Glomerular diseases最新文献

{"title":"Prostate Cancer Associated with Minimal Change Disease: A Case Report.","authors":"Yuta Nakano,&nbsp;Mariko Yoshida,&nbsp;Naohiro Muraki,&nbsp;Kouhei Sugita,&nbsp;Saori Ishihara,&nbsp;Jiro Kumagai,&nbsp;Hajime Fujisawa","doi":"10.1159/000525040","DOIUrl":"https://doi.org/10.1159/000525040","url":null,"abstract":"<p><strong>Introduction: </strong>Minimal change disease (MCD), a common cause of primary nephrotic syndrome that accounts for 10%-15% of all primary nephrotic syndrome cases in adults, is frequently associated with malignant lymphoma. However, studies on MCD associated with prostate cancer are scarce.</p><p><strong>Case presentation: </strong>A 73-year-old male with prostate cancer was referred to our department with hypoalbuminemia and severe proteinuria while waiting for prostatectomy. We diagnosed the patient with nephrotic syndrome and performed a renal biopsy. Renal pathological findings were consistent with those of MCD. The clinical course suggested an association between prostate cancer and MCD as our patient achieved complete remission of MCD after receiving androgen deprivation and radiation therapy for prostate cancer without the use of glucocorticoids or other immunosuppressants.</p><p><strong>Discussion: </strong>Although MCD can be associated with solid tumors, MCD associated with prostate cancer is very rare. The current case is the first to directly raise the possibility that secondary MCD may develop due to prostate cancer in some patients.</p>","PeriodicalId":73177,"journal":{"name":"Glomerular diseases","volume":"2 3","pages":"145-150"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a8/1c/gdz-0002-0145.PMC9710312.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10681234","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":"A Case of IgG4-Related Disease and Membranous Nephropathy Associated with Thrombospondin Type-1 Domain-Containing 7A.","authors":"Ryan Malcolm Hum,&nbsp;Sarah Elyoussfi,&nbsp;Benjamin J Parker,&nbsp;Graeme Reid,&nbsp;Durga A K Kanigicherla","doi":"10.1159/000524014","DOIUrl":"https://doi.org/10.1159/000524014","url":null,"abstract":"<p><strong>Background: </strong>IgG4-related disease (IgG4-RD) is a systemic multi-organ inflammatory disorder which affects the kidney 20% of the time. Patients with intrinsic IgG4-related kidney disease (IgG4-RKD) often have tubulointerstitial nephritis (TIN) whereas glomerular lesions like membranous nephropathy (MN) are less common. Antibodies to thrombospondin type-1 domain-containing 7A (THSD7A) have been described in primary MN, but never in association with IgG4-RKD.</p><p><strong>Case report: </strong>We report the first case of IgG4-MN associated with THSD7A antibodies in serum and positivity on glomerular staining, in a 57-year-old Caucasian male with IgG4-RD affecting the pancreas, liver, lacrimal glands, extraocular muscles, and kidneys. This patient presented initially with glomerular disease including significant proteinuria consistent with MN. Glomerular staining for THSD7A antigen and serum THSD7A antibody titres was positive. Treatment with corticosteroids and cyclophosphamide successfully induced remission with resolution of proteinuria, and improvement in renal function. However, despite maintenance azathioprine, the patient relapsed 39 months later. On relapse, there was minimal proteinuria but a significant rise in creatinine. Subsequent renal biopsy showed less glomerular disease and instead a TIN pattern. Subsequent treatment with Rituximab and corticosteroids successfully induced remission.</p><p><strong>Conclusion: </strong>The role of THSD7A autoantibodies in MN is emerging, and as both IgG4-MN and presence of THSD7A antibody are rare occurrences in themselves, we speculate that there may be an undiscovered association between THSD7A and IgG4-MN. Routine testing for THSD7A in IgG4-MN may help to identify the link.</p>","PeriodicalId":73177,"journal":{"name":"Glomerular diseases","volume":"2 3","pages":"139-144"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ca/3f/gdz-0002-0139.PMC9710322.