Frontiers in nephrology最新文献

{"title":"Triple monoclonal protein-related kidney lesions in a patient with plasma cell dyscrasia: a case report.","authors":"Arsalan Alvi, Alexander J Gallan, Nattawat Klomjit","doi":"10.3389/fneph.2024.1399977","DOIUrl":"10.3389/fneph.2024.1399977","url":null,"abstract":"<p><p>A toxic monoclonal protein typically results in a single kidney pathology due to the specific biophysical characteristics of monoclonal proteins. Multiple monoclonal protein lesions are rarely reported and often portend a poor prognosis. We present a 57-year-old male who developed rapidly progressive glomerulonephritis after concealed ruptured diverticulitis. A kidney biopsy showed light chain cast nephropathy, light chain proximal tubulopathy, and thrombotic microangiopathy. Laboratories showed IgG kappa with an M-spike of 0.2 g/dl and a kappa light chain of 16 mg/dl. A bone marrow biopsy showed 3% kappa-restricted plasma cells. The dramatic renal presentation despite the minimal hematological burden is suggestive of a highly toxic light chain, which is consistent with monoclonal gammopathy of renal significance (MGRS). Clone-directed therapy and a complement blockade were initiated. The patient remained dialysis-dependent despite a hematological response. This case highlights the importance of considering the toxic properties of monoclonal proteins in causing kidney diseases. Our case is the first report of an MGRS patient with three distinct kidney lesions. Triple monoclonal protein-related kidney lesions are very rare and are usually associated with multiple myeloma. Light chain cast nephropathy (LCCN) is a myeloma-defining event but his light chain (LC) (<50 mg/dl) and plasma cell (<10%) burdens were low which makes this case very unusual. Sepsis-induced low-flow stage and the toxic properties of LC may induce LCCN in this patient. Aggressive therapy is likely needed to eradicate the clone in order to achieve an organ response.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"4 ","pages":"1399977"},"PeriodicalIF":0.0,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11582032/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142711834","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}

{"title":"Commentary: Obstructive sleep apnea in the hemodialysis population: are clinicians putting existing scientific evidence into practice?","authors":"Aleena Jamal, Som P Singh, Fawad Qureshi","doi":"10.3389/fneph.2024.1450204","DOIUrl":"10.3389/fneph.2024.1450204","url":null,"abstract":"","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"4 ","pages":"1450204"},"PeriodicalIF":0.0,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11578962/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142689880","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}

{"title":"Prognostic significance of fibrinogen levels in sepsis-associated acute kidney injury: unveiling a nonlinear relationship and clinical implications.","authors":"Manqin Chen, Xinbin Chen, Huaxiang Ling, Chengwen Bai, Lihua Chen, Lin Zhong, Ping Gong, Fei Shi","doi":"10.3389/fneph.2024.1398386","DOIUrl":"10.3389/fneph.2024.1398386","url":null,"abstract":"<p><strong>Background: </strong>Fibrinogen plays a pivotal role in the inflammatory cascade and is intricately linked to the pathogenesis of sepsis. Nevertheless, its significance as a prognostic marker for sepsis-associated acute kidney injury (SA-AKI) remains uncertain. This study aimed to investigate the association between fibrinogen levels and 28-day mortality with sepsis-associated acute kidney injury.</p><p><strong>Method: </strong>The fibrinogen levels of patients admitted to the intensive care unit of Beth Israel Deaconess Medical Center between 2008 and 2019 were retrospectively assessed, and those diagnosed with SA-AKI were divided into low, middle and high fibrinogen level groups according to tertiles. Multivariate Cox proportional hazards model was used to assess the 28-day mortality risk of the SA-AKI patients.</p><p><strong>Results: </strong>A total of 3,479 patients with SA-AKI were included in the study. Fibrinogen demonstrated an independent association with 28-day mortality, yielding a hazard ratio (HR) of 0.961 (95% confidence interval [CI]: 0.923-0.999, <i>P</i> = 0.0471). Notably, a non-linear relationship between fibrinogen levels and 28-day mortality was observed, with the threshold observed at approximately 1.6 g/l. The effect sizes and corresponding CIs below and above this threshold were 0.509 (0.367, 0.707) and 1.011 (0.961, 1.064), respectively. Specifically, the risk of mortality among SA-AKI patients decreased by 49.1% for every 1 g/l increment in fibrinogen, provided that fibrinogen levels were less than 1.6 g/l.</p><p><strong>Conclusion: </strong>In patients with SA-AKI, a non-linear relationship was identified between fibrinogen levels and 28-day mortality. Particularly, when their fibrinogen levels were less than 1.6 g/l, a concomitant decrease in 28-day mortality was observed as fibrinogen levels increased.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"4 ","pages":"1398386"},"PeriodicalIF":0.0,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11576428/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142683696","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}

