The relationship between hyperuricemia and contrast-induced acute kidney injury undergoing primary percutaneous coronary intervention: secondary analysis protocol for the ATTEMPT RESCIND-1 study

Abstract

Background: Contrast-induced acute kidney injury (CI-AKI) contributes toward unfavorable clinical outcomes after primary percutaneous coronary intervention (pPCI). We will assess whether hyperuricemia is an independent predictor of CI-AKI and outcomes in patients undergoing pPCI. Methods/design: Our study is a secondary analysis for the database from ATTEMPT study, enrolling 560 STsegment elevation myocardial infarction (STEMI) patients undergoing pPCI. Patients will be divided into 2 groups according to the admission serum uric acid (SUA) level. Hyperuricemia will be defined as a SUA level > 7 mg/dL (417 mmol/L) in males and > 6 mg/dL (357 mmol/L) in females. The primary endpoint was CI-AKI, defined as > 25% or 0.5 mg/dL increase in serum creatinine from baseline during the first 48-72 h post-procedurally. Multivariate analyses for CI-AKI and long-term mortality will be performed using the logistic regression and Cox regression analyses, respectively. Discussion: This study will determine the predictive value of hyperuricemia for the development of CI-AKI and outcomes in patients with STEMI undergoing pPCI. We predict that hyperuricemia will be associated with a risk of CI-AKI in patients with pPCI. Furthermore, after adjusting for other variables, long-term mortality after pPCI may be higher in those with hyperuricemia than in those with normouricemia. Results of this study may provide scientific evidence for the effect of hyperuricemia on CI-AKI and long-term outcomes, thereby offering the potential possibility of lowering SUA on the development of CI-AKI and outcomes.

Clinical Feature-Based Machine Learning Model for 1-Year Mortality Risk Prediction of ST-Segment Elevation Myocardial Infarction in Patients with Hyperuricemia: A Retrospective Study

“…Although the pathophysiological mechanisms of adverse reactions to hyperuricemia have not been fully elucidated, it appears to be multifactorial. In the light of the experimental evidence, hyperuricemia was linked to a variety of proatherogenic processes, including increased oxi-dative stress, inhibition of endothelial nitric oxide, activation of the renin-angiotensin system, and increase in the microvascular damage via endothelial dysfunction and vascular smooth muscle cell proliferation [20][21][22][23].…”

Age-Related Effect of Uric Acid on Contrast-Induced Acute Kidney Injury of Patients Undergoing Coronary Angiography

“…Previous studies have also shown that excess uric acid is associated with the susceptibility of renal impairment on exposure to contrast medium, 17,18 The underlying mechanism of this relationship may be attributed to, the increased oxidative stress and crystals-related inflammation of high-level uric acid, leading to tubular injury, endothelial dysfunction and caused kidney injury following CAG. [19][20][21][22] However, young patients have been reported as not susceptible to oxidative stress induced than the elderly, 23 which may explain the insignificant association between uric acid and CI-AKI.…”

Correlation of Uric Acid with Disease Severity, Prognosis, and Complications in Patients with Severe Acute Pancreatitis

“…UA causes oxidative stress in cells, as well as the activation of various intracellular signaling pathways [22] . High blood uric acid modulates the leukocyte response to inflammatory patterns via epigenetic modifications such as histone methylation, promoting the release of pro-inflammatory cytokines such as IL-1b and IL-6, inhibiting the release of IL-1Ra, increasing ROS production, stimulating chemotaxis, and activating the NF-kB and mitogen-activated protein kinase pathways [27][28][29] . It has been shown that elevated serum uric acid levels are associated with high-sensitivity C-reactive protein(hs-CRP), tumor necrosis factor-α(TNF-α), superoxide anion (O 2 -), and hydrogen peroxide (H 2 O 2 ) [30][31] .…”