Nephron最新文献

{"title":"Unraveling the Molecular Nexus between Ankylosing Spondylitis and IgA Nephropathy: Insights from Mendelian Randomization and Bioinformatics Analysis.","authors":"Ningjun Shao, Kuibi Tan, Ping Chen, Qun Luo","doi":"10.1159/000544970","DOIUrl":"10.1159/000544970","url":null,"abstract":"<p><strong>Introduction: </strong>Renal complications are frequently observed in patients with ankylosing spondylitis (AS), with IgA nephropathy (IgAN) being a particularly significant concern. Although anecdotal evidence suggests a potential association between AS and IgAN, robust epidemiological data remain limited. Previous studies have reported varying prevalence rates of IgAN among AS patients, but these studies are often constrained by small sample sizes and inconsistent methodologies. Establishing a causal relationship between AS and IgAN through conventional observational studies has proven challenging due to confounding factors and reverse causality. Mendelian randomization (MR) offers a promising alternative, utilizing genetic variants to explore causal relationships. This study employs MR combined with bioinformatics analysis to investigate the molecular link between AS and IgAN, aiming to identify potential therapeutic targets.</p><p><strong>Methods: </strong>Two publicly available datasets were utilized: a genome-wide association study (GWAS) of AS (dataset ID: ebi-a-GCST005529) with 9,069 AS cases and 13,578 controls, and IgAN data from the FinnGen project, which included 653 cases and 411,528 controls. Instrumental variables were selected based on stringent criteria. MR analysis was conducted using the inverse variance weighted, weighted median, and MR-Egger methods to assess the causal relationship between AS and IgAN. Reverse MR analysis and sensitivity analysis were conducted to validate the findings. Bioinformatics analysis involved acquiring gene expression data from the GEO database and identifying differentially expressed genes (DEGs) using the limma package. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, protein-protein interaction (PPI) network construction, and hub gene identification were performed to elucidate the biological functions involved.</p><p><strong>Results: </strong>A total of 24 independent single-nucleotide polymorphisms (SNPs) associated with AS were identified through stringent SNP selection. MR analysis revealed a protective causal relationship between AS and IgAN (odds ratio = 0.552, 95% confidence interval, 0.339-0.900; p = 0.017). Analysis of DEGs identified 332 DEGs for IgAN and 5,521 DEGs for AS, with 59 common DEGs shared between the two diseases. Functional enrichment analysis highlighted significant changes in biological processes, cellular components, molecular functions, and KEGG pathways. PPI network analysis identified eight hub genes, including CX3CR1, which links AS and IgAN. External validation confirmed CX3CR1 as a crucial gene associated with both diseases.</p><p><strong>Conclusion: </strong>This study provides evidence of a protective causal relationship between AS and IgAN using MR analysis. Furthermore, bioinformatics analysis identifies CX3CR1 as a key gene, suggesting its role in mediating the protective link between AS and IgAN. These find","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-17"},"PeriodicalIF":2.3,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comments regarding \"Adoption of CKD-EPI (2021) for Glomerular Filtration Rate Estimation: Implications for UK Practice\".","authors":"Paul T Williams","doi":"10.1159/000545104","DOIUrl":"10.1159/000545104","url":null,"abstract":"","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-3"},"PeriodicalIF":2.3,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143605909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"When Proteins Go Berserk: The Unfolded Protein Response and ER Stress.","authors":"Doria Meiseles, Narkis Arbeli, Moran Dvela-Levitt","doi":"10.1159/000544971","DOIUrl":"10.1159/000544971","url":null,"abstract":"<p><strong>Background: </strong>The cellular proteostasis machinery is essential for maintaining protein homeostasis by employing quality control systems that identify, sequester, and eliminate damaged or misfolded proteins. However, the accumulation of misfolded proteins can overwhelm these protective mechanisms, disrupting proteostasis. This phenomenon is a hallmark of numerous pathologies, including a variety of genetic disorders. In the secretory pathway, the buildup of misfolded proteins triggers endoplasmic reticulum (ER) stress, which activates the unfolded protein response (UPR). The UPR serves as an adaptive mechanism, aiming to alleviate stress and restore cellular homeostasis. However, if ER stress is prolonged or severe, the UPR may fail to restore balance and apoptosis is induced.