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Abstract: SA-PO701

Clinicopathologic Spectrum of Renal Lesions Following Anti-TNF Alpha Inhibitor Therapy: A Single-Center Experience

Session Information

Category: Pathology and Lab Medicine

  • 1602 Pathology and Lab Medicine: Clinical

Authors

  • Usui, Joichi, University of Tsukuba, Tsukuba, Japan
  • Salvatore, Steven, Weill Cornell Medical College, New York, New York, United States
  • Yamagata, Kunihiro, University of Tsukuba, Tsukuba, Japan
  • Seshan, Surya V., Weill Cornell Medical Center, New York, New York, United States
Background

Anti-tumor necrosis factor (TNF)-alpha inhibitors, as biological agents, are used in a number of chronic immune mediated inflammatory states such as rheumatoid arthritis (RA), psoriatic arthritis (PA), and Crohns disease. This therapy can induce several autoimmune serologic markers and disorders including systemic vasculitis and lupus-like diseases, which may affect the kidney.

Methods

We studied the clinicopathologic features of kidney disease from our renal biopsy files from 2000-2018 and categorized them into pathogenic groups.

Results

45 patients using anti-TNF alpha inhibitors had renal biopsies, RA in 30, PA in 6, Crohns disease 7, RA and PA 1, RA and Crohns 1. Among these, 21 received etanercept, 16 adalimumab, 8 infliximab and 4 had 2 kinds of anti-TNF alpha inhibitors. The patients presented mostly with nephritic syndrome or CKD plus 1 case of AKI and 6 nephrotic syndrome. The main renal lesions on biopsy were classified into 3 groups: autoimmune and anti-TNF alpha induced lesions in 15, autoimmune disease-only 8, a variety of renal lesions unrelated to autoimmune or anti-TNF alpha therapy in 22 (diabetic nephropathy, interstitial nephritis, acute tubular injury, infection-related GN). Crescentic glomerulonephritis was seen in 6, 5 being pauci-immune type with 4 ANCA positive serology. Lupus or lupus-like nephritis was diagnosed in 6: ISN/RPS 2018 class II-2, class V-2, class III+V-1, class IV+V-1. Concurrent fibrillary GN, scleroderma renal crisis and renal amyloidosis were noted in 3 cases. In addition, active or chronic thrombotic microangiopathy was noted in 5, possibly associated to scleroderma or antiphospholipid antibodies, and nephrotic syndrome secondary podocytopathy in 2 cases.

Conclusion

The renal lesions during anti-TNF alpha therapy may have an autoimmune basis such as lupus, lupus-like or ANCA mediated disease, as well as secondary to endothelial or podocyte injury or related to the primary underlying systemic disease.