Journal of vascular surgery · 2015
Elevated serum cystatin C level is an independent predictor of contrast-induced nephropathy and adverse outcomes in patients with peripheral artery disease undergoing endovascular therapy.
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Kim Gwang-Sil, Ko Young-Guk, Shin Dong-Ho, Kim Jung-Sun, Kim Byeong-Keuk, Choi Donghoon, Hong Myeong-Ki, Jang Yangsoo
Аннотация
OBJECTIVE: The aim of this study was to investigate the association of serum cystatin C levels with contrast-induced nephropathy (CIN) and adverse clinical events in patients with peripheral artery disease (PAD).
METHODS: A total of 240 PAD patients who received endovascular therapy were included in this retrospective analysis. Serial serum levels of creatinine and cystatin C before and within 48 hours of endovascular therapy were evaluated for the incidence of CIN. The relationship between serum cystatin C levels and the incidence of major adverse events, defined as a composite of all-cause death, myocardial infarction, stroke, amputation, and target vessel revascularization, was investigated.
RESULTS: The incidence of CIN increased from 1.7% to 27.9%, depending on the quartile of baseline cystatin C level. Baseline serum cystatin C level (area under the curve of the receiver operating characteristic curve, 0.757; 95% confidence interval [CI], 0.696-0.735) predicted the incidence of CIN better than baseline serum creatinine level (area under the curve, 0.629; 95% CI, 0.563-0.691; P < .001). An elevated baseline cystatin C level was an independent predictor of CIN (hazard ratio, 14.37; 95% CI, 4.11-50.19; P < .001) and major adverse events in patients with PAD (hazard ratio, 2.57; 95% CI, 1.28-5.17; P = .008).
CONCLUSIONS: We found elevated baseline cystatin C level to be an independent risk factor for CIN and a predictor of all-cause mortality and major adverse events in patients with PAD undergoing endovascular therapy.
METHODS: A total of 240 PAD patients who received endovascular therapy were included in this retrospective analysis. Serial serum levels of creatinine and cystatin C before and within 48 hours of endovascular therapy were evaluated for the incidence of CIN. The relationship between serum cystatin C levels and the incidence of major adverse events, defined as a composite of all-cause death, myocardial infarction, stroke, amputation, and target vessel revascularization, was investigated.
RESULTS: The incidence of CIN increased from 1.7% to 27.9%, depending on the quartile of baseline cystatin C level. Baseline serum cystatin C level (area under the curve of the receiver operating characteristic curve, 0.757; 95% confidence interval [CI], 0.696-0.735) predicted the incidence of CIN better than baseline serum creatinine level (area under the curve, 0.629; 95% CI, 0.563-0.691; P < .001). An elevated baseline cystatin C level was an independent predictor of CIN (hazard ratio, 14.37; 95% CI, 4.11-50.19; P < .001) and major adverse events in patients with PAD (hazard ratio, 2.57; 95% CI, 1.28-5.17; P = .008).
CONCLUSIONS: We found elevated baseline cystatin C level to be an independent risk factor for CIN and a predictor of all-cause mortality and major adverse events in patients with PAD undergoing endovascular therapy.