, as the renal response is highly dependent on the hematologic response. In clone-negative monoclonal ITG, anti-B cell therapy is often used as a first-line therapy. Management of polyclonal ITG without an underlying hematologic disorder is poorly defined. Compared to monoclonal ITG, patients with polyclonal ITG have a higher risk of progression to end-stage kidney disease. Recurrence of ITG following kidney transplantation is common and is often associated with hematologic relapse.</p></div>","PeriodicalId":72096,"journal":{"name":"Advances in kidney disease and health","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141861786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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