Contrast-induced nephropathy in interventional cardiology

Abstract

Development of contrast-induced nephropathy (CIN), ie, a rise in serum creatinine by either ≥0.5 mg/dL or by ≥25% from baseline within the first 2–3 days after contrast administration, is strongly associated with both increased inhospital and late morbidity and mortality after invasive cardiac procedures. The prevention of CIN is critical if long-term outcomes are to be optimized after percutaneous coronary intervention. The prevalence of CIN in patients receiving contrast varies markedly (from <1% to 50%), depending on the presence of well characterized risk factors, the most important of which are baseline chronic renal insufficiency and diabetes mellitus. Other risk factors include advanced age, anemia, left ventricular dysfunction, dehydration, hypotension, renal transplant, low serum albumin, concomitant use of nephrotoxins, and the volume of contrast agent. The pathophysiology of CIN is likely to be multifactorial, including direct cytotoxicity, apoptosis, disturbances in intrarenal hemodynamics, and immune mechanisms. Few strategies have been shown to be effective to prevent CIN beyond hydration, the goal of which is to establish brisk diuresis prior to contrast administration, and to avoid hypotension. New strategies of controlled hydration and diuresis are promising. Studies are mixed on whether prophylactic oral N-acetylcysteine reduces the incidence of CIN, although its use is generally recommended, given its low cost and favorable side effect profile. Agents which have been shown to be ineffective or harmful, or for which data supporting routine use do not exist, include fenoldopam, theophylline, dopamine, calcium channel blockers, prostaglandin E1, atrial natriuretic peptide, statins, and angiotensin-converting enzyme inhibitors.

Network analysis of membranous glomerulonephritis based on metabolomics data

“…Notably, the hemodynamic actions of dopamine are dose-dependent; in low renal doses (0.5 to 2.5 µg/kg/min), dopamine stimulates the dopaminergic receptors in the renal and mesenteric vasculature, increases renal plasma flow, eGFR and sodium excretion in patients with normal renal function and with congestive heart failure ( 75 ). In addition, the decreased renal blood flow from the vasoconstriction caused by dopamine has been suggested as a contributing factor to the development of contrast-induced nephropathy; thus, dopamine failed to demonstrate a protective effect on renal function in patients undergoing contrast media exposure and was associated with a deleterious effect on the severity of renal failure and its duration ( 76 ). Therefore, it may be suggested that the renoprotective effects of dopamine occur only in low renal doses; conversely, decreased or increased levels of dopamine may have harmful effects on the kidney, which may result in enhanced nephropathy.…”

Meta-analysis of rosuvastatin efficacy in prevention of contrast-induced acute kidney injury

“… 2 Moreover, the incidence of contrast nephropathy was associated with patient characteristics that are risk factors for this disease. 3 , 4 As CI-AKI is associated with increased short- and long-term morbidity and mortality, nonfatal cardiovascular events, and a longer hospital stay, 5 the adoption of optimal therapeutic strategies is needed to prevent CIN, offering an opportunity to reduce patient morbidity and mortality.…”

Association of N-terminal pro-brain natriuretic peptide with contrast-induced acute kidney injury and long-term mortality in patients with heart failure and mid-range ejection fraction

“…[1,2] However, as effective treatment for CI-AKI is lacking, [3] risk identification is essential to ensuring that high-risk patients receive appropriate prophylactic measures. [4,5] …”