Contrast-Induced Nephropathy in the Cardiac Cath Lab

A patient who has renal insufficiency before the administration of contrast material is five to 10 times more likely to develop contrast-induced renal failure, (also known as contrast-induced nephropathy, CIN) than patients in the general population. Contrast-induced renal failure is related to the dose of contrast material used. Intravenous (and likely intra-arterial) administration of contrast material is responsible for more than 10% of cases of hospital-acquired renal failure. The incidence of renal failure following contrast administration is relatively uncommon, occurring in 0.1 to 13 percent of patients in the post-procedure period. The likelihood of CIN is related to the degree of preexisting renal insufficiency, diabetes and hydration. Fortunately, progression to complete renal failure requiring dialysis is very rare in patients without significant renal impairment beforehand. An especially vulnerable patient is the patient with multiple myeloma who is at increased risk, particularly if they are dehydrated. How contrast materials cause renal failure is unclear, but direct cellular toxicity and intrarenal vasoconstriction are believed to be the primary causes of renal function changes. A generally accepted definition of renal failure is an elevation of serum creatinine to greater than 25 percent of baseline within three days of receiving contrast material. Chronic renal insufficiency is considered to be baseline creatinine of > 1.5 ng/dl.

How should we treat our patients at risk for CIN before catheterization and angiography?
Conventional wisdom suggests that using the smallest amount of contrast material possible and low-molecular, nonionic contrast agents appears to decreases the relative risk of CIN. In addition, three clinical approaches to preventing CIN which can be instituted are: 1) ensuring adequate hydration, 2) discontinuing any nephrotoxic medications and 3) administering N-acetylcysteine for those at highest risk before the procedure (see table). How much contrast media is enough in patients at risk for CIN? Once the clinical indication for angiography exists and the patient understands the risks and benefits, the requirement for important diagnostic information trumps the amount of contrast to be used. The operator must use whatever amount of contrast is needed to obtain the critical information for making the potentially life and death decisions to come. Different procedures obviously require different amounts of contrast material to obtain the minimal diagnostic information. A patient with angina undergoing only native coronary angiography may require as little as 60 mL, compared to a patient with claudication after coronary bypass graft surgery, who may need over 150 mL of contrast for coronary, graft, aortic and peripheral angiography. Operators can limit contrast by skillful angiography, and withholding ventriculography and other marginally important studies. This can be especially challenging in the complex patient. On a personal note, in patients with only a minimally abnormal creatinine, I believe the small additional contrast load of a 20-25mL LVgram facilitates rapid and accurate decisions for revascularization in the CAD patient.

What pharmacotherapy is useful to prevent CIN?
Other than N-acetylcysteine (dose shown above), most other agents thought to prevent CIN have not been proven effective. For example, mannitol has been used in an attempt to increase or maintain the glomerular filtration rate (GFR), but little supporting evidence exists. A study comparing hydration with saline alone to saline plus mannitol showed that saline alone was more protective. Furosemide has not been shown to prevent contrast-induced renal failure. A significant decline in renal function may occur in some patients treated with furosemide before contrast administration. Oral calcium channel blockers may minimize the reduction of GFR. In a prospective study, patients treated with 20 mg per day of nitrendipine for three doses starting 24 hours before the procedure had sparing of GFR in the treatment group as compared to control patients. Protecting the kidney from the toxicity of contrast media in patients with borderline renal function will benefit these individuals over the long term, especially in view of the necessity for future studies to diagnosis and treat the progressive nature of atherosclerosis involving the coronary and peripheral arterial systems.

TABLE 1. Methods of Preventing Contrast-Induced Nephropathy: General Principles

1) Limit delivery of radiographic contrast material.

2) Discontinue any nephrotoxic drugs before the procedure.

3) Delay (i.e., rest the kidney) before performing second procedures.
*Conventional practice suggests allowing 2-5 days to recover renal function.

4) Hydration Oral: 500 mL before the procedure. Intravenous 0.9% or 0.45% saline 250cc/h x 4h, then oral fluids to total 2,500 mL x 24h post procedure.

5) N-acetylcysteine Mucomist, 600 mg orally every 12 hours for 48-72 hours, beginning the day before the procedure.