Antiglomerular Basement Membrane Disease Possibly Triggered by Undiagnosed Renal Cell Carcinoma: A Case Report

Abstract

Antiglomerular basement membrane (anti-GBM) disease is a rare, small-vessel vasculitis that affects the capillary beds of the kidneys and lungs. Although exceedingly rare, several case reports have described anti-GBM disease with a concurrent cancer diagnosis, suggesting a possible correlation between these 2 conditions. Herein, we describe the first known case to our knowledge of a woman in her early 60s with simultaneous anti-GBM disease and clear cell renal cell carcinoma, in which the tumor was thought to have been the substrate for anti-GBM disease. We believe that renal cell carcinoma may have contributed to the production of anti-GBM autoantibodies and, thus, anti-GBM disease. The concurrence of these 2 conditions complicated the treatment of the patient, who was hemodialysis-dependent at the time of hospital discharge. This report highlights the importance of considering anti-GBM disease as a potential diagnosis in patients with acute kidney failure, and how important it is to identify both clear cell renal cell carcinoma and anti-GBM disease at an early stage to improve outcomes.

Keywords: Antiglomerular basement membrane disease; acute kidney injury; immunosuppression; kidney failure; plasmapheresis; rapidly progressive glomerulonephritis; renal cell carcinoma; renal failure.

Figure 1

Timeline showing changes in the levels of anti-GBM in addition to important interventions during hospitalization. GBM, glomerular basement membrane

Figure 2

Ultrasonography (A) and computed tomography (CT) (B-D) imaging revealed a tumor in the patient’s right kidney. Fine-needle biopsies were obtained from both tumor and nontumor tissues (E-F). (A) Abdominal ultrasonography at the time of admission showed a tumor (red circle) with peripheral vascularization. No signs of hydronephrosis were observed. Both kidneys were hyperechogenic, swollen, and ∼13 cm long. (B) Axial CT slice (day 2) revealing a tumor in the right kidney (orange arrow) and a simple, hyperdense cyst in the lower pole of the left kidney (red arrow). Moreover, the CT imaging revealed ascites in the pelvis and edema in the subcutaneous adipose tissue near the kidneys and the tumor. There were no signs of hydronephrosis, and pelvic or abdominal CT revealed no lymphadenopathy. (C) Coronal CT imaging (day 2) revealing a mediolateral diameter of 53.2 mm. (D) Sagittal CT imaging (day 2) showing a craniocaudal diameter of 63.4 mm and an anteroposterior diameter of 65.2 mm. (E-F) Fine-needle aspiration biopsy of nontumor tissue (E: original magnification, ×10, F: original magnification, ×20) revealed crescentic lesions in all 10 glomeruli. Significant reactive changes were observed in the tubulointerstitium. Evaluation of possible interstitial fibrosis is challenging because of edema and the presence of inflammatory infiltrates. Moderate wall thickness and hyaline staining were observed in the small arteries. The arterioles showed signs of myocyte vacuolization and endothelial damage. Immunohistochemical staining was negative, except for C5b-9 staining along the capillary walls.