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10672234","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 Review with Emphasis on Ultrastructural Features.","authors":"Jean Hou,&nbsp;Kevin Yi Mi Ren,&nbsp;Mark Haas","doi":"10.1159/000524552","DOIUrl":"https://doi.org/10.1159/000524552","url":null,"abstract":"<p><p>C3 glomerulopathy (C3G) is a rare disease resulting from dysregulation of the alternative complement pathway, resulting in the deposition of complement component 3 (C3) in the kidney. It encompasses two major subgroups: dense deposit disease and C3 glomerulonephritis (C3GN). Although the alternative complement pathway is typically a very tightly controlled system, dysregulation can be a result of genetic mutations in the fluid phase or membrane-bound inhibitors or accelerators. In addition, de novo/acquired autoantibodies against any of the regulatory proteins can alter complement activation either by negating an inhibitor or activating an accelerator. Triggering events can be complex; however, the final pathway is characterized by the uncontrolled deposition of C3 in glomeruli and the formation of the membrane attack complex. Light microscopic findings can be quite heterogeneous with a membranoproliferative pattern most commonly encountered. Diagnostic confirmation of C3G is based on a characteristic pattern of glomerular immunofluorescence staining, with C3-dominant deposits that are at least 2 orders of intensity greater than staining for any immunoglobulin (Ig) or C1q. Electron microscopy is necessary for diagnosing DDD in particular, but can also help to distinguish C3GN from other glomerular disease mimickers.</p>","PeriodicalId":73177,"journal":{"name":"Glomerular diseases","volume":"2 3","pages":"107-120"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/6f/c7/gdz-0002-0107.PMC9710331.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10681241","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":"Quantitative Mass Spectrometry Normalization in Urine Biomarker Analysis in Nephrotic Syndrome.","authors":"Timothy D Cummins,&nbsp;David W Powell,&nbsp;Daniel W Wilkey,&nbsp;Makayla Brady,&nbsp;Fredrick W Benz,&nbsp;Michelle T Barati,&nbsp;Dawn J Caster,&nbsp;Jon B Klein,&nbsp;Michael L Merchant","doi":"10.1159/000522217","DOIUrl":"https://doi.org/10.1159/000522217","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) affects 30 million adults, costs ~$79 billion dollars (2016) in Medicare expenditures, and is the ninth leading cause of death in the United States. The disease is silent or undiagnosed in almost half of people with severely reduced kidney function. Urine provides an ideal biofluid that is accessible to high-sensitivity mass spectrometry-based proteomic interrogation and is an indicator of renal homeostasis. While the accurate and precise diagnosis and better disease management of CKD can be aided using urine biomarkers, their discovery in excessive protein or nephrotic urine samples can present challenges. In this work we present a mass spectrometry-based method utilizing multiplex tandem mass tag (TMT) quantification and improved protein quantification using reporter ion normalization to urinary creatinine to analyze urinary proteins from patients with a form of nephrotic syndrome (FSGS). A comparative analysis was performed for urine from patients in remission versus active disease flare. Two-dimensional LC-MS/MS TMT quantitative analysis identified over 1058 urine proteins, 580 proteins with 2 peptides or greater and quantifiable. Normalization of TMT abundance values to creatinine per ml of urine concentrated reduced variability in 2D-TMT-LC-MS/MS experiments. Univariate and multivariate analyses showed that 27 proteins were significantly increased in proteinuric disease flare. Hierarchical heatmap clustering showed that SERPINA1 and ORM1 were >1.5 fold increased in active disease versus remission urine samples. ELISA validation of SERPINA1 and ORM1 abundance agreed with our quantitative TMT proteomics analysis. These findings provide support for the utility of this method for identification of novel diagnostic markers of CKD and identify SERPINA1 and ORM1 as promising candidate diagnostic markers for FSGS.</p>","PeriodicalId":73177,"journal":{"name":"Glomerular diseases","volume":"2 3","pages":"121-131"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/6d/7e/gdz-0002-0121.PMC9529004.