Abstract
Fluid administration is the mainstay intervention effective in the prevention of radiocontrast-associated nephropathy (CAN) in high-risk patients. Vigorous hydration shortens intratubular solute transit-time and reduces tubular intraluminal concentration of contrast media (CM), decreasing exposure of tubular cells to CM and reducing renal parenchymal retention of the nephrotoxin. Lowered plasma and urine viscosity might also improve vasa recta flow and renal interstitial pressure, improving compromised renal parenchymal microcirculation and oxygenation. Herein we emphasize the overlooked plausible role of down-regulation of tubular transport, generated by vigorous hydration in the mitigation of medullary hypoxia and hypoxic medullary damage generated in CAN. Volume expansion triggers natriuretic peptides that improve renal parenchymal oxygenation and may attenuate hypoxic renal injury. Furthermore, enhanced large-volume hydration protocols used for high-risk patients undergoing coronary interventions or transcatheter aortic valve implantation include the administration of furosemide. Loop diuretics block oxygen consumption in medullary thick ascending limbs, improve medullary oxygenation and prevent outer medullary injury in experimental CAN. Thus, fluids are likely not the sole issue, and restoration of medullary oxygenation is critical in attenuating the risk of CAN by large volume hydration protocols for high-risk patients.