{"title":"Proteinuria and proximal tubular epithelial cells: correlation between immunofluorescence, histology, and degree of proteinuria.","authors":"Maria Bernadette Cy Chow, Vedat Yildiz, Laura Biederman, Alana Dasgupta, Anjali A Satoskar, Aaron Chow, Tibor Nadasdy, Sergey V Brodsky","doi":"10.3389/fneph.2024.1469388","DOIUrl":"10.3389/fneph.2024.1469388","url":null,"abstract":"<p><p>Proteins are filtered from the blood through the glomerular filtration barrier. Filtered proteins are reabsorbed by proximal tubular epithelial cells (PTECs), which have been shown to possess the ability to regulate protein reabsorption. Histologically, these reabsorbed proteins are seen as tubular protein reabsorption droplets (TPRDs). Experimental studies indicate that PTECs play an important role in regulating proteinuria but the correlations between TPRD and the degree of proteinuria in human kidney biopsies have not been investigated in detail. Consecutive native kidney biopsies with non-proliferative glomerular disease performed at the OSUWMC for a 1-year period were analyzed. Cases with acute glomerular diseases and inadequate biopsies were excluded. The staining intensity and the percentage of TPRDs, as well as other morphologic parameters, were assessed. A total of 109 kidney biopsies were included in the study. A reverse correlation was identified between the percentage of albumin TPRDs and proteinuria (<i>p</i> = 0.047). There were positive correlations between proteinuria and the staining intensity for IgG TPRDs (<i>p</i> = 0.05) and the degree of acute tubular necrosis (ATN) (<i>p</i> = 0.015). In patients with no ATN, positive correlations between proteinuria and albumin and IgG TPRDs were seen, whereas in patients with ATN, these correlations were lost. A positive correlation was seen between proteinuria and chronic kidney injury. A strong correlation was noted between the degree of proteinuria and podocyte foot process effacement. Our data indicate that PTECs regulate proteinuria by absorbing proteins from the urine filtrate. Therefore, based on the human renal biopsy material, our study confirms that well-functioning renal PTECs play an important role in the regulation of proteinuria.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"4 ","pages":"1469388"},"PeriodicalIF":0.0,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11560906/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142633958","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}

