{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T11:05:53Z","timestamp":1772190353562,"version":"3.50.1"},"reference-count":41,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2025,9,11]],"date-time":"2025-09-11T00:00:00Z","timestamp":1757548800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"Hanmi Pharmaceutical, Seoul, Korea"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,2,27]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Patients with immunoglobulin A nephropathy (IgAN) and moderate proteinuria are at risk of progressive renal failure despite the maximal use of renin\u2013angiotensin system blockers (RASBs). This study evaluated the efficacy of active vitamin D in reducing proteinuria in patients with IgAN receiving RASBs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In this double-blind, placebo-controlled trial, we enrolled biopsy-confirmed patients with IgAN and persistent proteinuria (0.5\u20133.5\u00a0g\/day) after maximal use of RASBs. Patients were randomized to receive either 0.25\u00a0\u03bcg\/day of calcitriol or placebo for 12\u00a0months. The primary outcomes were the change in the mean urinary protein:creatinine ratio (UPCR) and daily urinary protein excretion during the treatment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>A total of 138 patients from six medical centres were enrolled and assigned to receive a placebo (n\u00a0=\u00a069) or 0.25\u00a0\u03bcg of calcitriol (n\u00a0=\u00a069) and 115 patients (83.3%) completed the study. The calcitriol group showed a greater reduction in geometric means of UPCR {mean difference \u2212187\u00a0mg\/g [95% confidence interval (CI) \u2212370.6 to \u22124.0], P\u00a0=\u00a0.04} and urinary albumin:creatinine ratio [\u2212162\u00a0mg\/g (95% CI \u2212290.9 to \u221234.6), P\u00a0=\u00a0.01] than placebo. Changes in daily urinary protein excretion were \u22123.5% (from 1.32 to 1.02\u00a0g\/day) in the control group and \u221213.1% (from 1.29 to 0.97\u00a0g\/day) in the calcitriol group, without any statistically significant differences (P\u00a0=\u00a0.11). The annual decrease of the estimated glomerular filtration rate (eGFR) was \u22120.32\u00a0ml\/min\/1.73\u00a0m2 (95% CI \u22122.54 to 1.99) in the calcitriol group and \u22123.64\u00a0ml\/min\/1.73\u00a0m2 (95% CI \u22125.70 to \u22121.58) in the placebo group (calcitriol versus placebo over time, P\u00a0=\u00a0.02). Adverse events were comparable between the groups.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>The addition of 0.25\u00a0\u03bcg\/day calcitriol to RASBs safely lowered residual proteinuria and slowed the eGFR decline in patients with IgAN, suggesting a potential therapeutic role for calcitriol in this population.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/ndt\/gfaf187","type":"journal-article","created":{"date-parts":[[2025,9,11]],"date-time":"2025-09-11T11:54:52Z","timestamp":1757591692000},"page":"566-574","source":"Crossref","is-referenced-by-count":0,"title":["Additive renoprotective effects of oral calcitriol on patients with IgA nephropathy receiving RAS blockers"],"prefix":"10.1093","volume":"41","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7890-0928","authenticated-orcid":false,"given":"Young Su","family":"Joo","sequence":"first","affiliation":[{"name":"College of Medicine, Institute of Kidney Disease Research, Yonsei University Department of Internal Medicine, , Seoul ,","place":["Korea"]},{"name":"Yongin Severance Hospital, Yonsei University College of Medicine Division of Nephrology, Department of Internal Medicine, , Yongin ,","place":["Korea"]},{"name":"Institute for Innovation in Digital Healthcare, Yonsei University , Seoul ,","place":["Korea"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3311-6379","authenticated-orcid":false,"given":"Tae-Ik","family":"Chang","sequence":"additional","affiliation":[{"name":"National Health Insurance Service Medical Center, Ilsan Hospital Department of Internal Medicine, , Goyang ,","place":["Korea"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5195-7852","authenticated-orcid":false,"given":"Dong Ki","family":"Kim","sequence":"additional","affiliation":[{"name":"Seoul National University College of Medicine Department of Internal Medicine, , Seoul ,","place":["Korea"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7923-5635","authenticated-orcid":false,"given":"Seung Hyeok","family":"Han","sequence":"additional","affiliation":[{"name":"College of Medicine, Institute of Kidney Disease Research, Yonsei University Department of Internal Medicine, , Seoul ,","place":["Korea"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shin-Wook","family":"Kang","sequence":"additional","affiliation":[{"name":"College of Medicine, Institute of Kidney Disease Research, Yonsei University Department of Internal Medicine, , Seoul ,","place":["Korea"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9183-4507","authenticated-orcid":false,"given":"Tae-Hyun","family":"Yoo","sequence":"additional","affiliation":[{"name":"College of Medicine, Institute of Kidney Disease Research, Yonsei University Department of Internal Medicine, , Seoul ,","place":["Korea"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2025,9,11]]},"reference":[{"key":"2026022705020274400_bib1","doi-asserted-by":"publisher","first-page":"2402","DOI":"10.1056\/NEJMra1206793","article-title":"IgA nephropathy","volume":"368","author":"Wyatt","year":"2013","journal-title":"N Engl J Med"},{"key":"2026022705020274400_bib2","doi-asserted-by":"publisher","first-page":"275","DOI":"10.1038\/nrneph.2012.58","article-title":"Pathogenesis of IgA nephropathy","volume":"8","author":"Lai","year":"2012","journal-title":"Nat Rev Nephrol"},{"key":"2026022705020274400_bib3","doi-asserted-by":"publisher","first-page":"4","DOI":"10.1016\/j.semnephrol.2007.10.001","article-title":"Natural history of primary IgA nephropathy","volume":"28","author":"Berthoux","year":"2008","journal-title":"Semin Nephrol"},{"key":"2026022705020274400_bib4","doi-asserted-by":"publisher","first-page":"1050","DOI":"10.1038\/ki.1991.313","article-title":"Deterioration of GFR in IgA nephropathy as measured by 51Cr-EDTA clearance","volume":"40","author":"Rekola","year":"1991","journal-title":"Kidney Int"},{"key":"2026022705020274400_bib5","first-page":"619","article-title":"Clinico-pathological correlations and long-term follow-up of 253 United Kingdom patients with IgA nephropathy. 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