Abstract: FR-PO204
Panitumumab-Associated IgA Nephropathy With Membranoproliferative and Exudative Features
Session Information
- Onconephrology: Clinical and Research Advances - I
November 04, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1600 Onconephrology
Authors
- Yarandi, Niloufarsadat, Mayo Clinic Division of Nephrology and Hypertension, Rochester, Minnesota, United States
- Fidler, Mary E., Mayo Clinic Department of Laboratory Medicine and Pathology, Rochester, Minnesota, United States
- Leung, Nelson, Mayo Clinic Division of Nephrology and Hypertension, Rochester, Minnesota, United States
Introduction
Panitumumab is a monoclonal antibody(MAb)epidermal growth factor receptor (EGFR) inhibitor approved for metastatic colon cancer. EGFR inhibitors can cause tubular, electrolyte disorders and glomerulopathies.
Case Description
A 62-year-old male with metastatic colon cancer to the liver developed hypomagnesemia and nephrotic range proteinuria after 2 months of panitumumab. Magnesium 0.6 mg/dL, creatinine 0.72 mg/dL, albumin 3.4 g/dL, proteinuria 16.1 g/24hr, albumin/creatinine 4991 mg/gcr. Urinalysis 51- 100 RBCs(> 25%dysmorphic), 4 -10 WBCs, negative nitrite/leukocyte esterase. He required oral and IV magnesium supplements. Amiloride was attempted but resulted in hyperkalemia. Kidney biopsy revealed IgA nephropathy with exudative membranoproliferative features. Panitumumab was discontinued and prednisone 60 mg daily was started. Proteinuria improved to 6.9 g/24hr within 2 weeks; magnesium normalized.
Discussion
Tubular and electrolyte disorders are more common compared to glomerular lesions and are mainly associated with EGFR MAbs.
The main electrolyte disorder with EGFR inhibitor MAbs is hypomagnesemia via renal magnesium wasting. Proliferative IgA crescentic glomerulonephritis (GN), immune-complex GN, and pauciimmune crescentic GN have been reported with EGFR inhibitors. The exact mechanism for nephrotic/nephritic syndrome is not clear. Response to therapy varies from no response to complete response after discontinuing EGFR inhibitor +/- glucocorticoids or other immunosuppressives.
PAS-Jonesx40Endocapillary hypercellularity, segmental neutrophils, segmental glomerular basement membrane double-contouring
IF:IgA-dominant deposits involving mesangium and GBM EM: Endocapillary hypercellularity, mesangial/paramesangial, subendothelial deposits