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10656292","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":"Repository Corticotropin in Treating de novo C3 Glomerulonephritis after Transplantation.","authors":"Muhammad Saad Naseer,&nbsp;Ayush Singh,&nbsp;Neeraj Singh","doi":"10.1159/000520387","DOIUrl":"https://doi.org/10.1159/000520387","url":null,"abstract":"<p><strong>Introduction: </strong>De novo C3 glomerulonephritis (C3GN) after transplant is uncommon. Although eculizumab has been used successfully in several cases, the response is heterogeneous, and treatment strategies remain undefined. The use of repository corticotropin in C3GN has not been described in the literature.</p><p><strong>Case report: </strong>A 48-year-old African American male with kidney transplantation secondary to presumed diabetic nephropathy presented 6 years after transplant with lower extremity edema and nephrotic range proteinuria. His urine protein to creatinine ratio (UPCR) was 8.2 g/g. Renal allograft biopsy confirmed the diagnosis of C3GN. He was treated with eculizumab (Solaris®) 900 mg IV once weekly for 4 weeks and repository corticotropin (H.P. Acthar® gel) 80 units SQ twice weekly for 6 months with a near-complete resolution of proteinuria within 3 months of the treatment. The patient presented again 6 months after completing the therapy with a recurrence of proteinuria, which peaked at 11.6 g/g of UPCR. Repeat kidney allograft biopsy was consistent with C3GN. He was started on repository corticotropin 80 units SQ twice weekly, which resulted in a reduction of proteinuria to >50% within 2 months of therapy. When eculizumab 900 mg IV weekly for 4 weeks was added with repository corticotropin, the proteinuria resolved within 10 weeks of treatment. The patient was maintained on monotherapy of repository corticotropin and has been in complete remission of proteinuria for more than a year until his last follow-up.</p><p><strong>Conclusion: </strong>This is the first case report describing the role of repository corticotropin as an effective therapy in reducing proteinuria and maintaining patients with C3GN in proteinuria remission.</p>","PeriodicalId":73177,"journal":{"name":"Glomerular diseases","volume":"2 2","pages":"100-105"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/81/cc/gdz-0002-0100.PMC9670034.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10674928","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":"Erratum.","authors":"","doi":"10.1159/000522322","DOIUrl":"https://doi.org/10.1159/000522322","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1159/000521511.].</p>","PeriodicalId":73177,"journal":{"name":"Glomerular diseases","volume":"2 2","pages":"106"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/99/86/gdz-0002-0106.PMC9670031.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10733088","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":"Immunoglobulin-Negative Fibrillary Glomerulonephritis Masked in Diabetic Nephropathy: A Case Report and Discussion of a Diagnostic Pitfall.","authors":"Gabriel B W Lerner,&nbsp;Gary G Singer,&nbsp;Christopher P Larsen,&nbsp;Tiffany N Caza","doi":"10.1159/000520071","DOIUrl":"https://doi.org/10.1159/000520071","url":null,"abstract":"<p><strong>Introduction: </strong>Fibrillary glomerulonephritis (FGN) is a rare glomerular disease with poor prognosis, characterized by deposition of randomly arranged fibrillar material measuring 10-30 nm in diameter. This diagnosis is confirmed with DNAJB9 immunohistochemistry as well as ultrastructural examination. Ultrastructurally, the fibrillary material seen in this entity may be confused with diabetic fibrillosis occurring in diabetic nephropathy.</p><p><strong>Case presentation: </strong>We present a case of a 63-year-old African American male with remote hepatitis C virus (HCV) infection and type II diabetes mellitus who presented with chronic kidney disease and nephrotic range proteinuria. A kidney biopsy revealed PAS-positive mesangial matrix expansion consistent with diabetic nephropathy and focal randomly oriented fibril deposition on ultrastructural examination. Immunofluorescence for immunoglobulin G and light chains was negative by both routine and paraffin immunofluorescence. Immunohistochemistry for DNAJB9 was diffusely positive, confirming co-existing FGN.