medRxiv - Nephrology最新文献

{"title":"Long COVID and kidney function: A scoping review protocol","authors":"Marcella Frediani, Heitor S. Ribeiro, Geraldo Busatto, Carlos Carvalho, Emmanuel A Burdmann","doi":"10.1101/2024.02.29.24303559","DOIUrl":"https://doi.org/10.1101/2024.02.29.24303559","url":null,"abstract":"Introduction: The coronavirus disease 2019 (COVID-19) pandemic had catastrophic repercussions worldwide, including short- and long-term effects on multiple organs. The term long COVID encompasses signs and symptoms associated with COVID that persist for more than two months. However, the effects of long COVID on kidney function remain poorly understood. Objective: This scoping review aims to describe the effects of long COVID on kidney function and/or kidney-related outcomes. Methods: We will follow the Joanna Briggs Institute methodology and Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews. Based on the PCC framework, we will include studies that investigated long COVID survivors (Participants); describing kidney function and/or kidney-related outcomes (Concept); in all settings and designs (Context). A comprehensive literature search was performed using the MEDLINE, Embase, and LILACS databases without date or language restrictions from inception until August 2023. Websites, books, and guidelines will also be searched. Observational studies with retrospective, prospective, and case-control designs will be considered. Two independent reviewers will screen titles and abstracts and perform the full-text review. Data extraction will be done by the main reviewer and checked by a second one. Data about the diagnosis of COVID, follow-up time for long symptoms, and kidney function assessment and outcomes will be extracted from selected evidence. The quantitative results will be synthesized and presented in tables and figures along with a narrative summary. Ethics and dissemination: There is no requirement for ethical approval for this scoping review. On completion, it will be published in a peer-reviewed academic journal and presented at a conference.","PeriodicalId":501513,"journal":{"name":"medRxiv - Nephrology","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140001831","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}

{"title":"Quantitative susceptibility mapping for detection of kidney stones, hemorrhage differentiation and cyst classification in ADPKD","authors":"Karl Schumacher, Martin R. Prince, Jon D Blumenfeld, Hanna Rennert, Zhongxiu Hu, Hreedi Dev, Yi Wang, Alexey V. Dimov","doi":"10.1101/2024.02.24.24303322","DOIUrl":"https://doi.org/10.1101/2024.02.24.24303322","url":null,"abstract":"Background and purpose\u0000The objective is to demonstrate feasibility of quantitative susceptibility mapping (QSM) in autosomal dominant polycystic kidney disease (ADPKD) patients and to compare imaging findings with traditional T1/T2w magnetic resonance imaging (MRI). Methods\u0000Thirty-three consecutive patients (11 male, 22 female) diagnosed with ADPKD were initially selected. QSM images were reconstructed from the multiecho gradient echo data and compared to co-registered T2w, T1w and CT images. Complex cysts were identified and classified into distinct subclasses based on their imaging features. Prevalence of each subclass was estimated. Results\u0000QSM visualized two renal calcifications measuring 9 and 10 mm, and three pelvic phleboliths measuring 2 mm but missed 24 calcifications measuring 1mm or less and 1 larger calcification at the edge of the field of view. A total of 121 complex T1 hyperintense/T2 hypointense renal cysts were detected. 52 (43%) cysts appeared hyperintense on QSM consistent with hemorrhage; 60 (49%) cysts were isointense with respect to simple cysts and normal kidney parenchyma, while the remaining 9 (7%) were hypointense. The presentation of the latter two complex cyst subtypes is likely indicative of proteinaceous composition without hemorrhage. Conclusions\u0000Our results indicate that QSM of ADPKD kidneys is possible and uniquely suited to detect large renal calculi without ionizing radiation, and able to identify properties of complex cysts unattainable with traditional approaches.","PeriodicalId":501513,"journal":{"name":"medRxiv - Nephrology","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139979534","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}

