{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T06:00:34Z","timestamp":1792821634058,"version":"4.5.0"},"reference-count":105,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"12","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["CJASN"],"published-print":{"date-parts":[[2022,12]]},"abstract":"<jats:p>Idiopathic nephrotic syndrome often responds to immunosuppressive treatment. Nevertheless, this syndrome\u2014and the drugs used to treat it\u2014remain important causes of patient morbidity. Idiopathic nephrotic syndrome is usually caused by minimal change disease or FSGS, diseases that primarily affect the podocytes. In spite of decades of research, the underlying causes of both diseases remain incompletely understood. There is, however, a large body of observational and experimental data linking the immune system with both minimal change disease and FSGS, including associations with systemic infections and hematologic malignancies. Perhaps most compellingly, many different immunomodulatory drugs are effective for treating idiopathic nephrotic syndrome, including biologic agents that have well-defined immune targets. In fact, the unexpected efficacy of targeted therapeutic agents has provided important new insights into the pathogenesis of these diseases. Given the large number of drugs that are available to deplete or block specific cells and molecules within the immune system, a better understanding of the immunologic causes of idiopathic nephrotic syndrome may lead to better diagnostic and therapeutic approaches.<\/jats:p>","DOI":"10.2215\/cjn.07180622","type":"journal-article","created":{"date-parts":[[2022,10,5]],"date-time":"2022-10-05T13:45:12Z","timestamp":1664977512000},"page":"1823-1834","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":56,"title":["The Immune System and Idiopathic Nephrotic Syndrome"],"prefix":"10.2215","volume":"17","clinical-trial-number":[{"clinical-trial-number":"nct05183646","registry":"10.18810\/clinical-trials-gov"},{"clinical-trial-number":"nct03649152","registry":"10.18810\/clinical-trials-gov"}],"author":[{"given":"Ruth E.","family":"Campbell","sequence":"first","affiliation":[{"name":"Division of Renal Diseases and Hypertension, University of Colorado School of Medicine, Aurora, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua M.","family":"Thurman","sequence":"additional","affiliation":[{"name":"Division of Renal Diseases and Hypertension, University of Colorado School of Medicine, Aurora, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2022,12]]},"reference":[{"key":"B1-20241015","doi-asserted-by":"crossref","first-page":"529","DOI":"10.2215\/CJN.04121206","article-title":"A proposed taxonomy for the podocytopathies: A reassessment of the primary nephrotic diseases","volume":"2","author":"Barisoni","year":"2007","journal-title":"Clin J Am Soc Nephrol"},{"key":"B2-20241015","doi-asserted-by":"crossref","first-page":"68","DOI":"10.1038\/s41572-020-0196-7","article-title":"Podocytopathies","volume":"6","author":"Kopp","year":"2020","journal-title":"Nat Rev Dis 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