</p><p><strong>Discussion/conclusion: </strong>Patients with diabetic nephropathy and FGN have similar clinicopathologic presentations with a slowly progressive onset of kidney failure and proteinuria. In diabetic patients with fibrillary deposits under ultrastructural examination, concurrence of these disease entities must be considered. In this patient with remote HCV infection that was successfully treated years before, it is possible that in the absence of an FGN trigger, there was a loss of antigenicity with a loss of immunoglobulin staining. Therefore, we recommend DNAJB9 immunostaining for patients with remote HCV infection to avoid this diagnostic pitfall. Further studies are needed to determine the potential role of HCV infection in the initiation and etiopathogenesis of FGN.</p>","PeriodicalId":73177,"journal":{"name":"Glomerular diseases","volume":"2 2","pages":"95-99"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/89/c1/gdz-0002-0095.PMC9670039.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10681229","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":"Anti-Phospholipase A2 Receptor in Nonlupus Patients with Membranous Nephropathy and Crescents.","authors":"Yiqin Zuo,&nbsp;Livia Barreira Cavalcante,&nbsp;James Monroe Smelser,&nbsp;Neil Sanghani,&nbsp;Jamie P Dwyer,&nbsp;Julia Breyer Lewis,&nbsp;Agnes B Fogo","doi":"10.1159/000520641","DOIUrl":"https://doi.org/10.1159/000520641","url":null,"abstract":"<p><strong>Introduction: </strong>Anti-phospholipase A2 receptor (PLA2R) is detected in approximately 70% of biopsies of \"primary\" membranous nephropathy (MN). Crescents in MN in nonlupus patients suggest additional injury, such as antineutrophil cytoplasmic antibody (ANCA) or anti-glomerular basement membrane (anti-GBM)-associated glomerulonephritis and are postulated to reflect injury by a mechanism that unmasks cryptic epitopes leading to the second autoantibody.</p><p><strong>Methods: </strong>We studied PLA2R staining in nonlupus patients with MN and crescents. Native renal biopsies in 16 nonlupus patients with MN and crescents were stained for PLA2R.</p><p><strong>Results: </strong>The patients included 5 women and 11 men, with mean age 61 years and elevated serum creatinine (mean 4.68 mg/dL). Hematuria and proteinuria (mean 4.97 g/day) were documented in 13 patients. Two patients had positive serum anti-GBM antibody. Nine of 11 patients tested for ANCA were positive, with p-ANCA (<i>n</i> = 4), c-ANCA (<i>n</i> = 2), or both (<i>n</i> = 1), with 2 not specified. On average, 27% of glomeruli had crescents. One patient had an initial biopsy with MN, 4 years later had MN with crescent, and 7 years later had rebiopsy with persistent MN with crescents. One patient had ANCA-associated vasculitis, and 5 years later had MN and crescent. The remaining 14 patients had concurrent diagnoses of MN and crescents. PLA2R was positive in 5 cases, 3 with ANCA positivity, 2 with unknown ANCA status, and none with anti-GBM disease. The patient with initial MN preceding crescent was PLA2R positive; the patient with initial ANCA-associated vasculitis preceding MN was PLA2R negative.</p><p><strong>Conclusions: </strong>Most patients (64%) presented with concomitant MN and crescents, with rare occurrence of an initial disease process followed later by the second injury. PLA2R was positive in 31% of patients, suggesting most are secondary MN. Further study to determine the cryptic epitopes may shed light on the triggering mechanisms for these rare but unlikely coincidental glomerular injuries.</p>","PeriodicalId":73177,"journal":{"name":"Glomerular diseases","volume":"2 2","pages":"75-82"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/74/2d/gdz-0002-0075.PMC9670025.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10674929","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":"KM55 in the Evaluation of IgA-Containing Glomerular Diseases.","authors":"Rahul Raj,&nbsp;Alok Sharma,&nbsp;Adarsh Barwad,&nbsp;Soumita Bagchi,&nbsp;Sanjay Kumar Agarwal,&nbsp;Arvind Bagga,&nbsp;Amit Kumar Dinda,&nbsp;Geetika Singh","doi":"10.1159/000520640","DOIUrl":"https://doi.org/10.1159/000520640","url":null,"abstract":"<p><strong>Introduction: </strong>Mucosal-derived galactose-deficient IgA is central to the pathogenesis of primary IgA nephropathy (IgAN). Recent reports suggest similar pathogenesis in Henoch-Schonlein purpura (HSP) and secondary IgAN. Its role in other IgA-containing glomerular diseases is still under investigation. It can be detected in glomeruli with the recently described antibody KM55. We aimed to evaluate the role of KM55 by immunostaining a wide spectrum of IgA-containing glomerular diseases.