Contrast-induced acute kidney injury (CI- AKI) is usually considered to be a reversible form of acute renal impairment that develops soon after contrast administration. Peak serum creatinine levels typically occur at day 2 to 3 post procedure and return to normal within 2 weeks. Once CI-AKI develops, treatment is limited to supportive measures. Predisposing factors include advancing age, female gender, diabetes mellitus, dehydration, left ventricular dysfunction and pre-existing renal impairment.

The risk of CI-AKI is considerably higher among patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI) as compared to elective PCI [1,2].

 

A recent article in HEART by Wi et al [3] investigated the long-term prognostic implications of CI-AKI with transient or persistent renal impairment in AMI patients undergoing PCI.

 

This was a retrospective observational registry study with 1041 patients included between May 2005 and July 2009. The primary endpoint was a composite of all-cause death and renal impairment requiring dialysis.

 

CI-AKI was defined as an increase in serum creatinine > 25% or 44.2 mmol/l within 2 days post PCI.

 

CI-AKI was seen in 14.2% (n= 148) of patients. Persistent renal dysfunction (> 1 month post procedure) was documented in 45.9% (n=68) of this group. A patient with CI-AKI is more likely to be older, female and more likely to have multivessel coronary artery disease and a lower left ventricular ejection fraction.

 

Patients with CI-AKI had a higher rate of death or dialysis (25.4% vs 6.3%, p<0.001) at 2 years compared with patients without CI-AKI. CI-AKI was an important independent predictor of death or dialysis (HR 2.76, 95% CI 1.61 to 4.73, p<0.001). Patients with transient renal dysfunction showed a lower 2-year event rate of death or dialysis compared with those with persistent renal dysfunction (17.9% vs 34.1%, p=0.013); however, they showed a higher event rate compared with those without CI-AKI (17.9% vs 6.3%, p<0.001).

 

An important caveat from this study was that patients who developed even transient CI-AKI, had poorer outcomes than patients who did not develop any CI-AKI. Better preventive strategies including adequate hydration during the pre and postprocedural phase and utilising the minimal contrast load are to be highlighted. Most centres in the UK do not routinely perform renal function monitoring post procedure. This study highlights the need for more robust preventive strategies and post procedure monitoring to improve the long-term clinical outcome in patients at risk of developing CI-AKI.

 

 

1) Marenzi G, Lauri G, Assanelli E et al. Contrast-induced nephropathy in patients undergoing primary angioplasty for acute myocardial infarction. J Am Coll cardiol 2004;44:1780-5.

 

2) Van de Werf F, Ardissino D, Betriu A, et al. Management of acute myocardial infarction in patients presenting with ST-segment elevation. The Task force on the management of Acute Myocardial infarction of the European Society of Cardiology. Eur heart J 2003;24:28-66.