Serum Uric Acid and Risk for Acute Kidney Injury Following Contrast

Abstract

Contrast-induced acute kidney injury (CI-AKI) is a common cause of hospital-acquired acute kidney injury (AKI). We evaluated the evidence that uric acid (UA) plays a pathogenic role in CI-AKI. Ten studies were eligible for inclusion for meta-analysis. Hyperuricemia predicted risk for cases with AKI in prospective cohort studies. Higher levels of serum UA (SUA), as defined by the authors, were associated with a 2-fold increased risk to develop AKI (pooled odds ratio 2.03; 95% confidence interval [CI] 1.48-2.78). Significant heterogeneity was found in cohort studies ( P = .001, I = 85.7%). In 2 clinical trials, lowering of SUA with saline hydration was significantly associated with reduced risk for AKI compared with saline hydration alone or saline hydration with N-acetyl cysteine. An analysis of 2 randomized controlled trials found that allopurinol with saline hydration had a significant protective effect on renal function (assessed by serum creatinine values) compared with hydration alone (mean difference: -0.52 mg/dL; 95% CI: -0.81 to -0.22). Hyperuricemia independently predicts CI-AKI. Two clinical trials suggest lowering SUA may prevent CI-AKI. The mechanism by which UA induces CI-AKI is likely related to acute uricosuria.

Uric acid in the pathogenesis of metabolic, renal, and cardiovascular diseases: A review

“…The risk of AKI was 16% higher with each 1 mg increase in SUA [128]. SUA level is a significant predictor of contrast-induced nephropathy (CIN) [129], [130]. UA lowering with allopurinol in addition to saline hydration was associated with significantly lower incidence of CIN compared to saline hydration alone or saline hydration plus N-acetyl cysteine [130].…”

“…SUA level is a significant predictor of contrast-induced nephropathy (CIN) [129], [130]. UA lowering with allopurinol in addition to saline hydration was associated with significantly lower incidence of CIN compared to saline hydration alone or saline hydration plus N-acetyl cysteine [130]. UA potentially mediates AKI through vascular, pro-oxidative and inflammatory mechanisms [131].…”

Serum uric acid and acute kidney injury: A mini review

“…Indeed, an elevation in serum uric acid, even at modest levels, is known to increase the risk for contrast-induced AKI [47], [48]. A recent meta-analysis by Kanbay et al that included 10 studies reported that elevated levels of serum uric acid were associated with a twofold increased risk for the development of radiocontrast-induced AKI (pooled odds ratio 2.03; 95%CI 1.48–2.78) [49]. Prophylactic administration of allopurinol to subjects undergoing radiocontrast procedures was associated with significant renoprotection compared to hydration with or without N-acetyl cysteine [50], [51].…”

Elevation in serum uric acid levels predicts favourable response to erlotinib treatment in patients with metastatic non‐small‐cell lung cancer

“…11 Recently, uric acid has been a key area of focus as a potential causal factor in a multitude of diseases including but not limited to hypertension, nephropathy, atherosclerosis, heart failure and acute kidney injury. [12][13][14][15][16][17][18] The common pathophysiologic denominator of these pathways is thought to be oxidative stress and inflammation resulting from a hyperuricemic state. 19 In vitro studies demonstrated that the pro-oxidative and pro-inflammatory state induced by hyperuricemia leads to microvascular dysfunction through stimulation of vascular smooth muscle cell proliferation, inhibition of endothelial cell function and activation of renin-angiotensin system.…”