{"title":"The burden of patient healthcare activity in the first year of peritoneal dialysis","authors":"Kirsty Crowe, Eleanor C Murray, Joan MacLeod, Jamie P Traynor, Peter C Thomson","doi":"10.1101/2024.02.19.24301896","DOIUrl":"https://doi.org/10.1101/2024.02.19.24301896","url":null,"abstract":"Background: The healthcare-related burden associated with kidney replacement therapy (KRT) has not been characterised as comprehensively in peritoneal dialysis (PD) as in haemodialysis (HD) or kidney transplantation. This study aimed to capture the nature and extent of healthcare activity in the first year of PD therapy.\u0000Methods: Retrospective analysis was undertaken on consecutive incident adult patients on PD between 1st January 2015-31st December 2019 in the Glasgow Renal and Transplant Unit. Healthcare-related activity was captured up to the first 365 days post-commencement of PD. Data was collected on renal service contact and activity relating to dialysis access, radiological investigation, and relevant infection episodes. Carbon mapping of healthcare activity was estimated using postcode data and previously published carbon footprint estimations.\u0000Results: PD was initiated in 122 patients over the study period. Sixty-three patients (52%) transitioned to another KRT within 365 days of commencing PD. Patients had a mean 36.4 days (SD 22.7) of face-to-face contact days with renal services. This included a mean of 1.5 (SD 1.6) hospital admissions, with a median 5 (IQR 10.8) in-patient days. The estimated carbon footprint was 581kg CO2e/patient over the incident year. This included a median 207kg CO2e/patient for inpatient days and 26kg CO2e/patient for treatment of infections.\u0000Conclusions: There is a significant burden of kidney-associated healthcare on patients commencing their first year of PD despite it being a home-based therapy. Estimates of carbon footprint indicate hotspots include patient travel and hospital admissions, and episodes of peritonitis; a full life cycle analysis is merited.","PeriodicalId":501513,"journal":{"name":"medRxiv - Nephrology","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139918744","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}

{"title":"Contribution of variants across the allelic frequency spectrum to cystic kidney disease","authors":"Omid Sadeghi-Alavijeh, Melanie MY Chan, Gabriel Doctor, Catalin Voinescu, Alex Stuckey, Athanasios Kousathanas, Alexander Ho, Genomics England Research Consortium, Horia Stanescu, Horia Stanescu, Detlef Bockenhauer, Richard Sandford, Adam P Levine, Daniel P Gale","doi":"10.1101/2024.02.14.24302377","DOIUrl":"https://doi.org/10.1101/2024.02.14.24302377","url":null,"abstract":"Introduction\u0000Cystic kidney disease (CyKD) is frequently a familial disease, with ~85% of probands receiving a monogenic diagnosis. However, gene discovery has been led by family-based and candidate gene studies, limiting the ascertainment of non-Mendelian genetic contributors to the disease. Using whole genome sequencing data provided by the 100,000 Genomes Project (100KGP), we used hypothesis-free approaches to systematically characterize and quantify the genetic contributors to CyKD across variant types and the allele frequency spectrum. Methods\u0000We performed a sequencing-based genome-wide association study in 1,209 unrelated patients recruited to the 100,000 Genomes Project with CyKD and 26,096 ancestry-matched unaffected controls. The analysis was inclusive of individuals with diverse genetic ancestries. Enrichment of common, low-frequency (minor allele frequency [MAF] > 0.1%) and rare (MAF < 0.1%) single-nucleotide variants (SNV), indels and rare structural variants (SV) on a genome-wide and per-gene basis was sought using a generalised linear mixed model approach to account for population structure. Meta-analysis of CyKD cohorts from Finngen, the UK Biobank and BioBank Japan was performed. Results\u0000In 995 of the 1209 (82.30%) CyKD cases a likely disease-causing monogenic variant was identified. Gene-based analysis of rare SNVs/indels predicted to be damaging revealed PKD1 (P=1.13x10-309), PKD2 (P=1.96x10-150), DNAJB11 (P=3.52x10-7), COL4A3 (P=1.26x10-6) and truncating monoallelic PKHD1 (P=2.98x10-8) variants to be significantly associated with disease. Depleting for solved cases led to the emergence of a significant association at IFT140 (P=3.46x10-17) and strengthening of the COL4A3 (P=9.27x10-7) association, driven exclusively by heterozygous variants for both genes. After depleting for those harbouring IFT140 and COL4A3 variants , no other genes were identified. Risk of disease attributable to monoallelic defects of multiple genes linked with CyKD was quantified, with lower risk seen in rarer and more recently described genetic diagnoses.\u0000Genome-wide structural variant associations highlighted deletions in PKD1 (P=2.17x10-22), PKD2 (P=7.48x10-12) and the 17q12 locus containing HNF1B (P=4.12x10-8) as statistically significant contributors to disease. Genome-wide analysis of over 18 million common and low-frequency variants in the Finnish population revealed evidence of association (P=1.4x10-149) of a heterozygous stop-gain variant in PKHD1 that is endemic (MAF=4.7x10-03) in this population. Meta-analysis of 2,923 cases and 900,824 controls across 6,641,351 common and low frequency variants including UK, Japanese and Finnish biobanks did not reveal any novel significant associations. SNVs with a MAF>0.1% accounted for between 3 and 9% of the heritability of CyKD across three different European ancestry cohorts. Conclusions\u0000These findings represent an unbiased examination of the genetic architecture of a national CyKD cohort using ro","PeriodicalId":501513,"journal":{"name":"medRxiv - Nephrology","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139756896","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}

