A Clinical Study on Acute Kidney Injury in Cirrhotic Patients

Abstract

BACKGROUND The increased propensity for acute kidney injury (AKI) in patients with cirrhosis stems from haemodynamic abnormalities typical for patients with cirrhosis and ascites. 15 which is due to development of portal hypertension and portosystemic collaterals with splanchnic and systemic vasodilatation, resulting in decrease in effective arterial blood volume with increase in renin angiotensin-aldosterone system (RAAS), sympathetic nervous system and non-osmotic release of antidiuretic hormone causing sodium retention, increased intravascular volume, and a hyperdynamic circulatory state, 16 complemented with increased production of nitric oxide which is considered the main cause of vasodilatation in cirrhosis. Mechanism of renal dysfunction in cirrhosis includes portal hypertension & its accompanying haemodynamic abnormalities15 leading to increased synthesis of endogenous vasodilatory compounds such as nitric oxide leading to vasodilatation in splanchnic & systemic arterial systems ultimately leading to activation of reninangiotensinogen–aldosterone system causing compensatory renal vasoconstriction & hypo-perfusion resulting into renal failure. We wanted to study the clinical profile of patients with AKI who presented to a tertiary care hospital in Bangalore. METHODS Ninety-four patients of either gender admitted in the department of gastroenterology at a tertiary care hospital with age > 18 years with either diagnosed or newly diagnosed case of cirrhosis of liver (including both compensated & decompensated cases) admitted with acute kidney injury diagnosed according to International Club of Ascites Classification were enrolled in this study. The sample size was based on number of eligible patients admitted to tertiary care hospital during the study period. Details of the study were explained to them and consent was taken either from the patient or their attender. RESULTS Most patients were in the age group > 60 yrs. with 32 male patients (45.07 %) in the age group of 40 - 60 years & 13 female patients (56.52 %) in the age group of > 60 yrs. 78.7 % of patients developed AKI before hospital admission i.e., at community level; whereas 21.3 % of patients developed AKI after hospital admission i.e., they had normal creatinine level on admission. CONCLUSIONS Pre renal AKI was the most common cause of AKI followed by hepatorenal syndrome & acute tubular necrosis (ATN) comprising 52.1 %, 28.7 % & 19.1 % respectively. KEYWORDS AKI, Cirrhosis, ATN