A hypothesis on the conflicting results of angiotensin converting enzyme inhibitor in the prevention of contrast-induced nephropathy

Abstract

Contrast-induced nephropathy (CIN) is regarded as acute tubular necrosis resulting from the cytotoxicity of contrast media and the medullary hypoxia linking to the interplay of vasoconstriction and vasodilatation. Saline infusion may prevent CIN by inhibiting renin release and thus production of angiotensin II (ANG II), a vasoconstrictor, from angiotensin I (ANG I). Yet the use of angiotensin converting enzyme inhibitor (ACEI) yields conflicting results in the prevention of CIN. We hypothesise that ACEI will be useful for CIN prevention when the saline infusion is insufficient, useless when the saline infusion is sufficient, and counterproductive when the saline infusion is excessive, respectively. When the production of ANG I and thus ANG II is insufficiently inhibited by insufficient saline infusion, ACEI may help prevent CIN by conferring extra inhibition on the production of ANG II from ANG I. The counterproductive effect may result from ACEI blocking the generation of angiotensin 1–7, a potent vasodilator, from angiotensin 1–9 whose precursor, ANG I, is excessively diminished by excessive saline infusion. Clinical data suggest that normal saline infusion at a rate of 1ml/kg/h for 12h, 1ml/kg/h for 6h, and 2ml/kg/h for 6h before and after contrast injection provide sufficient, insufficient, and excessive hydration in the prevention of CIN, respectively. The mainstream guideline is to stop ACEI and provide sufficient hydration for CIN prevention. Alternatively one may continue to have ACEI but the use of normal saline infusion must be limited to 1ml/kg/h for 6h before and after contrast injection.