{"title":"Prevalence of Mendelian kidney disease among patients with high-risk APOL1 genotypes undergoing commercial genetic testing in the United States","authors":"Ronaldo da Silva Francisco, Sumit Punj, Lisa Vincent, Nina Sanapareddy, Vivek Bhalla, Glenn M. Chertow, Dianne Keen-Kim, Vivek Charu","doi":"10.1101/2024.02.13.24302777","DOIUrl":"https://doi.org/10.1101/2024.02.13.24302777","url":null,"abstract":"Background: Among individuals with high-risk APOL1 genotypes, the lifetime risk of developing kidney failure is ~15%, indicating that other genetic variants or non-genetic modifiers likely contribute substantially to an individual patient's risk of progressive kidney disease. Here we estimate the prevalence and distribution of molecularly diagnosed Mendelian kidney diseases among patients with high-risk APOL1 genotypes undergoing commercial genetic testing in the United States. Methods: We analyzed clinical exome sequencing data from 15,181 individuals undergoing commercial genetic testing for Mendelian kidney disease in the United States from 2020-2021. We identified patients with high-risk APOL1 genotypes by the presence of G1/G1, G1/G2, or G2/G2 alleles. Patients carrying single risk APOL1 alleles were identified as G1/G0, G2/G0; the remainder of patients were G0/G0. We estimated the prevalence and distribution of molecularly diagnosed Mendelian kidney disease stratified by APOL1 genotype. Results: Of 15181 patients, 3119 had genetic testing results consistent with a molecular diagnosis of Mendelian kidney disease (20.5%). 1035 (6.8%) had high-risk APOL1 genotypes. The prevalence of molecularly diagnosed Mendelian kidney diseases was lower in individuals with high-risk APOL1 genotypes (9.2%; n=95/1035) compared to single risk APOL1 allele carriers (14.4%; n=243/1687) and those with G0/G0 APOL1 genotypes (22.3%; n=2781/12459). The distribution of molecularly diagnosed Mendelian kidney diseases was broadly similar among patients with and without high-risk APOL1 genotypes. Conclusions: Among patients undergoing clinical genetic testing, we found a relatively high rate of molecularly diagnosed Mendelian kidney disease in patients with high-risk APOL1 genotypes. Mendelian kidney disease may contribute to wide variation in rates of progression observed among patients with high-risk APOL1 genotypes.","PeriodicalId":501513,"journal":{"name":"medRxiv - Nephrology","volume":"88 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139756516","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}

{"title":"Insights from Single-Cell RNA-seq: Identifying the Actin Gene Family as Novel Drivers in Parkinson's Disease","authors":"Saed Sayad, Mark Hiatt, Hazem Mustafa","doi":"10.1101/2024.02.12.24302696","DOIUrl":"https://doi.org/10.1101/2024.02.12.24302696","url":null,"abstract":"Background. Parkinson's disease (PD) is the second most common neurodegenerative disorder, affecting\u0000millions of individuals worldwide. The complex etiology of PD involves a combination of genetic and environmental factors. The Actin family encompasses a group of highly conserved cytoskeletal proteins that play a crucial role in maintaining cellular structure and function. Actin proteins are involved in various cellular processes, including cell motility, vesicle trafficking, and synaptic transmission. This\u0000paper delves into the exploration of the Actin family of genes, revealing their potential as key\u0000contributors to PD through the application of single-cell RNA-seq.\u0000Method. We obtained single-cell transcriptomes (GSE237133) from the NIH portal website. We\u0000conducted an extensive comparative analysis of single-cell transcriptomes derived from Parkinson's disease organoids and two control organoids to identify differentially expressed genes, pathways,\u0000and gene ontology terms.\u0000Results. We conducted a comparative analysis of single-cell transcriptomes from Parkinson's disease organoid and two control organoids, aiming to identify differentially expressed genes, pathways,\u0000and gene ontology items. In comparing the PD organoid with the control organoid, we observed that the ACTB and ACTG1 genes were common among 18 of the top 20 upregulated KEGG pathways and among\u000015 of the top 20 upregulated Reactome pathways. Additionally, when comparing the PD organoid with\u0000the isogenic control organoid, we found the ACTB and ACTG1 genes shared among 19 out of the top 20\u0000pathways and among 19 out of the top 20 upregulated Reactome pathways. An additional noteworthy\u0000finding includes the overexpression of several Mitochondrially Encoded NADH family genes in the PD organoid cells compare to the control organoids cells.\u0000Conclusion. The Actin family of genes in general and ACTB and ACTG1 genes in particular emerges as a\u0000potential new player in the convoluted landscape of Parkinson disease. Further research is needed to\u0000elucidate the precise mechanisms through which Actin dysregulation contributes to PD pathology and to develop targeted therapeutic approaches. Unraveling the connections between Actin and PD may pave the way for innovative strategies to intervene in the disease process, ultimately improving the lives of individuals affected by Parkinson's disease.","PeriodicalId":501513,"journal":{"name":"medRxiv - Nephrology","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139762530","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}

