A 68-year-old diabetic woman hospitalized for non-ST-segment elevation myocardial infarction develops increasing chest pain despite maximal appropriate medical therapy and is referred for urgent coronary angiography. She is normotensive, weighs 60 kg, and is without signs of congestive heart failure on examination. The serum creatinine is 1.6 mg/dL (her baseline). What is her risk for contrast media-induced nephropathy (CIN)? What measures can be undertaken to reduce her risk?
Radiocontrast agents are well-recognized nephrotoxins that can cause a usually reversible, non-oliguric form of renal failure within 24 hours and up to five days following administration. Contrast nephropathy is associated with longer hospital stays and higher mortality. The incidence varies widely according to patient characteristics and the type and quantity of contrast agent used.
The pathogenesis of CIN is not completely understood, but likely represents a combination of contrast-mediated renal vasoconstriction, oxidative damage, and direct cytotoxic effects. Newer low-osmolar or iso-osmolar contrast agents are associated with lower rates of CIN than high-osmolar contrast agents. Multiple pharmacologic strategies for CIN prevention have been investigated, with several important trials published in the past two years. This review summarizes the risk assessment and prophylactic strategies required for optimal protection of patients from CIN.
Assesment of Patient Risk
Contrast-induced nephropathy is defined variably in clinical trials, most commonly as a 25% increase in serum creatinine above baseline at 48 hours after contrast administration. The most important risk factor for CIN is pre-existing kidney disease—more specifically, a diminished glomerular filtration rate (GFR) below 60 mL/minute/1.73 m2 body surface area.1 The serum creatinine concentration can be misleading. Advancing age, female gender, low lean body mass, or unstable rising creatinine all can lead to overestimation of the GFR. The Modification of Diet in Renal Disease (MDRD) estimate of GFR and the Cockcroft-Gault estimate of creatinine clearance are calculated in a basic formula. (see Table 1, left)
Several other factors have been linked to increased risk for CIN. Table 2 (left) summarizes these risk factors and assigns them various point scores. In general, patients with chronic kidney disease or any of these risk factors should have a serum creatinine drawn before the contrast study to clarify their CIN risk and facilitate decisions regarding prophylaxis. Patients with a score of six or more are at substantial risk for CIN.1
Strategy for Prophylaxis
Low-osmolar and iso-osmolar contrast agents have been associated with lower rates of CIN compared to high-osmolar contrast. However, the referring hospitalist rarely determines the type and volume of contrast used. Fortunately, high-osmolar contrast is used infrequently today. The primary strategy for CIN prophylaxis is to:
1) Determine CIN risk using a validated tool (see Table 2).
2) If “at risk,” consider alternate diagnostic modalities that do not involve the intravenous administration of iodinated contrast. Consider delaying testing with contrast agents until potentially reversible conditions affecting GFR are addressed, such as volume depletion, recent contrast use, or concomitant use of nonsteroidal anti-inflammatory drugs or angiotensin-converting enzyme inhibitors.