Effects of Angiotensin Converting Enzyme Inhibitors and Angiotensin Receptor Blockers in Contrast-Induced Nephropathy

Abstract

Contrast-induced nephropathy (CIN) is considered the third leading cause of iatrogenic acute kidney injury in high-risk patients undergoing radiographic procedures. The main mechanism leading to CIN is medullary hypoxia due to decreased renal blood flow, secondary to renal artery vasoconstriction and direct tubular toxicity by contrast medium. Furthermore, experimental data suggests that an activated renin-angiotensin-aldosterone system (RAAS) plays a role in the pathophysiology of CIN. However, the role of RAAS blockers, including angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) in CIN is controversial. They have been reported to be effective in the prevention of CIN in previous studies, but some studies have concluded that they were associated with an increased risk of CIN, especially in patients with pre-existing renal impairment. In summary, there is no solid data to link ACE inhibitors and ARB to CIN, and larger randomised controlled trials are necessary to further investigate their role in the development of CIN. In this review, we discuss the pathophysiology of CIN, the role of RAAS on the development of CIN, and the effect of RAAS blockers on CIN.

Angiotensin-Converting Enzyme Inhibitor Prevents the Worsening of Renal Function in the Late Phase after Percutaneous Coronary Intervention

“…Cystatin C is a novel endogenous marker of renal whether treatment with renin -angiotensin -aldosterone system (RAAS) blockers, such as ACEI and ARB, decreases the frequency of AKI after PCI 16,17) . Dangas, et al reported that the use of ACEI might have a protective effect against AKI after PCI in patients with CKD 5)…”

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

“…Although hypoxia of the renal medulla [20–22] due to reduction of renal blood flow (RBF) especially in peritubular capillaries [23] and consequent oxidative stress are thought to be the major effectors of CI-AKI [13, 24–26], the exact pathomechanism is unknown [15, 20]. Thus CI-AKI is a subject of intense research.…”

Contemporary practice patterns related to the risk of acute kidney injury in the catheterization laboratory: Results from a survey of Society of Cardiovascular Angiography and Intervention (SCAI) cardiologists

“…Contrary to these data are several studies—both prospective and retrospective which have shown increased rates of AKI following contrast angiography on a background of RAS blockade therapy . Currently, the management of RAS antagonists before angiography remains an area of clinical equipoise and the results of the present survey support this uncertainty .…”