Angiotensin-converting enzyme inhibitors and their effects on contrast-induced nephropathy after cardiac catheterization or percutaneous coronary intervention

Patel, Kushal; King, Christopher A.; Jovin, Ion S.

doi:10.1016/j.carrev.2010.01.002

Cited by 18 publications

(12 citation statements)

References 18 publications

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“…Another strength of our study is the newly adopted analysis according to the status of chronic exposure to RAAS blocker, which has not been employed in previous meta-analyses or narrative reviews on this issue [16,17,18,19]. The major findings of this meta-analysis are that ACEI/ARB discontinuation in chronic users before contrast procedure is associated with less deterioration of renal function, whereas acute intervention of ACEI/ARB intake in drug-naïve patients did not affect CIN incidence.…”

Section: Discussionmentioning

confidence: 99%

The Impact of Renin-Angiotensin-Aldosterone System Blockade on Contrast-Induced Nephropathy: A Meta-Analysis of 12 Studies with 4,493 Patients

Lee

Park

et al. 2014

Cardiology

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Objectives: This meta-analysis investigated the impact of renin-angiotensin-aldosterone system (RAAS) blockade on the occurrence of contrast-induced nephropathy (CIN). Methods: Twelve studies comparing the use of RAAS blockade in a total of 4,493 patients undergoing a contrast-using procedure were included. The primary endpoint was the overall postprocedural incidence of CIN. Results: In the overall pooled analysis, there was no significant difference between the two groups, RAAS blockade ‘used' versus ‘not-used', in the incidence of postprocedural CIN in the random-effects model (OR 1.27, 95% CI 1.77-2.11, p = 0.351, I² = 61.9%). In the stratified analysis, however, for chronic RAAS blockade users, the continuation of the drug was significantly associated with a higher incidence of CIN compared with discontinuation (OR 2.06, 95% CI 1.62-2.61, p < 0.001, I² = 0.0%). A hazard of continuation was marked in a subgroup of older patients or in patients with chronic kidney disease. For drug-na9ve patients, however, administration of RAAS blockade before contrast procedures did not reduce the development of CIN significantly (OR 0.52, 95% CI 0.23-1.16, p = 0.108, I² = 34.2%). Conclusion: Discontinuation of RAAS blockade in chronic users is associated with a significantly lower incidence of CIN, whereas administration of RAAS blockade as a preventive measure for na9ve patients did not show a significant effect on the incidence of CIN. i 2014 S. Karger AG, Basel

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Section: Discussionmentioning

confidence: 99%

The Impact of Renin-Angiotensin-Aldosterone System Blockade on Contrast-Induced Nephropathy: A Meta-Analysis of 12 Studies with 4,493 Patients

Lee

Park

et al. 2014

Cardiology

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“…Based on these data they concluded that there is no definite correlation between ACEIs and the occurrence of CIN in the cardiac catheterization laboratory and withholding ACEIs prior to catheterization does not probably decrease the incidence of CIN and is not recommended. They also stated that starting ACEIs before the procedure for the sole purpose of lowering the risk of CIN cannot be recommended based on the current evidence (19). The presence of different conclusions can result from significant differences in methodology, study populations, interventions.…”

Section: Discussionmentioning

confidence: 99%

The effects of chronic usage of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers on contrast-induced nephropathy in low-risk patients

Barış¹,

Özpelit²,

Doğan³

et al. 2012

Anadolu Kardiyol Derg

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Objective: There is conflicting data about the role of renin-angiotensin-aldosterone system (RAAS) blockers in contrast-induced nephropathy (CIN) pathophysiology. In this study, we aimed to investigate the effects of chronic usage of RAAS blocker drugs on development of CIN in low risk patients. Methods: Study was designed as a prospective cohort study. A total of 295 patients were enrolled in the study. Study population was consisted of three subgroups according to prior usage of RAAS blockers: no RAAS blocker group (n=95), angiotensin-converting enzyme inhibitor (ACEI) group (n=106), angiotensin receptor blocker (ARB) group (n=94). CIN was defined as an increase of ≥25% in creatinine over the baseline value or 0.5 mg/dL rise within 48-72 h of angiography. Mehran score was calculated for each patient. Baseline variables and percentage of CIN were compared with ANOVA, Mann-Whitney U, Kruskal-Wallis and Pearson Chi-square tests between groups. In order to determine the independent predictors of CIN, binary logistic regression analyses were performed. Results: CIN occurred in 18 patients (17.0%) in the ACEI group, 17 patients (18.1%) in ARB group and 7 patients (7.4%) in the no RAAS group. CIN occurrence was significantly higher in RAAS than no RAAS group (17.5% vs. 7.4%, p=0.01). Chronic RAAS blocker administration was an independent predictor of CIN (OR=2.69; 95% CI: 1.025-7.067; p=0.04). Mehran score was the only other independent predictor for CIN (OR=1.15; 95% CI: 1.019-1.310; p=0.02).

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“…There was also no increased incidence of CIN with ACE inhibitors or ARBs in the subgroups at higher risk, such as those with diabetes mellitus [40]. Recently a review has been published by Patel et al [8]. In this review, the results of 5 randomised clinical trials and 678 patients were analysed.…”

Section: Effects Of Acei/arb In Cinmentioning

confidence: 99%

“…The role of renin-angiotensin-aldosterone system (RAAS)-blocking agents, including angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), in the pathophysiology of CIN is controversial because the available literature is conflicting [8,9,10,11]. Although several reports have suggested that these RAAS-blocking agents are nephrotoxic and worsen kidney failure in CIN [12], other reports have asserted that they protect the kidneys from the effects of CIN [13].…”

Section: Introductionmentioning

confidence: 99%

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

Zhou

Duan

2013

Kidney Blood Press Res

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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.

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Angiotensin-converting enzyme inhibitors and their effects on contrast-induced nephropathy after cardiac catheterization or percutaneous coronary intervention

Cited by 18 publications

References 18 publications

The Impact of Renin-Angiotensin-Aldosterone System Blockade on Contrast-Induced Nephropathy: A Meta-Analysis of 12 Studies with 4,493 Patients

The Impact of Renin-Angiotensin-Aldosterone System Blockade on Contrast-Induced Nephropathy: A Meta-Analysis of 12 Studies with 4,493 Patients

The effects of chronic usage of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers on contrast-induced nephropathy in low-risk patients

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

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