REVIEW ARTICLE Management of acute kidney injury in cirrhosis Suman Lata Nayak • Rakhi Maiwall • Ashish Nandwani • Sivaramakrishnan Ramanarayanan • R. P. Mathur • Ramesh Kumar • S. K. Sarin • Chitranshu Vashishtha Received: 25 January 2013 / Accepted: 29 June 2013 Ó Asian Pacific Association for the Study of the Liver 2013 Abstract Acute kidney injury (AKI) is a relatively fre- quent problem, occurring in approximately 20 % of hos- pitalized patients with cirrhosis. Although serum creatinine (S Cr) is the most commonly used method to determine AKI because of easy availability and low cost, practically it underestimates the extent of kidney injury in patients with chronic liver disease. AKI is defined as an abrupt rise in S Cr of 0.3 mg/dl or more ( [ 26.4 mmol/l) or an increase of 150 % or more (1.5-fold) from baseline. The cause of AKI in cirrhosis is multifactorial and is unique in terms of pathogenesis. The most common causes of AKI in cirrhosis can be subdivided into either functional or structural. The functional group includes volume-responsive (prerenal azotemia) and volume-unresponsive states (hepatorenal syndrome). Volume responsive is the most common type of AKI due to frequent use of diuretics, large volume abdominal paracentesis and gastrointestinal bleeding in patients with liver disease. The structural causes include acute tubular necrosis, tubulointerstitial and glomerular diseases. Patients with decompensated cirrhosis are in a vasodilatory state leading to a decrease in effective arterial blood volume, predisposing to AKI. Therefore, manage- ment of AKI depends on the underlying cause, and therapy should be directed toward removal of the cause. The out- come in cirrhosis when patients are on dialysis is very dismal. Every effort should be made to prevent AKI. Keywords Cirrhosis Á Acute kidney injury Á Hepatorenal syndrome Á Acute tubular necrosis Á Acute renal failure Á Chronic liver disease Abbreviations AKI Acute kidney injury HRS Hepatorenal syndrome ATN Acute tubular necrosis GI Bleed gastrointestinal bleed GFR Glomerular filtration rate S Cr Serum creatinine UNa Urinary sodium FENa Fractional excretion of sodium NE Norepinephrine OLT Orthotopic liver transplantation RRT Renal replacement therapy TIPS Transjugular intrahepatic portosystemic shunt MELD Model for End-Stage Liver Disease CLKT Combined liver–kidney transplantation NSAID Non-steroidal antiinflammatory drugs SBP Spontaneous bacterial peritonitis Introduction Acute kidney injury (AKI) occurs in up to 20 % of hos- pitalized liver disease patients and has been shown to have a significant adverse impact on patient survival depending on the type and duration of kidney injury [1]. Inclusion of serum creatinine (S Cr) as one of variables in the Model for End-Stage Liver Disease (MELD) score highlights the importance of renal function in this group of patients. AKI in cirrhotic patients is very much indicative of poor sur- vival [2]. S. L. Nayak (&) Á A. Nandwani Á S. Ramanarayanan Á R. P. Mathur Department of Nephrology, Institute of Liver & Biliary Sciences (ILBS), D-1, Vasant Kunj, New Delhi 110070, India e-mail: sumanmassu2000@yahoo.co.in R. Maiwall Á R. Kumar Á S. K. Sarin Á C. Vashishtha Department of Hepatology, Institute of Liver & Biliary Sciences, New Delhi, India 123 Hepatol Int DOI 10.1007/s12072-013-9456-x