Tsuyoshi Isono

Contrast-Induced Nephropathy in Patients Undergoing Emergency Percutaneous Coronary Intervention for Acute Coronary Syndrome

Contrast-induced nephropathy (CIN) is associated with significantly increased morbidity and mortality after coronary angiography and percutaneous coronary intervention (PCI). The aim of the present study was to assess the clinical features and in-hospital outcomes of CIN after emergency PCI. The serum creatinine (SCr) concentration was measured from days 0 to 30 in 338 consecutive patients with acute coronary syndrome undergoing emergency PCI. CIN was defined as an increase in SCr of >25% or >0.5 mg/dl within 2 days after PCI. Overall, 94 patients (28%) developed CIN. The mean SCr on admission was not significantly different between patients with CIN and those without CIN. The CIN group had significantly greater SCr at days 1, 2, and 30 than did the no CIN group. Multivariate analysis showed female gender (odds ratio [OR] 2.38, 95% confidence interval [CI] 1.12 to 5.07, p = 0.025), a culprit lesion in the left anterior descending artery (OR 2.37, 95% CI 1.31 to 4.27, p = 0.0042), contrast agent volume >200 ml (OR 3.60, 95% CI 1.96 to 6.62, p <0.001) and end-diastolic pulmonary arterial pressure >15 mm Hg (OR 2.03, 95% CI 1.02 to 4.04, p <0.01) to all correlate independently with CIN. The in-hospital mortality rate was greater in the CIN group than in the no CIN group (9.6% vs 3.3%, respectively; p = 0.025). In conclusion, CIN is a frequent complication of emergency PCI for acute coronary syndrome and is associated with a greater mortality rate and persistent renal dysfunction.

A new protocol using sodium bicarbonate for the prevention of contrast-induced nephropathy in patients undergoing coronary angiography.

Contrast-induced nephropathy (CIN) is associated with increased morbidity and mortality rates. Although a previous study reported that pretreatment with sodium bicarbonate is more effective than sodium chloride for prophylaxis of CIN, this has not been a universal finding. We performed a prospective randomized trial to investigate whether CIN can be avoided using sodium bicarbonate. In total 155 patients with a glomerular filtration rate (GFR) <60 ml/min/1.73 m(2) who were undergoing coronary angiography were enrolled. We assigned patients to sodium chloride plus sodium bicarbonate (bicarbonate group, n = 78) or sodium chloride alone (chloride group, n = 77). Infusion of sodium bicarbonate at 1 ml/kg/hour continued from 3 hours before to 6 hours after coronary angiography. CIN was defined as a 25% increase in serum creatinine from baseline value or an absolute increase of ≥0.5 mg/dl, which appeared within 2 days of contrast. Baseline GFR was not significantly different between the 2 groups. Patients in the bicarbonate group had a higher GFR than those in the chloride group on day 2 (45.8 ± 13.4 vs 40.9 ± 14.6 ml/min/1.73 m(2), p = 0.031) and at 1 month (49.5 ± 14.7 vs 43.7 ± 15.5 ml/min/1.73 m(2), p = 0.019). CIN occurred in 10 patients (13%) in the chloride group but in only 2 patients (2.6%) in the bicarbonate group (p = 0.012). Sodium chloride plus sodium bicarbonate is more effective than sodium chloride alone for prophylaxis of CIN and can lead to retention of better long-term renal function.