Abstract: TH-PO160
Intravitreal Injection of Avastin over Time Can Be Associated with Thrombotic Microangiopathy in the Native Kidney
Session Information
- Drug Events Trainee Case Reports
November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 1602 Pathology and Lab Medicine: Clinical
Authors
- Yin, Wenqing, Boston Medical Center, Boston, Massachusetts, United States
- Zhang, Ping L., William Beaumont Hospital, Royal Oak, Royal Oak, Michigan, United States
Introduction
Avastin, an inhibitor of vascular endothelial growth factor, has been used for treating various metastatic cancers. Its side effects leading to renal thrombotic microangiopathy (TMA) has been well known. Intravitreal injection of Avastin (IIA) has been used to treat macular proliferation or degeneration in patients. A recent study of 69 patients with IIA showed no side effects, while there were two case reports suggested a link with IIA and native renal failure in 5 patients without proven biopsies. Whether IIA over time can lead to renal TMA in diabetic patients remain controversial. This case reports the presence of renal TMA after months of IIA in a diabetic patient.
Case Description
A 56 years old diabetic man received IIA for macular edema and proliferative retinopathy over the past few months was found to have deteriorated renal function (serum creatinine up to 2.47 mg/dl) with a nephrotic range of proteinuria (protein/creatinine ratio 4.7). All his serology tests were negative. A renal biopsy was performed to evaluate pathologic changes in the kidney (Light microscopy revealed mesangial nodular expansion, characteristic for diabetic nephropathy but with additional sub-endothelial expansion and lamination around the diabetic nodules. The acute tubular injury was present on PAS-stained sections. No thrombi formation was noted in glomeruli or vessels. Immunofluorescent studies reveal moderate nearly linear IgM staining around diabetic nodules with positive fibrinogen staining. Electron microscopy showed double contoured glomerular basement membranes with subendothelial edema causing detachment of glomerular endothelial cells. Overall findings supported a diagnosis of chronic active TMA on top of diabetic nephropathy background and secondary acute tubular injury.
Discussion
Patient’s ophthalmologist was informed of the result. A follow-up will be conducted (IIA may be discontinued). The finding of this case suggestive the link between repeat IIA and renal TMA, where a small leakage of Avastin from repeat IIA could be a thread to interact with glomerular podocytes and endothelial cells leading to chronic active TMA in the kidney, resulting in renal failure and proteinuria.