Anti-tumor necrosis factor (TNF)-alpha inhibitors, as biological agents, are used in autoimmune inflammatory states, rheumatoid arthritis (RA), psoriatic arthritis (PA), and Crohn’s disease. They can induce autoimmune serologic responses and clinical disorders including systemic vasculitis and lupus-like diseases, affecting the kidney.
Retrospective analysis of clinicopathologic features of kidney disease following anti-TNF alpha therapy (treatment group) from our renal biopsy files from 2000-2018 is conducted and compared with 106 cases without therapy (control group).
Forty-eight patients using anti-TNF-alpha agents had renal biopsies, RA in 30, PA in 6, Crohn’s disease 6, RA and PA 1, RA and Crohn’s disease 1, and others 4. 20 received etanercept, 15 adalimumab, 8 infliximab and 5 had 2 forms of agents manifesting new onset nephritic syndrome or CKD, 17 with acute kidney injury and 16 nephrotic syndrome, with recent ANCA and/or lupus serology. The renal lesions were crescentic glomerulonephritis in 8, 5 pauci-immune type and 5 ANCA+. Lupus or lupus-like nephritis seen in 6: ISN/RPS 2018 class II-2, class V-2, class III+V-1, class IV+V-1, 3 with concurrent fibrillary GN, scleroderma/TMA and amyloidosis. Renal lesions unrelated to anti-TNF-alpha therapy or underlying autoimmune disease in 23 (eg diabetic nephropathy, interstitial nephritis, acute tubular injury, infection-related GN), IgA nephropathy, renal sarcoidosis and AA amyloidosis were noted in 5 cases. Thrombotic microangiopathy was recognized in 5 cases, 1 associated with scleroderma and 1 antiphospholipid antibodies, and 2 nephrotic syndrome secondary to podocytopathy. The control group was similar with higher immune mediated GN, interstitial nephritis and amyloidosis.
The renal lesions during anti-TNF-alpha therapy have an autoimmune basis such as ANCA, 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.