{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T23:30:26Z","timestamp":1789601426875,"version":"build-2803163510"},"reference-count":17,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,11,6]],"date-time":"2025-11-06T00:00:00Z","timestamp":1762387200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>Nephrotic syndrome (NS) in IgA nephropathy (IgAN) may indicate concurrent minimal change disease (MCD). This study characterized the IgAN-MCD overlap phenotype using anti-nephrin autoantibodies (IgG co-localization) in NS-IgAN patients, assessing its prevalence and therapeutic implications.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We conducted a retrospective analysis of 67 biopsy-confirmed NS-IgAN patients (2010-2024) with \u22651-year follow-up. Patients were stratified by treatment response into complete remission (CR, n = 24) and non-remission (NR, n = 26) groups. Renal biopsies were evaluated for anti-nephrin autoantibodies via IgG co-localization and podocyte ultrastructure. Longitudinal data were analyzed using repeated-measures ANOVA with Benjamini-Hochberg correction; time-to-remission was assessed by Kaplan-Meier and Cox regression analyses.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      CR patients showed significantly lower baseline serum albumin (18.8 \u00b1 4.0 vs. 24.1 \u00b1 4.2 g\/L,\n                      <jats:italic>P<\/jats:italic>\n                      &amp;lt;\u00a00.001) and higher eGFR (101 \u00b1 29 vs. 62 \u00b1 35 mL\/min\/1.73m\u00b2,\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&amp;lt;\u00a00.001) compared to NR patients. Anti-nephrin IgG co-localization was detected in 54.2% of CR patients but absent in NR patients (\n                      <jats:italic>P<\/jats:italic>\n                      &amp;lt;\u00a00.001). Cox regression identified anti-nephrin positivity as a strong predictor of faster remission (HR: 0.40, 95% CI: 0.17-0.90;\n                      <jats:italic>P<\/jats:italic>\n                      =\u00a00.028). CR patients achieved rapid proteinuria remission (0.1 \u00b1 0.1 vs. 7.0 \u00b1 0.8 g\/24h at 1 month,\n                      <jats:italic>P<\/jats:italic>\n                      &amp;lt;\u00a00.001) with significant time\u00d7group interactions for proteinuria (\n                      <jats:italic>P<\/jats:italic>\n                      =\u00a00.001) and serum albumin (\n                      <jats:italic>P<\/jats:italic>\n                      =\u00a00.004). An estimated 35.8% of NS-IgAN cases represented IgAN-MCD overlap.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>A significant subset (~36%) of NS-IgAN patients exhibit an IgAN-MCD overlap state identifiable by renal anti-nephrin IgG co-localization, demonstrating MCD-like pathology and excellent corticosteroid response. This biomarker integration can guide personalized therapy, enabling effective short-course treatment for overlap cases while avoiding unnecessary long-term immunosuppression in classic NS-IgAN.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2025.1669276","type":"journal-article","created":{"date-parts":[[2025,11,6]],"date-time":"2025-11-06T06:22:46Z","timestamp":1762410166000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["How to identify IgA nephropathy presenting as nephrotic syndrome coexisting with minimal change disease? A 15-year single-center clinicopathological analysis"],"prefix":"10.3389","volume":"16","author":[{"given":"Yue","family":"Yang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lu-xian","family":"Duan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zheng","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qian-qian","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Zhuo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wen-ge","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2025,11,6]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"67","DOI":"10.1038\/s41572-023-00476-9","article-title":"IgA nephropathy","volume":"9","author":"Stamellou","year":"2023","journal-title":"Nat Rev Dis Primers"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00837.x","article-title":"Epidemiologic data of renal diseases from a single unit in China: analysis based on 13,519 renal biopsies","volume":"66","author":"Li","year":"2004","journal-title":"Kidney Int"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018101017","article-title":"Mortality in igA nephropathy: A nationwide population-based cohort study","volume":"30","author":"Jarrick","year":"2019","journal-title":"J Am Soc Nephrol"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2019.02.016","article-title":"Prediction and risk stratification of kidney outcomes in igA nephropathy","volume":"74","author":"Chen","year":"2019","journal-title":"Am J Kidney Dis"},{"key":"B5","doi-asserted-by":"publisher","first-page":"S1","DOI":"10.1016\/j.kint.2021.05.021","article-title":"KDIGO 2021 clinical practice guideline for the management of glomerular diseases","volume":"100","author":"Rovin","year":"2021","journal-title":"Kidney Int"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1080\/0886022X.2023.2267138","article-title":"Clinical significance of massive proteinuria in primary IgA nephropathy with and without nephrotic syndrome: a single center cohort study","volume":"45","author":"Hu","year":"2023","journal-title":"Ren Fail"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1007\/s10238-019-00580-9","article-title":"Clinical and pathological features of immunoglobulin A nephropathy patients with nephrotic syndrome","volume":"19","author":"Han","year":"2019","journal-title":"Clin Exp Med"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.04820511","article-title":"Clinical features and outcomes of IgA nephropathy with nephrotic syndrome","volume":"7","author":"Kim","year":"2012","journal-title":"Clin J Am Soc 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with clinical outcome in igA nephropathy","volume":"32","author":"Canney","year":"2021","journal-title":"J Am Soc Nephrol"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.08600718","article-title":"Proteinuria reduction as a surrogate end point in trials of igA nephropathy","volume":"14","author":"Thompson","year":"2019","journal-title":"Clin J Am Soc Nephrol"}],"container-title":["Frontiers in 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