What interventions most effectively protect against contrast media-induced nephropathy?

Case

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?

Key Points

  • Serum creatinine may overestimate glomerular filtration rate (GFR) in older, female, and low-body-mass patients. Determine contrast media-induced nephropathy (CIN) risk based upon an estimate of GFR. A less-than-60 mL/min is a potent CIN risk factor.
  • Identify overall CIN risk early and according to a validated tool.
  • Consider alternate diagnostic testing to avoid contrast administration, if feasible.
  • Consider delaying contrast testing while undertaking efforts to improve GFR: fluid resuscitation, stopping NSAID medications, stopping diuretics or ACE-inhibitors if feasible.
  • Use N-acetylcysteine and isotonic IVF, preferably sodium bicarbonate, to protect against CIN.

Additional Reading

McCullough PA. State of the art paper: contrast-induced acute kidney injury. J Am Coll Cardiol. 2008;51:1419-1428.

Background

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)

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