{"title":"Increased levels of antibodies to synaptopodin and annexin 1 in patients with primary podocytopathies.","authors":"Natalia V Chebotareva, Evgeniya A Charionovskaya, Evgenia A Biryukova, Anatoliy A Vinogradov, Igor I Alentov, Natalia S Sergeeva, Alexey S Kononikhin, Evgeny N Nikolaev, Sergey V Moiseev","doi":"10.3389/fneph.2024.1471078","DOIUrl":"10.3389/fneph.2024.1471078","url":null,"abstract":"<p><strong>Introduction: </strong>Circulating anti-podocyte antibodies have been proposed as potential factors contributing to increased permeability in primary podocytopathies, such as Minimal Change Disease (MCD) and Focal Segmental Glomerulosclerosis (FSGS). The aim of the study was to to assess the levels of antibodies targeting synaptopodin and annexin 1 in the blood serum of patients diagnosed with nephrotic syndrome, with the aim of evaluating their potential utility in diagnosing primary podocytopathies and predicting therapeutic response.</p><p><strong>Methods: </strong>The study included a total of 72 patients diagnosed with nephrotic syndrome, alongside 21 healthy subjects for comparison. Among the patients, 38 were diagnosed with FSGS, 12 with MCD, and 22 with MN. The levels of anti-synaptopodin and anti-annexin-1 antibodies were quantified using Enzyme-Linked Immunosorbent Assay.</p><p><strong>Results: </strong>The levels of antibodies to annexin 1 and anti-synaptopodin in the blood were found to be higher in patients diagnosed with MCD and FSGS compared to those with MN and healthy individuals. The elevated levels of antibodies to annexin 1 and synaptopodin showed area under the curve values of 0.826 (95% CI 0.732-0.923) and 0.827 (95% CI 0.741-0.879), respectively. However, a model incorporating both antibodies demonstrated higher sensitivity (80.9%) and specificity (81.3%) with an AUC of 0.859 (95% CI 0.760-0.957). Notably, serum levels of annexin 1 and anti-synaptopodin antibodies did not predict the response to prednisolone and/or CNI therapy.</p><p><strong>Discussion: </strong>Levels of antibodies targeting synaptopodin and annexin 1 were notably elevated in patients diagnosed with MCD and FSGS compared to those with MN and healthy controls. A panel comprising both antibodies demonstrated moderate to high sensitivity and specificity for diagnosis MCD or FSGS.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"4 ","pages":"1471078"},"PeriodicalIF":0.0,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11560892/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142633956","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}

{"title":"C3 glomerulopathy: a kidney disease mediated by alternative pathway deregulation.","authors":"Karin Heidenreich, Deepti Goel, P S Priyamvada, Sagar Kulkarni, Vipul Chakurkar, Dinesh Khullar, Ravi Singh, Charan Bale, Peter F Zipfel","doi":"10.3389/fneph.2024.1460146","DOIUrl":"https://doi.org/10.3389/fneph.2024.1460146","url":null,"abstract":"<p><p>C3 glomerulopathy (C3G) is an ultra-rare complement-mediated kidney disease caused by to the deregulation of the alternative pathway (AP) of proximal complement. Consequently, all effector loops of the complement are active and can lead to pathologies, such as C3a- and C5a-mediated inflammation, C3b opsonization, surface C3b-mediated AP C3 convertase assembly, C3 cleavage product deposition in the glomerulus, and lytic C5b-9/MAC cell damage. The most common pathologic mechanisms are defective chronic alternative pathway deregulation, mostly occurring in the plasma, often causing C3 consumption, and chronic complement-mediated glomerular damage. C3G develops over several years, and loss of renal function occurs in more than 50% of patients. C3G is triggered by both genetic and autoimmune alterations. Genetic causes include mutations in individual complement genes and chromosomal variations in the form of deletions and duplications affecting genes encoding complement modulators. Many genetic aberrations result in increased AP C3 convertase activity, either due to decreased activity of regulators, increased activity of modulators, or gain-of-function mutations in genes encoding components of the convertase. Autoimmune forms of C3G do also exist. Autoantibodies target individual complement components and regulators or bind to neoepitopes exposed in the central alternative pathway C3 convertase, thereby increasing enzyme activity. Overactive AP C3 convertase is common in C3G patients. Given that C3G is a complement disease mediated by defective alternative pathway action, complement blockade is an emerging concept for therapy. Here, we summarize both the causes of C3G and the rationale for complement inhibition and list the inhibitors that are being used in the most advanced clinical trials for C3G. With several inhibitors in phase II and III trials, it is expected that effectice treatment for C3G will become availabe in the near future.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"4 ","pages":"1460146"},"PeriodicalIF":0.0,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11554616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142633955","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}

