What is the role of renin-angiotensin-aldosterone system (RAAS) blockade in the prevention of contrast-induced nephropathy (CIN)?

Updated: Feb 21, 2020
  • Author: Anita Basu, MD, FACP; Chief Editor: Vecihi Batuman, MD, FASN  more...
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A prospective, 50-month Mayo study found that renin-angiotensin-aldosterone system (RAAS) blockade, particularly in older patients with coronary heart disease, exacerbates CIN (43% incidence of dialysis and 29% progression to ESRD). [63] The marker used for renal function was eGFR, as calculated by the MDRD formula. The study recommended that RAAS blockade be withheld 48 hours prior to contrast exposure.

RAAS blockade, however, can improve renal perfusion and decrease proximal tubular reabsorption, including CM absorption by the tubular cells. This effect can be documented with the increase in the fractional excretion of urea seen with low-dose RAAS therapy in patients with CHF and moderate CKD (the majority of the CIN-susceptible population). [64] In this group, reduction in intraglomerular pressure and filtration fraction from RAAS therapy might decrease tubular CM concentration and therefore lessen its adverse effects.

In a randomized pilot study conducted in 208 patients with moderate renal insufficiency who were undergoing cardiac catheterization, withholding of an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker (ACEI/ARB) 24 hours or longer preprocedure resulted in a non-significant reduction in contrast-induced AKI and a significant reduction in post-procedural rise of creatinine. The authors suggested considering withdrawal of ACEI/ARB therapy as a low-cost intervention when referring a patient for cardiac catheterization. [65]

Despite some of the above data, current KDIGO guidelines do not support stopping RAS blockade [1]

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