VEGF inhibitor systemic use, known toxicity, and scientific mechanism
Figure: molecular physiology of VEGF cellular function and blockade Hanna et.al. CKJ 2019 open access [9]
VEGF inhibition is well known to upset homeostatic equilibrium inside the two main cell types in the kidney (the podocyte and the endothelial cell) [1-4].
VEGF inhibition results in the loss of signals that tell podocytes and endothelial cells how to survive function, organize the tubule networks, as well as to properly regulate clotting in the cells that line blood vessels (endothelial cells) and the blood urine barrier [9].
Too much or too little VEGF both result in abnormal protein leakage, inflammation through the renin angiotensin aldosterone system targets, higher blood pressure by suppressing nitric oxide synthesis, and clotting by dysregulation of the Di-Acyl-Glycerol (DAG) signaling [9].
Risks of VEGF inhibition extend beyond the kidney and include a higher risk of stroke, heart attacks, deep venous thrombosis (leg vein clots) that can extend to a pulmonary embolus (lung venous clots) [1-3].