{"title":"Desidustat: a novel PHD inhibitor for the treatment of CKD-induced anemia.","authors":"Amit Joharapurkar, Vrajesh Pandya, Harilal Patel, Mukul Jain, Ranjit Desai","doi":"10.3389/fneph.2024.1459425","DOIUrl":"10.3389/fneph.2024.1459425","url":null,"abstract":"<p><p>Desidustat is a small molecule inhibitor of hypoxia-inducible factor-prolyl hydroxylase (HIF-PH) discovered and developed by Zydus Lifesciences for the treatment of anemia associated with chronic kidney disease (CKD). This review summarizes the preclinical and clinical profile of desidustat which led to its approval and clinical use in India.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"4 ","pages":"1459425"},"PeriodicalIF":0.0,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11534831/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142585144","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}

{"title":"The clinical course of SARS-CoV-2 infection in patients with glomerular diseases and evaluation of the subsequent risk of relapse.","authors":"Sophia Lionaki, Evangelia Dounousi, Smaragdi Marinaki, Konstantia Kantartzi, Marios Papasotiriou, Dimitra Galitsiou, Ioannis Bellos, Aggeliki Sardeli, Petros Kalogeropoulos, Vassilios Liakopoulos, Christos Mpintas, Dimitrios Goumenos, Sophia Flouda, Aliki Venetsanopoulou, Paraskevi Voulgari, Eva Andronikidi, Georgios Moustakas, Stylianos Panagoutsos, Ioannis Boletis","doi":"10.3389/fneph.2024.1472294","DOIUrl":"10.3389/fneph.2024.1472294","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to describe the clinical course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in patients with glomerular diseases (GDs) and its impact on the probability of relapse.</p><p><strong>Methods: </strong>Patients with biopsy-proven GD and positive PCR test for SARS-CoV-2 from glomerular clinics across Greece were studied retrospectively. Those who received the GD diagnosis after the SARS-CoV-2 vaccination or coronavirus disease 2019 (COVID-19) or ended in ESKD prior to infection were excluded. Demographics, histopathological diagnoses, past medical history, immunosuppression, and GD activity status were recorded.</p><p><strong>Results: </strong>A total of 219 patients with GDs and documented SARS-CoV-2 infection were included. The mean time from the diagnostic kidney biopsy to SARS-CoV-2 infection was 67.6 ( ± 59.3) months. Among the participants, 82.5% had been vaccinated against SARS-CoV-2 with three doses (range: 2.5-3) without subsequent GD reactivation in 96.2% of them. Twenty-two patients (10%) were hospitalized for COVID-19 and one (0.5%) required mechanical ventilation. Four (1.8%) died due to COVID-19 and one (0.5%) had long COVID-19 symptoms. Among patients in remission prior to SARS-CoV-2 infection, 22 (11.2%) experienced a GD relapse within 2.2 (range: 1.5-3.7) months from the diagnostic test. The relapse-free survival after COVID-19 was significantly shorter for patients with minimal change disease, pauci-immune glomerulonephritis, and focal segmental glomerulosclerosis. No difference was observed in the relapse-free survival post-COVID-19 based on the history of SARS-CoV-2 vaccination.</p><p><strong>Conclusions: </strong>SARS-CoV-2 infection appears to have a symptomatic but uncomplicated sequence in vaccinated patients with GDs, with a significant impact on the clinical course of GD, associated with an increased probability of relapse in certain histopathological types.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"4 ","pages":"1472294"},"PeriodicalIF":0.0,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11532109/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142577403","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}

