A 72-year-old man was addressed to the nephrology department for acute kidney injury with increased creatininemia at 2.2 mg/dL (N: 0.72-1.17) corresponding to an estimated glomerular filtration rate (eGFR) of 30 mL/min/1.73 m2 according to the CKD-EPI formula. He was asymptomatic. He had no personal or family history of kidney disease. He did not travel, had no allergies, and had no known contact with ill patients. He was not taking any nonsteroidal anti-inflammatory drugs. His medical history comprised of pleural tuberculosis treated 20 years before, well controlled hypertension under treatment with calcium antagonists and glaucoma treated by monthly intravitreal injections of bevacizumab in the past 6 months. Physical examination and blood pressure were normal. There was no swelling. Laboratory investigations did not show any sign of TMA, with normal haemoglobin and platelet count. Immunological testing was positive only for antiphospholipid antibodies. Infectious serology was negative. The urinalysis showed no haematuria but increase of albuminuria from 2.9 to 226 mg/g of creatinine (N: <30). Urine cultures were negative. Kidney ultrasound was normal. A renal biopsy performed two weeks after showed ten glomeruli. Two of them were obsolescent glomeruli with complete glomerulosclerosis. The other glomeruli demonstrated thickening of capillary wall (Figure 1(a)). There were segmental glomerular capillary microaneurysms, filled with pale material, and segmental hyaline thickening of the glomerular basement membrane (Figure 1(b)). Silver staining showed some double contours (Figure 1(c)). Mild focal interstitial fibrosis and tubular atrophy with a mononuclear cells infiltrate were seen. Immunofluorescence for IgA, IgG, IgM, C1q, kappa, and lambda was negative. However, C3 immunofluorescence showed a sparse endothelial positivity in arterioles (not shown). On electron microscopy, the endothelial cells showed irregularities, and focal loss of fenestrations. Subendothelial space expansion by electron-lucent material was visible (Figure 1(d)). This was consistent with signs of endothelial injury. Intravitreal injections of anti-VEGF were suspended. Four months after withdrawal, serum creatinine was of 1.20 mg/dL, and albuminuria normalized, supporting our hypothesis of intravitreal anti-VEGF induced renal microangiopathy. One year after bevacizumab was stopped, serum creatinine was of 0.95 mg/dL, and urinary albumin-creatinine ratio was of 3.3 mg/g. The patient did not present any thromboembolic event.