BACKGROUND: Recent research has shown cystatin C to predict mortality and cardiovascular morbidity independent of renal function. The aim of this study was to evaluate the prognostic value of cystatin C on mortality in adult general ICU patients with acute kidney injury (AKI). We later expanded the study and included patients without signs of AKI. METHODS: A total of 845 ICU patients were analysed for cystatin C and classified according to the RIFLE criteria. Of these, 271 patients with either creatinine >150 micromol/l, urea >25 or anuria/oliguria entered the AKI cohort. The remaining 562 patients entered the non-AKI cohort. Both cohorts were divided into quartiles according to cystatin C at entry. In the non-AKI cohort, we split the highest cystatin C quartile into two. The relationship between the different cystatin C quartiles and mortality in patients with and without AKI was estimated by hazard ratios (HR) derived from the Cox proportional hazards regression model. RESULTS: A relationship between cystatin C and mortality was found in patients with and without AKI, being stronger in patients without AKI. In AKI patients, the HR comparing cystatin C above and below the median more than doubled from the second year on compared to the first year follow-up. After exclusion of patients in the non-AKI cohort with 'potential AKI' (creatinine >100 micromol/l or urea > 20 mmol/l), the correlation between cystatin C levels and risk of death was strengthened. CONCLUSIONS: Cystatin C is correlated with mortality independently of renal function measured by creatinine in patients entering the general ICU.
BACKGROUND: Recent research has shown cystatin C to predict mortality and cardiovascular morbidity independent of renal function. The aim of this study was to evaluate the prognostic value of cystatin C on mortality in adult general ICU patients with acute kidney injury (AKI). We later expanded the study and included patients without signs of AKI. METHODS: A total of 845 ICU patients were analysed for cystatin C and classified according to the RIFLE criteria. Of these, 271 patients with either creatinine >150 micromol/l, urea >25 or anuria/oliguria entered the AKI cohort. The remaining 562 patients entered the non-AKI cohort. Both cohorts were divided into quartiles according to cystatin C at entry. In the non-AKI cohort, we split the highest cystatin C quartile into two. The relationship between the different cystatin C quartiles and mortality in patients with and without AKI was estimated by hazard ratios (HR) derived from the Cox proportional hazards regression model. RESULTS: A relationship between cystatin C and mortality was found in patients with and without AKI, being stronger in patients without AKI. In AKI patients, the HR comparing cystatin C above and below the median more than doubled from the second year on compared to the first year follow-up. After exclusion of patients in the non-AKI cohort with 'potential AKI' (creatinine >100 micromol/l or urea > 20 mmol/l), the correlation between cystatin C levels and risk of death was strengthened. CONCLUSIONS:Cystatin C is correlated with mortality independently of renal function measured by creatinine in patients entering the general ICU.
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