{"title":"<i>Inside CKD</i>: a microsimulation modelling study projects the clinical and economic burden of chronic kidney disease in Hungary.","authors":"Lilla Szabó, Luca Adél Halmai, Erzsébet Ladányi, Juan Jose Garcia Sanchez, Salvatore Barone, Claudia Cabrera, Lise Retat, Laura Webber, István Wittmann, Boglárka Laczy","doi":"10.3389/fneph.2024.1458607","DOIUrl":"10.3389/fneph.2024.1458607","url":null,"abstract":"<p><strong>Objectives: </strong>The <i>Inside CKD</i> programme implemented a microsimulation modelling approach to project the clinical and economic burden of chronic kidney disease (CKD) between 2024 and 2027 in Hungary.</p><p><strong>Methods: </strong>Using the peer-reviewed <i>Inside CKD</i> microsimulation, a virtual Hungarian population was generated that was derived from national records, local demographic data and published epidemiological data. These inputs defined the likelihood of a change in health state for each individual as they progressed through the model in annual increments. Individual CKD status, including disease progression, cardiorenal complications and associated costs, was tracked annually to generate the population-level projections of the clinical and economic burden of CKD.</p><p><strong>Results: </strong>By 2027, people with CKD were projected to constitute 13.3% of the Hungarian national population. The prevalence of heart failure, myocardial infarction and stroke in people with CKD were projected to remain consistently high, reaching 323 447, 69 188 and 120 118 by 2027, respectively. Kidney replacement therapy cases were predicted to remain high at 20 515 in 2024 and 22 325 in 2027, with associated costs increasing from 71.4 billion HUF in 2024 to 79.6 billion HUF in 2027. Total annual healthcare costs associated with treating CKD were projected to constitute 5.4% of the overall national healthcare budget in 2027.</p><p><strong>Conclusions: </strong><i>Inside CKD</i> demonstrates that the future burden of CKD in Hungary will be substantial unless current management strategies change. The high prevalence of undiagnosed CKD and associated cardiorenal complications highlight the urgent need for policy interventions focused on early diagnosis and timely intervention to mitigate the future burden of CKD.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"4 ","pages":"1458607"},"PeriodicalIF":0.0,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11527778/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142570501","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}

{"title":"Quantifying measurement uncertainty in renal transplant biopsy assessment.","authors":"Xavier Loizeau, Marina Romanchikova, Spencer A Thomas, Moulham Alsuleman, John O O Ayorinde, Gavin J Pettigrew","doi":"10.3389/fneph.2024.1458491","DOIUrl":"https://doi.org/10.3389/fneph.2024.1458491","url":null,"abstract":"<p><strong>Introduction: </strong>Renal transplant biopsies provide insights into graft health and support decision making. The current evidence on links between biopsy scores and transplant outcomes suggests there may be numerous factors affecting biopsy scores. Here we adopt measurement science approach to investigate the sources of uncertainty in biopsy assessment and suggest techniques to improve its robustness.</p><p><strong>Methods: </strong>Histological assessments, Remuzzi scores, biopsy processing and clinical variables are obtained from 144 repeat biopsies originating from 16 deceased-donor kidneys. We conducted sensitivity analysis to find the morphometric features with highest discriminating power and studied the dependencies of these features on biopsy and stain type. The analysis results formed a basis for recommendations on reducing the assessment variability.</p><p><strong>Results: </strong>Most morphometric variables are influenced by the biopsy and stain types. The variables with the highest discriminatory power are sclerotic glomeruli counts, healthy glomeruli counts per unit area, percentages of interstitial fibrosis and tubular atrophy as well as diameter and lumen of the worst artery. A revised glomeruli adequacy score is proposed to improve the robustness of the glomeruli statistics, whereby a minimum of 104 µm² of cortex tissue is recommended to keep type 1 and type 2 error probabilities below 0.15 and 0.2.</p><p><strong>Discussion: </strong>The findings are transferable to several biopsy scoring systems. We hope that this work will help practitioners to understand the sources of statistical uncertainty and improve the utility of renal biopsy.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"4 ","pages":"1458491"},"PeriodicalIF":0.0,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11519413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142549270","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}