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The renal vasculature encompasses the network of arteries, arterioles, glomerular and peritubular capillaries, and veins that deliver approximately 22% of cardiac output to the kidneys for oxygenation, filtration, and waste removal. It branches from the renal artery through interlobar, arcuate, and interlobular arteries to afferent arterioles entering glomeruli, with efferent arterioles feeding peritubular capillaries around tubules. In disease states like CKD, AKI, and renovascular disease, it undergoes functional rarefaction (vasoconstriction, endothelial dysfunction) and structural rarefaction (remodeling, loss of vessels), reducing RBF, GFR, and tubular function while promoting hypoxia and fibrosis. Factors like reduced VEGF impair angiogenesis and repair, while TGF-β and CTGF drive fibrosis and lumen narrowing. Therapeutic strategies target preservation via pro-angiogenic agents (e.g., VEGF), endothelin blockers, statins, or localized deliveries like KTP-ELP-VEGF fusions to inhibit rarefaction and improve hemodynamics, though clinical challenges persist due to nonspecificity and translation gaps.
Preservation of microvascular function and promotion of proliferation/stabilization. Reduction of vasoconstriction and endothelial dysfunction. Inhibition of vascular rarefaction via angiogenesis or anti-fibrotic effects. Improvement of renal hemodynamics and function.
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