Open AccessIs Angiotensin‐Converting Enzyme Inhibitor a Contraindication for Contrast‐Induced Nephropathy Prophylaxis? A Review About its Paradox
Author(s) -
Li Ximing,
Li Tingting,
Cong Hongliang
Publication year - 2012
Publication title -
cardiovascular therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 46
eISSN - 1755-5922
pISSN - 1755-5914
DOI - 10.1111/j.1755-5922.2011.00299.x
Subject(s) - medicine , nephropathy , angiotensin converting enzyme , renin–angiotensin system , contraindication , pathogenesis , ace inhibitor , context (archaeology) , angiotensin ii , aldosterone , contrast induced nephropathy , vasoconstriction , endocrinology , cardiology , pharmacology , pathology , blood pressure , paleontology , alternative medicine , biology , diabetes mellitus
SUMMARY Contrast‐induced nephropathy (CIN) is reported to be the third leading cause of acute renal failure. The role of angiotensin‐converting enzyme (ACE) inhibitors in CIN is controversial. Some studies pointed out that it was effective in the prevention of CIN, while some concluded that it was associated with increased risk of CIN, especially for patients with preexisting renal impairment. Nevertheless, it is a common practice in many centers to prescribe ACE inhibitors before coronary angiography. The most likely mechanisms leading to CIN are medullary hypoxia due to decreased renal blood flow (RBF) secondary to renal artery vasoconstriction and direct tubular toxicity by contrast medium (CM). Furthermore, experimental data suggest that an activated renin–angiotensin–aldosterone system, increased endothelin‐1, and reactive oxygen species play a role in the pathogenesis of CIN and these can be inhibited by using ACE inhibitors. In this context, we review the medical literatures and discuss the pathogenesis, the role of renin–angiotensin–aldosterone system on the development of CIN and ACE inhibitors’ effect on CIN.