Abstract: SA-PO279
Secondary (AA) Amyloidosis Associated with Checkpoint Inhibition
Session Information
- Trainee Case Reports - VI
October 27, 2018 | Location: Exhibit Hall, San Diego Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Reports
- 1202 Glomerular Diseases: Immunology and Inflammation
Authors
- Sebastian, Anne D., Rush University Medical Center, Chicago, Illinois, United States
- Whittier, William Luke, Rush University Medical Center, Chicago, Illinois, United States
- Cimbaluk, David J., Rush University Medical Center, Chicago, Illinois, United States
Introduction
Nivolumab (Nb) is an immune checkpoint inhibitor (CPI) which targets solid tumors but can cause nephrotoxicity by accelerating systemic inflammation. We report a case of a patient who achieved partial remission of squamous cell lung cancer (SCLC) with Nb but later developed nephrotic syndrome from secondary (AA) amyloidosis.
Case Description
A 75 y.o. white man presented with anasarca. He was diagnosed with metastatic SCLC 2 years ago and received 4 cycles of Nb. His last dose was 10 months ago. It was stopped due to failure to thrive as he had acheived partial remission. Exam notable for diffuse anasarca. Alb 1.1 g/dL, Cr 0.76 mg/dL. ANA (-). C3 77, C4 25 mg/dL, RF 67 IU, CRP 86.8 mg/L, ESR >140 mm/hr. SIEP and UIEP (-) for monoclonal protein. A year ago, Alb 2.6 g/dL, UA trace protein.
Renal biopsy demonstrated apple green birefringent deposits in the glomeruli and arterioles on Congo red (Figure 1). Amyloid A immunostain was (+). IF was (+) for full house mesangial staining of IgG (3+), IgA (3+), IgM (2+), C3 (3+), C1q (3+) and C4 (1+) and equal for κ & λ stain (3+). EM with randomly arranged fibrils 8-12 nm in the GBM & mesangium. He was started on prednisone, bactrim, and colchicine and his U P/C improved to 5.1 g/g in 3 months. His inflammatory markers improved and his SCLC remained in partial remission.
Discussion
We present a patient with secondary (AA) amyloidosis with diffusely positive mesangial IF 10 months after receiving Nb. Although progressive cancers can be associated with AA amyloidosis, his SCLC was in partial remission, making it an unlikely etiology. In addition, his elevated ESR, CRP, RF, and full house IF are signs of active inflammation. CPIs exert their antineoplastic action by accelerating inflammation, causing interstitial nephritis. In contrast, our case illustrates the possibility that the immune checkpoint inhibitor created an uncontrolled inflammatory response leading to secondary (AA) amyloidosis.