CIN - Contrast Induced Nephropathy Doubt cast on sodium bicarb defense against contrast nephropathy: http://www.theheart.org/viewArticle.do?primaryKey=841545&nl_id=tho13mar08 According to: Prevention of contrast induced nephropathy: recommendations for the high risk patient undergoing cardiovascular procedures - from the SCAI (Society of Cardiovascular Angiography and Interventions): - pts at risk: GFR <60 cc/min - A minimum 1 L of isotonic saline should be administered three hours before and continuing at least six to eight hours after the procedure. - There are limited data that suggest a modified regimen with sodium bicarbonate may be effective in high-risk patients. Catheter Cardiovasc Interv. 2007 Jan;69(1):135-40. JWatch: Meta-Analysis: N-Acetylcysteine Is Effective for Preventing ContrastInduced Nephropathy Meta-analysis revealed that, compared with periprocedural saline alone, N-acetylcysteine is the only drug that significantly lowers risk for contrast-induced nephropathy. Contrast-induced nephropathy (CIN) is a common cause of acute renal failure in hospitalized patients. Using low doses of intravenous contrast, preprocedural hydration, and low- or iso-osmolar contrast agents lowers, but does not eliminate, this risk. Therefore, clinicians must consider the use of renoprotective agents in patients with marked kidney disease who are to receive contrast loads. However, previous studies of various drugs have not shown consistent benefits. In a meta-analysis of 41 randomized controlled trials (that involved 6379 patients who had received elective radiographic procedures with IV iodinated contrast agents), researchers evaluated the effectiveness of various drugs (N-acetylcysteine [NAC], theophylline, fenoldopam, dopamine, iloprost, simvastatin, furosemide, or mannitol) plus saline infusion for preventing CIN; saline infusion alone was the standard treatment in all these studies. The primary outcome, CIN, was defined as an absolute increase of >0.5 mg/dL or a relative increase >25% of baseline serum creatinine level at 48 hours after contrast injection. Only NAC lowered risk for CIN significantly more than did saline infusion alone (relative risk, 0.62; 95% confidence interval, 0.44–0.88). Comment: This meta-analysis was limited by the fact that the evaluated endpoint in all included trials was CIN rather than a clinical outcome, such as dialysis dependency or in-hospital morbidity and mortality (see note below). CIN usually is a transient phenomenon, and whether using prophylactic pharmacologic therapy results in any meaningful clinical benefit is unclear. Nonetheless, NAC is an inexpensive drug with very few side effects, and it effectively lowers risk for CIN when it is used with IV saline supplementation. NAC should be considered for all patients who are at high risk for CIN and who require contrast radiologic studies. Published in Journal Watch Hospital Medicine February 25, 2008 Citation(s): Kelly AM et al. Meta-analysis: Effectiveness of drugs for preventing contrast-induced nephropathy. Ann Intern Med 2008 Feb 19; 148:284. Note: N-acetylcysteine reduces contrast-associated nephropathy but not clinical events during long-term follow-up. Abs: Background: Contrast-associated nephropathy (CAN) is associated with increased morbidity and mortality following percutaneous coronary intervention (PCI). N-acetylcysteine (NAC) has been shown to reduce the risk of nephropathy; however, the impact of NAC on long-term clinical outcomes has not been assessed. Methods: This randomized, double-blind, placebo-controlled trial enrolled 180 patients with moderate renal dysfunction undergoing PCI or coronary angiography with a high likelihood of ad hoc PCI; 171 patients completed the clinical follow-up. Patients received oral NAC (2000 mg/dose, n = 95) or placebo (n = 85) twice a day for 3 doses if randomized the night prior to the procedure, and 2 doses if randomized the day of the procedure. The primary end point was the incidence of a >=25% increase in serum creatinine level 48 to 72 hours after PCI. Secondary end points were the inhospital incidence of death, nonfatal myocardial infarction, or urgent dialysis, and the 9-month incidence of death, nonfatal myocardial infarction, need for dialysis, or repeat hospitalization for cardiac reasons. Results: CAN occurred in 9.6% of patients assigned to NAC and 22.2% of patients assigned to placebo (P = .04); 1 patient receiving NAC required urgent dialysis. The inhospital composite end point occurred in 7 (7.4%) NAC-treated and 3 (3.5%) placebo-treated patients, P = NS. At 9 months, the composite end point occurred in 23 (24.2%) NAC-treated patients and 18 (21.2%) placebo-treated, P = NS. Conclusion: Although high-dose NAC prevented periprocedural CAN, this benefit did not translate into a decrease in adverse outcomes over 9 months. Further studies to determine the clinical utility of this drug are required. American Heart Journal. 148(4):690-695, October 2004.
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