The spectrum of bevacizumab-induced renal injury: A systematic review of published case reports.

Abstract

e24143 Background: Bevacizumab, a monoclonal antibody targeting vascular endothelial growth factor (VEGF), is widely used across solid tumors. Despite its therapeutic benefit, renal toxicity remains an important and incompletely characterized adverse effect. Available evidence is limited to case reports and small series. We therefore performed a systematic review to clarify the clinical spectrum and outcomes of bevacizumab-induced renal injury. Methods: A systematic search of PubMed, Google Scholar, EMBASE, and Scopus was conducted from inception through November 2025 to identify case reports and case series describing renal injury attributed to bevacizumab. Extracted variables included demographics, malignancy type, bevacizumab exposure, clinical presentation, biochemical findings, renal pathology, management, and outcomes. Duplicate cases and reports lacking sufficient clinical detail were excluded. Descriptive statistics were used. Results: 31 patients from 21 publications were included. Mean age was 64 years, and 58.1% were women. Underlying malignancies included colorectal (25.8%), breast (22.6%), ovarian (16.1%), and lung cancers (12.9%), with most patients having advanced or metastatic disease. Clinical presentation was dominated by hypertension (71%), nephrotic-range proteinuria (48.4%), acute kidney injury (41.9%) and nephrotic syndrome (32.3%). Kidney biopsy was performed in 22 patients, with thrombotic microangiopathy (TMA) representing the predominant lesion (50% of biopsied cases; 35.5% overall). Other pathologies included immune-complex glomerulonephritis, membranoproliferative patterns, IgA nephropathy with superimposed TMA, endothelial injury, and acute interstitial nephritis. Bevacizumab was discontinued in 74.2% of cases, with dose reduction or interruption in the remainder. Management strategies varied and included supportive care, antihypertensives, corticosteroids, dialysis and complement inhibition with eculizumab in 5 cases. Full renal recovery occurred in 48.4% of patients, partial recovery in 38.7%, while 12.9% progressed to end-stage kidney disease or had no meaningful recovery. Overall mortality was 25.8%, mainly attributable to underlying malignancy progression rather than renal failure. Conclusions: Bevacizumab-induced renal injury encompasses a broad clinicopathologic spectrum, with hypertension and TMA emerging as the most frequent presentation and biopsy-proven pattern. Although most patients experience complete or partial renal recovery after drug withdrawal, a notable minority progress to severe or irreversible renal dysfunction. These findings highlight the importance of early recognition, blood pressure and proteinuria monitoring, and timely bevacizumab discontinuation to reduce renal morbidity. Prospective studies are needed to better define risk factors and optimal management strategies.