C-Reactive Protein and the Risk of Contrast-Induced Acute Kidney Injury in Patients Undergoing Percutaneous Coronary Intervention

Abstract

Background: The relationship between preprocedural C-reactive protein (CRP) levels and the incidence of contrast-induced acute kidney injury (CI-AKI) is unknown. Methods: Documents of 7,310 consecutive patients undergoing percutaneous coronary intervention (PCI) were screened. Patients with acute myocardial infarction, cardiogenic shock, concomitant inflammatory conditions or undergoing CABG within 48 h were excluded due to potential confounding effects. Results: A total of 4,522 patients were valid for analysis. The median follow-up was 26 months (interquartile range 20–33 months). According to preprocedural CRP values, patients were divided into 3 groups: group 1: CRP <1.0 mg/l (n = 1,523); group 2: 1.0 mg/l ≤ CRP ≤ 3.0 mg/l (n = 1,626); group 3: CRP >3.0 mg/l (n = 1,373). Patients with higher preprocedural CRP levels were associated with a significantly increased rate of CI-AKI (10.6 vs. 14.9 vs. 23.5%, p < 0.0001). After adjustment for baseline covariates, CRP level was still an independent predictor for the incidence of CI-AKI, either as a continuous variable or a categorical variable. Patients with higher CRP values had a significantly higher rate of all-cause mortality and myocardial infarction during follow-up. Conclusion: Elevated preprocedural CRP is associated with an increased risk for CI-AKI in patients undergoing PCI. Preprocedural risk stratification with CRP as an adjunct to established clinical risk factors might be useful.

Risk factors for contrast induced nephropathy: A study among Italian patients

“…The elderly remain at a higher risk of CIN after PCI, a few studies have found age older than 70 years to be an independent predictor of CIN in multivariate analysis. 29 Mehran et al, similarly, found eight variables for patients who underwent PCI (hypotension, intra-aortic balloon pump, congestive heart failure, chronic kidney disease, diabetes, age 75 years, anemia, and volume of contrast) and assigned a weighted integer to each variable to make up a score cumulatively so as to divide low risk (5) and high risk (16) scores. 7 Many studies have found Diabetes Mellitus (DM) as an independent risk factor for CIN.…”

“…Gao et al in their study demonstrated that elevated preprocedural CRP was associated with an increased risk for CIN in patients undergoing PCI. 16 Lyu et al showed that CRP was a significant and independent predictor of CIN after primary PCI in patients with STEMI. 17 Some studies indicated that the administration of statins was associated with reduced incidence of CIN in patients undergoing PCI and the beneficial effect of statins on systemic inflammation and endothelium dysfunction has been well documented.…”

“…Some recent studies found that elevated preprocedural C-reactive protein (CRP) levels may be associated with an increased risk for CIN after percutaneous coronary intervention (PCI). 16,17 The aim of our study was to make a profile of patients at highest risk of developing CIN after coronary angiography and/or percutaneous coronary intervention, in order to take appropriate prevention measures, analyzing the risk factors, evaluated extensively in the literature, and assessing if other markers of inflammation and atherosclerosis, may be considered as risk factors for CIN.…”

Role of Reactive Oxygen Species-Mediated Endoplasmic Reticulum Stress in Contrast-Induced Renal Tubular Cell Apoptosis

“…In some special populations, such as patients with underlying hypertension, cardiovascular diseases, diabetes mellitus, or preexisting renal insufficiency, the incidence is higher and may be as high as 20-50% [2,3,4]. In patients undergoing coronary angiography in China, the incidence of CI-AKI is 8.7-23.5% [5,6]. The precise mechanisms underlying CI-AKI are not fully understood, especially its cellular and molecular mechanism.…”

Xuezhikang ameliorates contrast media-induced nephropathy in rats via suppression of oxidative stress, inflammatory responses and apoptosis

“…[12][13][14] The former one altered oxygen balance leading to medullary hypoxic injury manifesting as cell apoptosis and necrosis. 12,13 The later one initiated the tissue damage through inflammatory factors, [14][15][16] i.e. TNF-A and IL-6.…”