We record here a unique case of early endothelial cells injury induced by intravitreal injection of bevacizumab. primarily reported after its systemic injection. Podocytes produce VEGF that interacts with endothelial cells VEGF receptor-2 keeping glomerular basement membrane integrity. Bevacizumab induce the detachment of endothelial cells from glomerular basement membrane leading to the proteinuria and renal function decrease. Intravitreal bevacizumab is generally supposed to be safe. However, glomerular injury with microangiopathy features, actually after intravitreal injection is possible. Summary We statement the electron microscopy evidence that intravitreal injection of anti-VEGF induces glomerular endothelial cells injury. Nephrologists and ophthalmologists should be aware of this complication. 1. Intro Antiangiogenic providers that inhibit vascular endothelial growth factor (VEGF) have emerged as important tools to treat metastatic cancer and various ocular diseases [1, 2]. Their systemic use can induce nephrotoxicity, primarily glomerular injury characterized by minimal switch disease, or most frequently features of renal limited microangiopathy, BC 11 hydrobromide leading to proteinuria, nephrotic syndrome, and hypertension [3, 4]. This anti-VEGF induced renal microangiopathy is definitely rarely associated to the classical hematologic abnormalities found in acute thrombotic microangiopathy (TMA), as it happens among other things in standard, atypical haemolytic uremic syndrome, or malignant hypertension . Intravitreal injection of anti-VEGF agent is supposed to be safe. However, BC 11 hydrobromide systemic absorption may occur. We statement here an exceptional case of kidney injury related to glomerular microangiopathy after intravitreal injection of bevacizumab, an anti-VEGF humanized antibody. 2. Case Demonstration COG3 A 72-year-old man was addressed to the nephrology division for acute kidney injury with increased creatininemia at 2.2?mg/dL (406.25? em /em g/mL) in experimental rabbit model . In glomeruli, podocytes produce BC 11 hydrobromide VEGF that binds to VEGF receptor-2 indicated on endothelial cells. This connection is necessary to the normal function of the glomerular filtration barrier and for recovery of renal microvascular injury . Ultrastructure study inside a murine model of doxycycline induced VEGF deletion in podocytes showed swelling of the endothelial cells. This indicate the crucial part of VEGF in keeping glomerular endothelium integrity . The endothelial cells injury in our individual after intravitreal bevacizumab injections, indicate that actually very low systemic concentrations of anti-VEGF could significantly impair connection between VEGF derived from podocytes, and VEGF receptor within the endothelial cells. As far as we know, we statement for the first time the electron microscopy evidence that intravitreal injection of anti-VEGF induces glomerular endothelial cells injury. As the use of anti-VEGF therapy is definitely increasing, particularly in ocular diseases with local injections, ophthalmologists, and nephrologists should be aware of this complication. A regular monitoring of renal function and proteinuria after introducing anti-VEGF antibodies is advised. Ethical Approval This short article does not contain any studies with human participants or animals performed by any of the authors. Conflicts of Interest The authors declare no discord of interest..
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