{"title":"Spatial Multi-Omics Connect SHROOM3 and COL18A1 in Chronic Kidney Disease","authors":"Pukhraj S. Gaheer, Nikhil Uppal, Amy Paul, Pedrum Mohammadi-Shemirani, Nicolas Perrot, Guillaume Pare, Darren Bridgewater, Matthew B. Lanktree","doi":"10.1101/2024.02.09.24301246","DOIUrl":"https://doi.org/10.1101/2024.02.09.24301246","url":null,"abstract":"Shroom Family Member 3 (<em>SHROOM3</em>) encodes an actin-binding protein that impacts kidney development. Genome-wide association studies (GWAS) identified CKD-associated common variants around <em>SHROOM3</em> and Shroom3 knock-out mice develop glomerular abnormalities. We sought to evaluate the impact of genetically predicted <em>SHROOM3</em> expression on kidney traits and the circulating proteome, and validate findings in a mouse model. Genetic instruments for <em>SHROOM3</em> expression in distinct kidney compartments (glomerular n=240, tubulointerstitial n=311) were constructed using single cell sequencing data from NephQTL2. Using two-sample Mendelian randomization, we evaluated the effects of glomerular and tubulointerstitial <em>SHROOM3</em> expression on kidney traits and the concentration of 1,463 plasma proteins in the UK Biobank and CKDGen Consortium. Genetically predicted tubulointerstitial <em>SHROOM3</em> expression colocalized with the genetic signals for eGFR and albuminuria. A 34% reduction in genetically predicted tubulointerstitial <em>SHROOM3</em> expression was associated with a 0.3% increase in cross-sectional eGFR (P = 6.8x10-4), a 1.5% increase in albuminuria (P = 0.01), and a 2.2% reduction in plasma COL18A1 concentration (P = 1.2x10-5). In contrast, genetically predicted glomerular <em>SHROOM3</em> expression showed neither colocalization nor significant Mendelian randomization results. Using immunofluorescence, heterozygous Shroom3 knockout mice had a concordant reduction of Col18a1 in their kidneys, primarily around the tubules. Thus, reduced tubulointerstitial <em>SHROOM3</em> expression, but not glomerular, is associated with increased cross-sectional eGFR, increased uACR, and reduced plasma COL18A1 and Shroom3 knockout leads to reduced kidney Col18a1, agnostically linking <em>SHROOM3</em> and COL18A1 in CKD pathogenesis.","PeriodicalId":501513,"journal":{"name":"medRxiv - Nephrology","volume":"26 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139762615","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}

{"title":"Acute kidney injury outcomes of COVID-19 confirmed patients in a Philippine tertiary hospital: A retrospective study","authors":"Joberly Sayson, Reginald Kalaw, Bernadette Ecunar Ordona, Marissa Elizabeth Lim","doi":"10.1101/2024.02.05.24302369","DOIUrl":"https://doi.org/10.1101/2024.02.05.24302369","url":null,"abstract":"The novel coronavirus (COVID-19) is known to be the fifth pandemic causing massive deaths worldwide. This virus has not only been deeply associated with acute respiratory distress, but also acute kidney injury (AKI). This study describes the baseline characteristics and various outcomes of AKI based on the KDIGO 2012 Clinical Practice Guidelines in patients hospitalized with COVID-19 at a Philippine tertiary hospital. A total of 195 patient records were retrospectively reviewed for the study. Of the 195 patients, 81(42%) patients developed AKI. Significant baseline characteristics included older age (56.28 + 14.12), presence of hypertension (p=0.004), diabetes mellitus (p=0.002), and cardiovascular disease (p=0.003). Also, the use of diuretics, inotropes and antibiotics were more prevalent in patients who developed AKI. Most of the patients who had AKI were categorized as stage 1 (49.38%). Mechanical ventilation was significantly (p&lt;0.001) more prevalent in patients with AKI (20.99%) compared to patients without AKI (5.26%). There was significantly higher rates (p&lt;0.001) of renal replacement therapy in patients with AKI (30.86%). Lastly, higher mortality rates were observed in patients with AKI (50.62%) versus patients without AKI (12.28%). Our study demonstrated that patients with COVID-19 can develop AKI and tend to have a poorer prognosis.","PeriodicalId":501513,"journal":{"name":"medRxiv - Nephrology","volume":"108 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139762516","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}

