Uptal D Patel and Brahmajee K Nallamothu

KEY POINTS

■ Renal dysfunction after cardiac catheterization and percutaneous coronary intervention (PCI) is common, is primarily due to exposure to contrast agents, and is associated with worse clinical outcomes.

■ The prevalence of chronic kidney disease is rising, and it is a key risk factor for renal dysfunction after cardiac catheterization and PCI.

■ The presence of chronic kidney disease and end-stage renal disease is associated with worse short- and long-term outcomes even after successful PCI, including higher rates of restenosis and repeat revascularization. The use of coronary stenting and drug-eluting stents may diminish this risk.

■ Calculation of glomerular filtration rates and a simple risk score can help identify high-risk patients before their procedure beyond the use of serum creatinine levels alone.

■ Established keys to preventing renal dysfunction after cardiac catheterization and PCI include periprocedural hydration and use of low- or iso-osmolar contrast agents.

■ Evidence appears to favor the safety and efficacy of antioxidant agents such as N-acetylcysteine in high-risk patients, but not all trials are consistent.

■ Intraprocedural strategies should consistently be used to minimize the volume of contrast agent exposure as much as possible.

Renal dysfunction is a widely-recognized complication of cardiac catheterization and percutaneous coronary intervention (PCI). A transient rise in serum creatinine levels, a common marker for the development of mild renal dysfunction, occurs in up to 15% of patients undergoing these procedures. Although many of these rises are unlikely to be clinically significant, even short-term renal dysfunction after cardiac catheterization and PCI has been associated with longer hospital stays and greater inpatient costs, as well as worse short- and long-term mortality.

Renal dysfunction after cardiac catheterization and PCI is believed to be primarily caused by intraproce-dural exposure to contrast agents that are nephro-toxic in high doses.1 The single most important risk factor that has been linked to the development of renal dysfunction after cardiac catheterization and PCI is the presence of preexisting chronic kidney disease (CKD). Other clinical factors such as diabetes mellitus and hemodynamic instability, which are also highly prevalent in this population, may also contribute to and exacerbate its clinical course. In a small proportion of patients, renal dysfunction is related to renal atheroembolic disease from diffuse atherosclerosis of the aorta. In patients without CKD or other risk factors, the development of renal dysfunction after these procedures is rare.

Importantly, recent diagnostic and therapeutic advances have improved our ability to identify those patients who are at the highest risk for developing renal dysfunction and, further, to minimize its occurrence. In this chapter we provide a summary of these data, with an additional focus on patients with CKD, given its strong association with worsening renal dysfunction as well as subsequent cardiovascular complications. We also briefly comment on patients with end-stage renal disease (ESRD), a group that represents a growing segment of the population undergoing coronary revascularization. Finally, we discuss the role of nonpharmacologic and pharmacologic strategies for reducing the likelihood of developing renal dysfunction in high-risk patients.

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