{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T12:26:31Z","timestamp":1792153591339,"version":"4.4.0"},"reference-count":34,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2017,4]]},"abstract":"<jats:p>\n                    IgA nephropathy frequently leads to progressive CKD. Although interest surrounds use of immunosuppressive agents added to standard therapy, several recent studies have questioned efficacy of these agents. Depleting antibody\u2013producing B cells potentially offers a new therapy. In this open label, multicenter study conducted over 1-year follow-up, we randomized 34 adult patients with biopsy\u2013proven IgA nephropathy and proteinuria &gt;1 g\/d, maintained on angiotensin\u2013converting enzyme inhibitors or angiotensin receptor blockers with well controlled BP and eGFR&lt;90 ml\/min per 1.73 m\n                    <jats:sup>2<\/jats:sup>\n                    , to receive standard therapy or rituximab with standard therapy. Primary outcome measures included change in proteinuria and change in eGFR. Median baseline serum creatinine level (range) was 1.4 (0.8\u20132.4) mg\/dl, and proteinuria was 2.1 (0.6\u20135.3) g\/d. Treatment with rituximab depleted B cells and was well tolerated. eGFR did not change in either group. Rituximab did not alter the level of proteinuria compared with that at baseline or in the control group; three patients in each group had \u226550% reduction in level of proteinuria. Serum levels of galactose-deficient IgA1 or antibodies against galactose-deficient IgA1 did not change. In this trial, rituximab therapy did not significantly improve renal function or proteinuria assessed over 1 year. Although rituximab effectively depleted B cells, it failed to reduce serum levels of galactose-deficient IgA1 and antigalactose\u2013deficient IgA1 antibodies. Lack of efficacy of rituximab, at least at this stage and severity of IgA nephropathy, may reflect a failure of rituximab to reduce levels of specific antibodies assigned salient pathogenetic roles in IgA nephropathy.\n                  <\/jats:p>","DOI":"10.1681\/asn.2016060640","type":"journal-article","created":{"date-parts":[[2016,11,7]],"date-time":"2016-11-07T22:13:56Z","timestamp":1478556836000},"page":"1306-1313","source":"Crossref","is-referenced-by-count":282,"title":["A Randomized, Controlled Trial of Rituximab in IgA Nephropathy with Proteinuria and Renal Dysfunction"],"prefix":"10.1681","volume":"28","author":[{"given":"Richard A.","family":"Lafayette","sequence":"first","affiliation":[{"name":"Division of Nephrology and Hypertension, Stanford University, Stanford, California;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pietro A.","family":"Canetta","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Columbia 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