P2759Value of biomarkers (urinary KIM-1, NGAL, albumin, serum Cys C) for predicting renal lesions and prognosis in patients with infective endocarditis

Abstract Background Infective endocarditis (IE) is frequently complicated by kidney damage of various pathogenesis. The essential differences in pathophysiological mechanisms of kidney lesions (glomerular and tubular damage, mixed mechanisms) create different therapeutical targets. Nowadays these mechanisms are only possible to differentiate with the use of nephrobiopsy or autopsy. Non-invasive methods to assess the genesis of kidney damage are eagerly wanted. It is possible that kidney biomarkers may be such method. Materials and methods 209 patients with verified IE (DUKE 2009, 2015), hospitalized and treated in city clinical hospital named after V.V. Vinogradov in Moscow from January 2010 to June 2018, were included in the study. Kidney function was assessed using CKD-EPI formula. Acute kidney injury (AKI) and acute kidney disease (AKD) were diagnosed according to current guidelines (KDIGO 2012) and the work group consensus (ADQI 16 Workgroup 2017). Serum creatinine decrease on ≥26,5 mcmol/L in 48 hours after the hospitalization was counted as early-onset AKI. Patients with serum creatinine elevation on ≥26,5 mcmol/L in 48 hours during the hospitalization were diagnosed with late-onset AKI. Biomarkers were assessed at the admission. Cystatin C level was assessed in serum; neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule 1 (KIM-1), albumin levels were assessed in urine. Results Kidney damage biomarkers' levels were analyzed in 65 patients with IE. Patients with kidney dysfunction (n=45) comparing to ones without AKI (n=20) had higher mean value of all kidney biomarkers, however, the significant difference was established only for cystatin C. (1.9 vs 1.3 mg/l respectively; p<0.001). Patients with early-onset AKI (n=11) next to patients without AKI had significantly higher cystatin C value at admission (1.9 vs 1.3 mg/l respectively; p=0,0186). In similar manner patients with late-onset had had significantly higher cystatin C value at admission (1.9 vs 1.3 mg/l respectively; p=0,002). Cystatin C appeared to be an independent AKI predictor with threshold value 1.35 mg/l (OR 14.0; 95% CI 1.74–112.2; p=0.013), and also cystatin C was an independent predictor of the in-hospital mortality with threshold 1.87 mg/l (OR 3.16; 95% CI 1.25–7.99; p=0.006). After analysis of patients with AKD it was established that they had significantly higher levels of cystatin C (1.7 vs 1.3 mg/l respectively; p=0.035) and NGAL (19 vs 1.9 ng/ml; p=0.05) in comparison with patients without AKD. Albumin and KIM-1 didn't show significant associations. Conclusions The results of a study allow to consider serum cystatin C as AKI marker, AKI predictor and in-hospital mortality predictor in patients with IE, and urinal NGAL and serum cystatin C may be considered as AKD markers.