</p><p><strong>Summary: </strong>This review introduces the intricate signaling pathways activated by the three UPR transmembrane sensors: protein-kinase R-like endoplasmic reticulum kinase (PERK), inositol requiring enzyme 1 (IRE1), and activating transcription factor 6 (ATF6). We briefly present the roles of the distinct transcriptional programs activated by each sensor in modulating the cellular response to protein stress and in determining cell fate. We discuss how genetic variants and environmental factors contribute to the heterogeneity observed in protein misfolding diseases. Finally, we critically evaluate select therapeutic strategies, specifically protein stabilization, trafficking modulation, and UPR sensor targeting approaches.</p><p><strong>Key messages: </strong>This review introduces the potential consequences of protein misfolding, which may not only impair protein function but can also lead to toxic protein accumulation and stress induction. Using Fabry disease as a compelling example, we suggest that future therapeutic intervention may require nuanced, combination approaches that address both loss and gain of protein function.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-11"},"PeriodicalIF":2.3,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143557483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Home-Based Dialysis and Person-Centered Care: A Scoping Review.","authors":"Beate Nygaard-Andersen, Astrid Torbjørnsen, Peter Forde Hougaard, Ann-Chatrin Linqvist Leonardsen, Axel Wolf, Jeanette Finderup","doi":"10.1159/000544699","DOIUrl":"10.1159/000544699","url":null,"abstract":"<p><strong>Introduction: </strong>Managing dialysis at home requires the involvement of the patient in decisions, treatment, and their illness and health. Evidence-based person-centered care interventions focus on listening to the patient's narrative, establishing a partnership between patients and healthcare professionals, and documenting care and treatment in a shared health plan. Therefore, a person-centered care intervention is expected to enhance the patient's ability to manage dialysis at home. This study aimed to identify and map evidence for person-centered interventions and home-based dialysis for individuals with kidney failure.</p><p><strong>Methods: </strong>A scoping review was conducted based on the approach of Arksey and O'Malley. A systematic search was carried out in Medline, CINAHL, and Scopus for articles in all languages and without time restrictions. Person-centered care interventions concerning home dialysis were included. Two independent researchers assessed the literature. Data were extracted using NVIVO, and a relational analytical framework was employed to synthesize the data.</p><p><strong>Results: </strong>The search identified 9,443 articles, of which 16 met the inclusion criteria. A total of 13 person-centered care interventions were identified. Eight interventions aimed to involve the patient in the decision regarding the type of dialysis modality, with six interventions identified to involve the patient in treatment, illness, and health. Only one intervention was identified to involve the patient in the decisions that follow once the patient has commenced dialysis treatment. Five interventions showed a correlation between a person-centered care intervention and the number of patients in home dialysis.</p><p><strong>Conclusion: </strong>There is a need for interventions for patients in home dialysis to be adapted to a more person-centered care approach, particularly regarding the involvement of the patient in their treatment, illness, and health, as well as the decisions that follow the initiation of dialysis treatment.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-16"},"PeriodicalIF":2.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Inflammatory Pathogenetic Pathways of Fabry Nephropathy and Agalopathy: GLA Variant Induction of Endoplasmic Reticulum Stress.","authors":"Sandro Feriozzi, Paula Rozenfeld","doi":"10.1159/000544760","DOIUrl":"10.1159/000544760","url":null,"abstract":"<p><strong>Background: </strong>Fabry disease (FD) is a monogenic disease with highly variable clinical features. This variability suggests that additional pathogenetic pathways may exist besides the intra-lysosomal deposition of globotriaosylceramide (Gb3) and its deacylated form globotriaosylsphingosine (LysoGb3) caused by an enzyme deficiency.