</p><p><strong>Methods: </strong>After standardization and colocalization in a case of IgAN, a spectrum of 60 cases including IgAN, HSP, chronic liver disease (CLD)-related IgAN, other secondary IgAN, IgA-dominant/codominant membranoproliferative glomerulonephritis (MPGN), and lupus nephritis were subjected to immunofluorescence with KM55. KM55 was used to resolve diagnostic dilemma in cases of IgA deposition with confounding histology.</p><p><strong>Results: </strong>The group of primary IgAN (17 cases), HSP (4 cases), and secondary IgAN (19 cases) including CLD showed 2-3+ granular staining with KM55, suggesting mucosal-derived IgA. In contrast, cases of IgA-dominant/codominant MPGN (8 cases) and lupus nephritis (12 cases) were negative for KM55, suggesting systemic derivation of IgA. In cases of IgA deposition with confounding histology such as membranoproliferative or diffuse endocapillary proliferative pattern, KM55 helped to resolve the diagnosis.</p><p><strong>Discussion/conclusion: </strong>This cross-sectional study concludes that KM55 is useful in the evaluation of IgA-containing glomerular diseases from a pathogenetic perspective and is a practical tool in resolving differential diagnosis in cases with overlapping histopathological features.</p>","PeriodicalId":73177,"journal":{"name":"Glomerular diseases","volume":"2 2","pages":"59-74"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a8/d4/gdz-0002-0059.PMC9670030.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10674926","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":"Glomerular Disease Education Experience across Nephrology Fellowship Programs: An International Survey.","authors":"Harish Seethapathy,&nbsp;Sayna Norouzi,&nbsp;Kate J Robson,&nbsp;Lida Gharibvand,&nbsp;Ali Poyan Mehr","doi":"10.1159/000521598","DOIUrl":"https://doi.org/10.1159/000521598","url":null,"abstract":"<p><strong>Introduction: </strong>Glomerulonephritis (GN) education is an important, albeit a challenging, component of nephrology fellowship training. We hypothesized that trainee experience varies widely across programs, leading to differences in self-reported competency levels in the diagnosis and management of glomerular diseases.</p><p><strong>Methods: </strong>The Glomerular Disease Study & Trial Consortium (GlomCon) conducted an anonymous online survey to determine the educational experience of nephrology trainees. We used multiple-choice questions to obtain data about (a) curriculum-based education, (b) dedicated specialty clinic, and (c) exposure to pathology. We leveraged a visual analog scale of 1-100 (with a higher number indicating a higher comfort level) to assess self-reported levels of clinical competency. The survey was disseminated via email to the subscribing members of GlomCon and through Twitter.</p><p><strong>Results: </strong>In total, there were 109 respondents to our survey, and 56% were from training programs in the USA. Exposure to a specialized GN clinic was reported by 45%, while 77% reported the presence of an onsite nephropathologist at their training program. Self-reported competency scores were 59 ± 25 and 52 ± 25 for diagnosis and treatment of glomerular diseases, respectively. Days spent in a GN clinic per year, years of fellowship, and dedicated nephropathology didactics were associated with higher diagnosis and treatment competency scores.</p><p><strong>Conclusion: </strong>Trainees report a wide variation in glomerular disease education across fellowship programs. A lack of nephropathology exposure and a dedicated GN curriculum was associated with lower scores in self-reported clinical competency in caring for patients with glomerular disease.</p>","PeriodicalId":73177,"journal":{"name":"Glomerular diseases","volume":"2 2","pages":"89-94"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b1/53/gdz-0002-0089.PMC9670032.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10681231","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}