%0 Journal Article
%T Urinary Biomarkers of Acute Kidney Injury in Patients with Liver Cirrhosis
%A Anass Ahmed Qasem
%A Salama Elsayed Farag
%A Emad Hamed
%A Mohamed Emara
%A Ahmed Bihery
%A Heba Pasha
%J ISRN Nephrology
%D 2014
%R 10.1155/2014/376795
%X Acute kidney injury (AKI) is a common complication in cirrhotic patients. Serum creatinine is a poor biomarker for detection of renal impairment in cirrhotic patients. This study aimed to evaluate urinary neutrophil gelatinase-associated lipocalin (NGAL) and urinary interleukin-18 (IL-18) as early biomarkers of acute kidney injury in cirrhotic patients. 160 patients with cirrhosis admitted to the Liver Units at Zagazig University Hospitals were classified into three groups: (I) nonascitic patients, (II) ascitic patients without renal impairment, and (III) ascitic patients with renal impairment. Patients with renal impairment were further divided into four subgroups: [A] prerenal azotemia, [B] chronic kidney disease (CKD), [C] hepatorenal syndrome (HRS), and [D] acute tubular necrosis (ATN). Significant elevation of both urinary NGAL and urinary IL-18 in cirrhotic patients with renal impairment especially in patients with ATN was observed. Urinary NGAL and urinary IL-18 have the ability to differentiate between AKI types in patients with cirrhosis. This could improve risk stratification for patients admitted to the hospital with cirrhosis, perhaps leading to early ICU admission, transplant evaluation, and prompt initiation of HRS therapy and early management of AKI. 1. Introduction Egypt was blessed with the River Nile and ancient culture but was deemed with liver diseases. Liver cirrhosis is a common disease in Egypt as Egypt has the highest incidence rate of HCV infection worldwide [1]. Acute kidney injury (AKI) in patients with cirrhosis is common. Up to 20% of hospitalized patients with cirrhosis develop AKI [2] and once AKI occurs, there is a reported fourfold increased risk of mortality [3]. Typically, patients with decompensated liver cirrhosis have significant circulatory dysfunction, which is characterized by a vasodilatory state, lower total peripheral resistance, activated renin-angiotensin-aldosterone system (RAAS), and finally renal arterial vasoconstriction [4]. In cirrhosis, AKI types include prerenal azotemia, hepatorenal syndrome (HRS), and acute tubular necrosis (ATN) with prevalence rates of 68%, 25%, and 33%, respectively, but their effect on mortality risk varies [2]. Unfortunately, these forms of AKI are difficult to distinguish clinically as serum creatinine (sCr), the clinical standard to define kidney function, poorly discriminates AKI type in cirrhosis [5]. Furthermore, various factors can affect serum creatinine in cirrhotic patients such as age, gender, nutritional status, muscle mass, and drug and volume distribution; in
%U http://www.hindawi.com/journals/isrn.nephrology/2014/376795/