</p><p><strong>Summary: </strong>It has been demonstrated that intralysosomal accumulation of Gb3 and LysoGb3 triggers an inflammatory response. Monocytes, macrophages, and dendritic cells overexpress the adhesion molecules, and cytokines release occurs, including interleukin β, tumor necrosis factor-alpha (TNFα), and transforming growth factor beta. These processes determine the activation of inflammation processes associated with chronic inflammation and tissue fibrosis. The pathogenetic mechanisms stimulated by Gb3 and LysoGb3 deposition could break free from the original activation, causing an irreversible effect, in which Fabry disease-specific therapy can play a limited role. A new disease mechanism, \"Agalopathy\" would coexist with enzyme deficiency. Missense variants in the coding sequence of the GLA gene would generate the misfolding of the altered protein alpha-galactosidase A. Emergence of misfolded proteins may generate stress of the endoplasmic reticulum, leading to induction of the unfolded protein response (UPR). The UPR causes the release of pro-inflammatory cytokines and contributes to inflammatory status. This mechanism could be activated independently of glycolipid deposition, and its relationship with inflammatory pathways deserves more research. Strikingly, a zebrafish GLA knockout model that naturally lacks the enzyme that synthesizes Gb3 shows many alterations in lysosomal functions.</p><p><strong>Key messages: </strong>These pieces of evidence suggest the involvement of alternative pathways independent of Gb3 in FD pathogenesis. This review aims to describe these processes' role in the pathogenesis of renal damage in FD or Agalopathy nephropathies.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-6"},"PeriodicalIF":2.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Subclinical Inflammation and Renal Allograft Dysfunction: Myth or Reality?","authors":"Carlos Couceiro, Maria Visent, Josep M Cruzado","doi":"10.1159/000544762","DOIUrl":"10.1159/000544762","url":null,"abstract":"<p><strong>Background: </strong>Since the implementation of the Banff classification, the diagnosis and treatment of transplant rejection have been standardised. However, the rigid categorisation of transplant pathology has limited our perspective on allograft inflammation, particularly disregarding those inflammatory infiltrates who do not reach the category of rejection.</p><p><strong>Summary: </strong>The term subclinical inflammation was introduced to designate the inflammation found in protocol biopsies, without significant renal function deterioration. Following the introduction of modern immunosuppression with tacrolimus and mycophenolate, subclinical rejection rate decreased, and less attention was paid to this entity. However, in the last decades, several studies have evaluated the impact of lower levels of inflammation and demonstrated its negative consequences on long-term outcomes. Although, in some patients, this subclinical inflammation is not permanent and can spontaneously disappear. The uncomplete definition of subclinical inflammation, which only considers renal function stability, and the evaluation of the biopsy as a definitive diagnosis, and not as a picture of an evolving process, are the main reasons why managing this inflammation represents a challenge, especially when there is no pathogenic mechanism identified.</p><p><strong>Key messages: </strong>In this review, we revise the \"natural\" history of inflammation in the kidney allograft and its possible origins based on cellular composition and transcriptomic expression changes in kidney biopsies. In addition, we propose an updated definition and an approach to manage it.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-6"},"PeriodicalIF":2.3,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143441530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CHA2DS2-VASc Score as a Predictor of Cardiovascular and All-Cause Mortality in a Prospective Cohort of Hemodialysis Patients of Predominantly African Ancestry: The PROHEMO.","authors":"Gabriel Brayan Gutiérrez-Peredo, Andrea Jimena Gutiérrez-Peredo, Iris Montaño-Castellón, Marinho Marques da Silva Neto, Fernanda Albuquerque da Silva, Marcia Tereza Silva Martins, Cacia Mendes Matos, Jean Michell Correia Monteiro, Pedro Guimarães Silva, Gildete Barreto Lopes, Marcelo Barreto Lopes, Luis Claudio Correia, Roberto Pecoits-Filho, Keith C Norris, Antonio Alberto Lopes","doi":"10.1159/000543720","DOIUrl":"10.1159/000543720","url":null,"abstract":"<p><strong>Background: </strong>Patients with chronic kidney disease undergoing maintenance hemodialysis (MHD) have an increased mortality. The CHA2DS2-VASc score, initially used for stroke prediction in atrial fibrillation, is relevant for various cardiovascular conditions. This study evaluates its effectiveness in predicting cardiovascular and all-cause mortality in MHD patients.