4.8 Article

Persistent Renal Damage After Contrast-Induced Acute Kidney Injury Incidence, Evolution, Risk Factors, and Prognosis

Journal

CIRCULATION
Volume 125, Issue 25, Pages 3099-+

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCULATIONAHA.111.085290

Keywords

angiography; chronic kidney disease; contrast-induced nephropathy; acute kidney injury; contrast media; catheter based coronary intervention

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Background-The temporal evolution of renal function in patients with acute kidney injury after contrast medium (CI-AKI) is not well known. The aim of this observational study was to evaluate the incidence, risk factors, and prognostic implications of persistent renal damage (RD) in patients with preexistent moderate-to-severe renal dysfunction. Methods and Results-From June 2003 to March 2008, 3986 patients underwent coronary angiography at our institution; 1490 of 3986 had an estimated creatinine clearance of <60 mL/min and were enrolled. CI-AKI was defined as an absolute increase >= 0.5 mg/dL over baseline serum creatinine within 3 days after the administration of contrast medium (iodixanol). In patients who developed CI-AKI, persistent RD was defined as a relative decrease of creatinine clearance >= 25% over baseline at 3 months. Patients whose creatinine clearance returned to baseline (or nearly) were classified as transient RD. The overall incidence of CI-AKI was 12.1%, and persistent RD occurred in 18.6% of CI-AKI patients. At Cox regression analysis, nephropathy risk score >= 17, left ventricular ejection fraction <= 30%, and increased value of serum creatinine >= 1.5-fold from baseline within 5 days were found to be significant risk factors for persistent RD. At 5 years, the incidence of death was significantly higher in patients with persistent RD than in both patients with transient RD (P = 0.015) and those without CI-AKI (P = 0.0001). A similar trend was observed for the combined end point of death, dialysis and cardiovascular events. Conclusions-These results suggest that CI-AKI is not always a transient, benign creatininopathy, but rather a direct cause of worsening renal function. The occurrence of CI-AKI can identify patients at increased risk of cardiovascular events. (Circulation. 2012;125:3099-3107.)

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