{"title":"Clinical Predictors of Long-term Outcomes in C3 Glomerulopathy and Immune-Complex Membranoproliferative Glomerulonephritis within the UK RaDaR Registry","authors":"Sherry Masoud, Katie Wong, Lewis Downward, David Pitcher, Nicholas J.A. Webb, Clare Proudfoot, RaDaR Consortium, Edwin K.S. Wong, Daniel P. Gale","doi":"10.1101/2024.02.03.24301605","DOIUrl":"https://doi.org/10.1101/2024.02.03.24301605","url":null,"abstract":"Background C3 glomerulopathy (C3G) and immune-complex membranoproliferative glomerulonephritis (IC-MPGN) are rare disorders that often result in kidney failure over the long-term. While there is much interest in the therapeutic potential of complement inhibition, the limited duration and necessarily small size of controlled trials, means there is a need to define how well short-term changes in eGFR and proteinuria predict clinically important outcomes such as kidney failure. We aimed to address this using longitudinal data from the UK National Registry of Rare Kidney Diseases (RaDaR). Methods 287 patients with biopsy-proven C3G (135, 47%) or IC-MPGN (152, 53%) were included. Analyses of kidney survival were conducted using Kaplan Meier and Cox regression. eGFR slope was estimated using linear mixed models with random intercept and slope. Results 85/135 (63%) C3G and 107/152 (70%) IC-MPGN patients reached kidney failure over follow-up after a median of 9.7 years (95% CI 7.6-12.4). Median time to first allograft loss following transplantation was 4.9 years (95% CI 1.7-6.5). Kidney survival was strongly associated with eGFR at baseline and 12-month timepoints (p&lt;0.001). Proteinuria at diagnosis, although high, was not associated with long-term kidney failure risk. In contrast, both a time averaged 0.44g/g (50mg/mmol) and 50% reduction in UPCR at 12 months (from either diagnosis or 6 months) was strongly associated with a lower risk of kidney failure (≤0.002). Most notably those with a UPCR &lt;0.88g/g (&lt;100mg/mmol) at 12 months had a substantially lower rate of progression to kidney failure (HR adjusted for eGFR 0.13 (95% CI 0.03-0.56), p=0.007). Conclusions We quantified the relationships between early changes in both eGFR and proteinuria with long-term kidney survival. We demonstrate that proteinuria a short time after diagnosis is a strong predictor of long-term outcomes and that a UPCR &lt;0.88g/g (&lt;100mg/mol) at 1 year is associated with a substantially lower kidney failure risk.","PeriodicalId":501513,"journal":{"name":"medRxiv - Nephrology","volume":"57 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139679269","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}

{"title":"A web-based tool for real-time adequacy assessment of kidney biopsies","authors":"Meysam Ahangaran, Emily Sun, Khang Le, Jiawei Sun, William Wang, Tian Herng Tan, Lyle Burdine, Zeljko Dvanajscak, Clarissa Cassol, Shree Sharma, Vijaya B Kolachalama","doi":"10.1101/2024.02.01.24302147","DOIUrl":"https://doi.org/10.1101/2024.02.01.24302147","url":null,"abstract":"The escalating incidence of kidney biopsies providing insufficient tissue for diagnosis poses a dual challenge, straining the healthcare system and jeopardizing patients who may require re-biopsy or face the prospect of an inaccurate diagnosis due to an unsampled disease. Here, we introduce a web-based tool that can provide real-time, quantitative assessment of kidney biopsy adequacy directly from photographs taken with a smartphone camera. The software tool was developed using a deep learning-driven automated segmentation technique, trained on a dataset comprising nephropathologist-confirmed annotations of the kidney cortex on digital biopsy images. Our framework demonstrated favorable performance in segmenting the cortex via 5-fold cross-validation (Dice coefficient: 0.788+/-0.130) (n=100). Offering a bedside tool for kidney biopsy adequacy assessment has the potential to provide real-time guidance to the physicians performing medical kidney biopsies, reducing the necessity for re-biopsies. Our tool can be accessed through our web-based platform: http://www.biopsyadequacy.org.","PeriodicalId":501513,"journal":{"name":"medRxiv - Nephrology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139679165","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}