</p><p><strong>Methods: </strong>Data are from the \"Prospective Study of the Prognosis of Patients on Chronic Hemodialysis\" (PROHEMO) in Salvador, Brazil. Patients were divided by CHA2DS2-VASc scores: ≤2 and >2. Cox regression estimated hazard ratios (HR) for death, both unadjusted and adjusted for confounders. We assessed the distribution of each score variable and its association with mortality. A modified CHA2DS2-VASc score was created due to the low percentage of patients over 75 (1.3%) and normotensive (4.6%).</p><p><strong>Results: </strong>A total of 237 patients (mean age 51.6 years; 57.0% male) were included in the study. There were 55 deaths, 21 from cardiovascular causes. For patients with a CHA2DS2-VASc score >2, the unadjusted hazard of all-cause mortality was doubled (HR = 2.05; 95% CI: 1.20, 3.49) compared to those with a score ≤2, and the risk for cardiovascular deaths was more than threefold (HR = 3.53; 95% CI: 1.46, 8.54). These ratios remained consistent after adjusting for covariates. In the most comprehensive Cox model, the HR for all-cause mortality was 2.43 (95% CI: 1.38, 4.23) and for cardiovascular mortality was 3.52 (95% CI: 1.40, 8.84), similar to results from the modified CHA2DS2-VASc score.</p><p><strong>Conclusions: </strong>The results support the CHA2DS2-VASc score as a practical tool for identifying MHD patients at higher risk of mortality, especially from cardiovascular causes.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-12"},"PeriodicalIF":2.3,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12060819/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recurrence of Glomerular Diseases after Kidney Transplantation: What Do We Know New?","authors":"Emilio Rodrigo, Lara Belmar, José Luis Pérez-Canga","doi":"10.1159/000543268","DOIUrl":"10.1159/000543268","url":null,"abstract":"<p><strong>Background: </strong>The recurrence of primary glomerulonephritis (GN) following kidney transplantation poses a significant threat to graft survival. To enhance kidney transplant outcomes, we must lessen the burden of recurrence. In recent years, there has been progress in understanding the incidence, risk factors for recurrence, pathophysiology, biomarkers, and therapeutics, making it worthwhile to conduct an update on primary GN that may recur following kidney transplantation.</p><p><strong>Summary: </strong>We conducted a narrative review of the literature on the novel discoveries of primary GN that can recur following kidney transplantation. To summarize, developing a broad consensus on recurrence diagnosis would greatly advance our understanding, and its development would be a valuable collaborative effort. The key risk factors for recurrence have been better understood, particularly in individuals with complement-related or monoclonal gammopathy-related recurrent membranoproliferative GN. Furthermore, we can identify better recurrent IgA nephropathy patients who are more likely to experience graft loss. New biomarkers for membranous nephropathy (anti-PLA2R-Ab) and focal and segmental glomerulosclerosis (anti-nephrin-Ab) can assist in identifying and monitoring patients at risk of recurrence. Regarding therapy, the focal and segmental glomerulosclerosis consensus will enhance recurrence treatment. Some complement inhibitors and anti-CD38 monoclonal antibodies are already promising in treating and healing recurrent C3 glomerulopathy and focal and segmental glomerulosclerosis, respectively. Finally, new drugs developed specifically to treat IgA nephropathy in the native kidney will also change the outcome of IgA nephropathy recurrence.</p><p><strong>Key messages: </strong>Although there has been progress in understanding the recurrence of primary GN following kidney transplantation, a worldwide effort should be undertaken to gather research that will allow for improved diagnosis, monitoring, and management of these patients.