The most commonly used definition of renal dysfunction after cardiac catheterization and PCI in the literature (which refers primarily to contrast-related nephropathy) is a rise in serum creatinine levels of 0.5 mg/dL or a 25% increase from baseline. Although its reported incidence ranges from 8% to 15% in the general population,8 the clinical importance of this change in most cases is uncertain given its transitory nature. In only a few of these patients (<1%) will this abnormality extend beyond a few weeks and require the need for renal replacement therapy with either hemodialysis or peritoneal dialysis. In most cases with long-term complications, patients have preexisting evidence of advanced CKD.
In addition to CKD, several other risk factors for developing renal dysfunction after cardiac catheter-ization and PCI have been identified (Table 5-2). Most importantly, these appear to be related to demographic factors such as advanced age, comor-bidities (e.g., diabetes mellitus), periprocedural factors such as hemodynamic instability or heart failure, and evidence of volume depletion.9 Additional factors include the use of intra-aortic balloon pumps and nephrotoxic medications such as nonsteroidal anti-inflammatory drugs (NSAIDs). A key and potentially modifiable factor is the use of high volumes of contrast agents. Several investigators have suggested a maximum allowable contrast dose that is dependent on the degree of CKD at baseline (Fig. 5-1).10,11
Over the last several years, several risk-prediction models have been developed to predict a patient's risk of developing renal dysfunction (and specifically contrast-related nephropathy) after cardiac catheter-ization and PCI. A recent model by Mehran and colleagues, developed in 8357 patients undergoing PCI, uses eight readily-available variables to calculate an
Table 5-1. Concomitant Drugs to Monitor with Exposure to Contrast Agents
Drugs influencing renal hemodynamics
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Angiotensin-converting enzyme (ACE) inhibitors
Angiotensin receptor blockers
Drugs that cause tubular toxicity
Diuretics, including mannitol
Antibiotics, including aminoglycosides, vancomycin, amphotericin B
Immunosuppressants, including tacrolimus and cyclosporine A
Drugs with potentially enhanced toxicity after contrast-induced nephropathy
Table 5-2. Risk Factors for the Development of Contrast-Induced Nephropathy
Acute coronary syndrome Hypotension Heart failure Volume depletion
Concomitant nephrotoxic medications Anemia
Intra-aortic balloon pump placement
Adapted from Erley C: Concomitant drugs with exposure to contrast media. Kidney Int Suppl 2006;(100):S20-S24.
overall risk score for predicting both contrast-related nephropathy and nephropathy requiring dialysis (Fig. 5-2).12 Variables in this model are scored from 1 to 6 and then summed to generate risks of contrast-related nephropathy ranging from 7.5% to 57.3% and risks of nephropathy requiring dialysis from 0.04% to 12.6%. Use of models such as these allows clinicians to appropriately discuss the potential benefits and risks of cardiac catheterization with high-risk patients before their procedure. It also may help target potential strategies to minimize the risk of developing renal dysfunction.
In most cases, renal dysfunction after cardiac catheterization and PCI is completely reversible and has no apparent long-term effects. Contrast-related nephropathy typically results in a clinical course consistent with acute tubular necrosis and nonoliguric renal dysfunction. Abnormalities in serum creatinine levels start within 24 to 48 hours after the procedure, peak at 5 days, and then completely resolve within 2 to 4 weeks.13 The need for renal replacement therapy with hemodialysis or peritoneal dialysis is extremely rare.11 Among those who do require renal replacement therapy, fewer than 50% require it permanently. The requirement for renal replacement
Maximum allowable contrast dose (MACD) =
(5* kg of body weight) Serum creatinine (mg/dL)
Figure 5-1. Calculation of maximum allowable contrast dose based on degree of chronic kidney disease. (Redrawn from Cigarroa RG, Lange RA, Williams RH, et al: Dosing of contrast material to prevent contrast nephropathy in patients with renal disease. Am J Med 1989;86:649.)
therapy appears to be more likely in the setting of renal atheroembolic disease, which has a more progressive course than contrast-related nephropathy and a lower likelihood of recovery.
Importantly, both the presence of CKD at baseline and the development of renal dysfunction after cardiac catheterization and PCI have been associated with several clinical outcomes unrelated to renal disease. Several studies have shown that patients with CKD at baseline who undergo PCI are at a higher risk of mortality and major adverse clinical events, both in routine cases and in the setting of ST-elevation myocardial infarction.14,15 In addition, the development of renal dysfunction after cardiac catheterization and PCI has been shown to result in longer hospital stays and greater inpatient costs.16 Recent reports also suggest that the development of contrast-related nephropathy predicts short- and long-term mortality.17-20 What remains unclear from this literature, however, is whether the presence of CKD at baseline or the development of renal dysfunction after PCI is simply a marker of greater disease acuity or represents an additional comorbidity like diabetes mellitus.
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