{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T21:06:42Z","timestamp":1791925602191,"version":"4.3.4"},"reference-count":27,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2023,3,1]],"date-time":"2023-03-01T00:00:00Z","timestamp":1677628800000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Kidney360"],"published-print":{"date-parts":[[2023,3]]},"abstract":"<jats:sec>\n                    <jats:title>Key Points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>\n                            This renal biopsy study documents clinical renal dysfunction and pathologic lesions encountered in patients after anti-TNF\n                            <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                            therapy and compares them with similar patients without treatment.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            This study highlights the spectrum of autoimmune, serologic, and other kidney adverse effects of anti-TNF\n                            <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                            therapy.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Unrelated active or chronic renal lesions including amyloidosis secondary to the underlying systemic inflammatory states may be observed.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Anti-TNF\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      inhibitors, as biological agents, are used in autoimmune inflammatory states, rheumatoid arthritis (RA), psoriatic arthritis (PA), and Crohn disease. They can induce autoimmune serologic responses and clinical disorders, including systemic vasculitis and lupus-like diseases, affecting the kidney.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Retrospective analysis of clinicopathologic features of kidney disease after anti-TNF\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      therapy (treatment group) from our renal biopsy files from 2000 to 2018 is conducted and compared with 106 patients without therapy (control group).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Forty-eight patients using anti-TNF\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      agents had renal biopsies: RA in 30, PA six, Crohn disease six, RA and PA one, RA and Crohn disease one, and others four. Twenty received etanercept, 15 adalimumab, eight infliximab, and five two forms of agents manifesting new-onset nephritic syndrome or CKD, 17 with AKI and 16 nephrotic syndrome, with recent ANCA and\/or lupus serology. The renal lesions were crescentic GN in eight, pauci-immune\u2013type in five, and ANCA+ in five. Lupus or lupus-like nephritis was seen in six: International Society of Nephrology\/Renal Pathology Society 2018 class II\u20142, class V\u20142, class III+V\u20141, and class IV+V\u20141, and concurrent fibrillary GN, scleroderma\/thrombotic microangiopathy (TMA), and amyloidosis in three. Renal lesions unrelated to anti-TNF\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      therapy or underlying autoimmune disease were noted in 23 patients (\n                      <jats:italic toggle=\"yes\">e.g.<\/jats:italic>\n                      , diabetic nephropathy, interstitial nephritis, acute tubular injury, infection-related GN); immunoglobulin A nephropathy, renal sarcoidosis, and amyloid A amyloidosis were noted in five patients. TMA was recognized in five patients, one associated with scleroderma and one anti-phospholipid antibodies, and two had nephrotic syndrome secondary to podocytopathy. The control group was similar with higher number of immune-mediated GN, interstitial nephritis, and amyloidosis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>\n                      The renal lesions during anti-TNF\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      therapy have an autoimmune basis such as ANCA and lupus or lupus-like disease, correlated with new-onset serology, while others were similar to those observed in the control group. Renal biopsy findings integrated with clinical features and therapy can identify the underlying pathophysiologic process for appropriate management.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.34067\/kid.0000000000000063","type":"journal-article","created":{"date-parts":[[2023,1,27]],"date-time":"2023-01-27T17:26:10Z","timestamp":1674840370000},"page":"363-373","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":13,"title":["Clinicopathologic Spectrum of Renal Lesions Following Anti-TNF-\u03b1 Inhibitor Therapy: A Single Center Experience"],"prefix":"10.34067","volume":"4","author":[{"given":"Joichi","family":"Usui","sequence":"first","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, New York"},{"name":"Department of Nephrology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven P.","family":"Salvatore","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kunihiro","family":"Yamagata","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Surya V.","family":"Seshan","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"issue":"12","key":"B1-20250823","doi-asserted-by":"crossref","first-page":"1267","DOI":"10.2165\/00003495-200464120-00001","article-title":"Biological agents for rheumatoid arthritis: targeting both physical 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