MP298BIOMARKERS IN EARLY DIAGNOSTIC OF ACUTE KIDNEY INJURY IN PATIENTS WITH ACUTE CARDIORENAL SYNDROME

Abstract

INTRODUCTION AND AIMS: Acute kidney injury (AKI) is a common complication of critical illnesses and has a significant impact on outcomes, including mortality and morbidities. Unfortunately, apart from prophylactic measures, no effective treatment for this syndrome is known. Therefore, early recognition of AKI not only can provide better opportunities for preventive interventions, but also opens many gates for research and development of effective therapeutic options. Over the last few years, several new AKI biomarkers have been discovered and validated to improve early detection, differential diagnosis, and differentiation of patients into risk groups for progressive renal failure, need for renal replacement therapy (RRT), or death. These novel AKI biomarkers complement serum creatinine (SCr) and urine output, which are the standard diagnostic tools for AKI detection. To most significant biomarkers include neutrophil gelatinase-associated lipocalin (NGAL), a proinflammatory -IL-18, cystatin C and KIM-1. Explore the place biomarkers damage the heart and kidneys in the development of risk assessment, early detection and prediction of short-term outcomes of acute cardiorenal syndrome. METHODS: On admission, 109 randomly selected patients using immunoassay ELISA analysis to determine the level of biomarkers AHF / AD CHF (NT-pro BNP in serum) and kidney damage (cystatin C in serum; NGAL, KIM-1 and IL-18 in the urine). Statistical analysis was performed using statistical software application package STATISTICA-10 and SPSS -22 using standard algorithms of variation statistics. For all quantitative traits in the two groups was carried out. RESULTS: In 109 patients were examined biomarkers heart damage (NT-pro BNP) and kidney (cystatin C in serum, NGAL, and IL-18 KIM-1 in urine). Patients with AKI as compared with patients with stable renal function were detected higher levels of NGAL (p <0.001) and KIM-1 (p <0.01) in all groups, the differences of IL-18 levels in the urine and cystatin C in blood were higher in ACS without elevation ST than in patients with AD CHF (p <0.001 and p <0,01), NT-pro BNP levels were higher in ACS without elevation ST (p <0.001) in patients with AKI compared with patients with stable renal function and no difference in AD CHF group. Based on the identified association diagnostically significant markers connection with the development of renal damage AKI, all patients were divided into 4 groups depending on the level of structural damage markers (NGAL ≥60,1 ng / ml and / or a KIM-1 ≥ 0,519 ng / ml) and presence AKI: in group 1 included patients with stable renal function and the level of biomarkers following diagnosis, group 2 included patients with stable renal function and diagnostically relevant levels of biomarkers in the third group were patients with AKI and low levels of biomarkers in 4th group included patients with AKI and diagnostically relevant levels of markers The test includes two markers of kidney damage (NGAL and / or KIM-1) has 95% sensitivity and 59% specificity. CONCLUSIONS: : Patients with subclinical clinical and laboratory changes (changes in serum creatinine by 10-50% from baseline) did not differ from patients with acute kidney injury on major risk factors, hospital mortality in these patients is lower than in patients with AKI (30% and 12%, p <0.05), but higher than in the group with stable renal function. Defining two structural renal damage markers (NGAL and KIM-1) in high-risk patients to diagnose AKI 95%.