CONTRAST-INDUCED NEPHROPATHY IN THE CONTEXT OF INTERVENTIONAL CARDIOLOGY

Abstract

Contrast-induced nephropathy (CIN), defined as an increase in serum creatinine by at least 0.5 mg/dL or 25% from baseline within the initial 2–3 days following contrast administration, is strongly linked to heightened in-hospital and long-term morbidity and mortality following invasive cardiac procedures. Preventing CIN is crucial for optimizing long-term outcomes post percutaneous coronary intervention. The incidence of CIN in patients exposed to contrast ranges widely (from less than 1% to 50%), influenced by well-defined risk factors, notably chronic renal insufficiency and diabetes mellitus. Additional risk factors encompass advanced age, anemia, left ventricular dysfunction, dehydration, hypotension, renal transplant, low serum albumin, concomitant nephrotoxin use, and contrast volume. The pathophysiology of CIN is likely multifactorial, involving direct cytotoxicity, apoptosis, disturbances in intrarenal hemodynamics, and immune responses. Few strategies have demonstrated efficacy in CIN prevention beyond hydration, aiming to establish robust diuresis before contrast exposure and prevent hypotension. Emerging approaches include controlled hydration and diuresis, showing promise. Studies vary regarding the effectiveness of prophylactic oral N-acetylcysteine in reducing CIN incidence, though it's generally recommended due to its affordability and favorable side effect profile. Conversely, several agents have proven ineffective or harmful, lacking supporting evidence for routine use, including fenoldopam, theophylline, dopamine, calcium channel blockers, prostaglandin E1, atrial natriuretic peptide, statins, and angiotensin-converting enzyme inhibitors.