EJMS

Abstract

Acute kidney injury (AKI) is a common medical condition with significant associated morbidity and mortality. It is defined by the Acute Kidney Injury Network (AKIN) as an abrupt (within 48 h) reduction in kidney function manifested by an absolute rise of serum creatinine (SCr) of at least 0.3 mg/dL (26 μmol/L) or the equivalent to a percentage increase of 50% (1.5-fold) from baseline, or a urine output < 0.5 mL/kg per hour for > 6 h. Definition of AKI still depends on the rise of SCr although this is not occur in a proper time because there is some delay from the onset of AKI. So, the physician is always delayed in both diagnostic and therapeutic intervention. After AKI kidney biomarkers that are released into the blood or urine enable earlier detection and nephrology consultation, more optimal dosing of antibiotics, avoidance of nephrotoxic agents and even earlier specific intervention. Till now, no single validated ideal biomarker for AKI. This study focused on the potential role of urinary liver fatty acid binding protein (u-LFABP) in detection of AKI in patients with liver cirrhosis compared to serum cystatin C (SCy C) and SCr. The study was carried out on 57 patients with liver cirrhosis divided into two groups: group (1) with active hematemesis (36) and group (2) stable patient with liver cirrhosis where urine and serum samples were taken at base line and 6, 12, 36 hours from hematemesis for assay. All patients (57) had Child-Pugh score: A (n=25), B (n=23) or C (n=9). Eleven (11) patients (n=11 about 30.56%) from thirty six patients with cirrhosis with active hematemesis (group 1) developed AKI based on urine output criteria, only 3 cases were based on serum creatinine. Our results show no significant difference between levels of SCyC and u-LFABP, and SCr at base line between the different studied groups (p=0. 352, 0.704, 0.094 respectively). Also there was no significant difference between levels of SCy C and u-LFABP at base line between the different stages of chronic liver disease in hematemesis group (p=0. 801 and 0.539 respectively). There was no significant difference between SCy C levels in AKI (0.905±0.11) and non AKI group (0.887±0.11) at 6 hours (p=0.396). While at 12 and 36 hours there is a significant higher level in AKI group (1.485±0.20,1.456±0.40) than non AKI (0.890±0.11, 0.893±0.11) (p=0.0001 and 0.002 respectively). At 6, 12, and 36 H. there was significant higher levels of u-LFABP in AKI group (37.475±5.17, 44±8.52 and 46.43±24.56 respectively) than non AKI group (7.429±1.19, 7.443±1.20 and 7.471±1.21 respectively) (p=0001 for all). Regarding SCr only significant higher difference between AKI (1.382±0.38) and non-AKI (0.854±0.14) appear at 36 h (p=0.001). While at 6 and 12 H there was no significant difference in AKI (0.815±0.38 and 0.936 ±0.15) and non AKI (0.837±0.14 and 0.851±0.14) (p=0.962 and 0.084) respectively). There was positive correlation between SCy C and u-LFABP in AKI group at 12 H. We concluded that in AKI u-LFABP significantly rise within 6 hours while SCy C significantly rise within 12 hours. Both of them are considered early markers of AKI. Either of both could detect subclinical AKI in cirrhotic patients before rise of SCr by 24 hours. From our results we recommend to add u-LFABP to the list of biomarkers that help in diagnosis of AKI among patients with cirrhosis. Larger studies are needed to evaluate the diagnostic and prognostic significance of biomarker levels in AKI and their role in clinical nephrology practice. A new standard definition of AKI that is not based on a change in SCr is urgently needed.