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-12"},"PeriodicalIF":2.3,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142952054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the Critical Role of Tight Junction Proteins in Kidney Disease Pathogenesis.","authors":"David Jayne, Corentin Herbert, Vincent Anquetil, Geoffrey Teixeira","doi":"10.1159/000542498","DOIUrl":"10.1159/000542498","url":null,"abstract":"<p><strong>Background: </strong>Kidney disease poses a significant global health challenge, marked by a rapid decline in renal function due to a variety of causative factors. A crucial element in the pathophysiology of kidney disease is the dysregulation of epithelial cells, which are vital components of renal tissue architecture. The integrity and functionality of these cells are largely dependent on tight junctions (TJ) proteins, complex molecular structures that link adjacent epithelial cells. These TJ not only confer cellular polarity and maintain essential barrier functions but also regulate epithelial permeability.</p><p><strong>Summary: </strong>TJ proteins are pivotal in their traditional role at cell junctions and in their non-junctional capacities. Recent research has shifted the perception of these proteins from mere structural elements to dynamic mediators of kidney disease, playing significant roles in various renal pathologies. This review explores the multifaceted roles of TJ proteins, focusing on their functions both within and external to the renal epithelial junctions. It highlights how these proteins contribute to mechanisms underlying kidney disease, emphasizing their impact on disease progression and outcomes.</p><p><strong>Key messages: </strong>TJ proteins have emerged as significant players in the field of nephrology, not only for their structural role but also for their regulatory functions in disease pathology. Their dual roles in maintaining epithelial integrity and mediating pathological processes make them promising therapeutic targets for kidney disease. Understanding the intricate contributions of TJ proteins in kidney pathology offers potential for novel therapeutic strategies, aiming to modulate these proteins to halt or reverse the progression of kidney disease.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"240-250"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11991748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urinary Complement C3 and Vitamin D-Binding Protein Predict Adverse Outcomes in Patients with Acute Kidney Injury after Cardiac Surgery.","authors":"Joseph Hunter Holthoff, Joseph L Alge, John M Arthur, Fatima Ayub, Wadhah Bin Homam, Michael G Janech, Sreelakshmi Ravula, Nithin Karakala","doi":"10.1159/000540664","DOIUrl":"10.1159/000540664","url":null,"abstract":"<p><strong>Introduction: </strong>Acute kidney injury (AKI) is associated with adverse outcomes, including death and dialysis. The goal of this study was to identify prognostic biomarkers of AKI that could be used across multiple phenotypes of AKI and across different species.</p><p><strong>Methods: </strong>Liquid chromatography/tandem mass spectrometry analysis of urine samples from three species (human, rat, and mouse) and four etiologies of AKI identified five potential biomarkers, of which two were validated, complement C3 and vitamin D-binding protein, in a cohort of 157 patients that developed AKI following cardiothoracic surgery. We studied the relationship between the biomarker's concentration in the urine and the development of a composite primary endpoint (stage 3 AKI within 10 days or death within 30 days).</p><p><strong>Results: </strong>Of the 153 patients who developed AKI following cardiovascular surgery, 17 met the combined primary outcome. The median concentration of urine complement C3 adjusted to urine creatinine had the best predictive value and was significantly higher in the primary outcome group than in the controls. Similarly, the median concentration of vitamin D-binding protein was higher in the primary outcome group.</p><p><strong>Conclusions: </strong>The studies provide proof in principle that cross-species discovery analyses could be a valuable tool for identifying novel prognostic biomarkers in AKI. Urine complement C3 and vitamin D-binding protein could be promising early predictors of adverse outcomes in patients who develop AKI after cardiac surgery.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"66-76"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142350544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}