Definitions

Alcoholic hepatitis was diagnosed in patients with an average alcohol intake of more than 50 g per day during the 3 months before enrollment and/or liver histologic findings consistent with alcoholic hepatitis (Mallory bodies surrounded by polymorphonuclear neutrophils) [1,2]

Maddrey’s discriminant function was calculated as [4.6 × (patient’s prothrombin time − control prothrombin time, in seconds)] + serum bilirubin level, in milligrams per deciliter.[1,2]

ABIC Score was calculated as (age x 0.1) + (serum bilirubin x 0.08) + (serum creatinine x 0.3) + (INR x 0.8). Patients were stratified based on ABIC score with low risk (6.71 points), intermediate (6.71–8.99 points), and high risk (9 points) of death. [7]

Acute Kidney Injury : According to the criteria proposed by the International Ascites Club and the Acute Dialysis Quality Initiative (ADQI) group i.e. an increase in serum creatinine level of 0.3 mg/dL(26.4 mmol/L) in less than 48 hours or a 50% increase in serum creatinine level from a stable baseline reading [8]

Staging based on AKIN criteria :defined and staged according to the AKI criteria i.e. AKI Stage 1 as an abrupt (within 48 hours) increase in serum creatinine of more than or equal to 0.3 mg/dl (≥ 26.4 μmol/l), a percentage increase in serum creatinine of more than or equal to 50% (1.5-fold from baseline) AKI Stage 2 ; increase of serum creatinine to > 200-300% from baseline, AKI Stage 3; increase of serum creatinine to > 300% from baseline or serum creatinine 4.0 mg/dL or treatment with renal replacement [3]

Progression of AKI- Progression to higher AKIN stage or need of RRT [3]

Peak AKIN stage as the highest AKIN stage reached during hospital [19]

Resolution of peak AKI stage as lowering of sCr from the baseline value or less [19]

Type 1 HRS : Rapidly progressive reduction in renal function, eg, a doubling of SCr to ≥2.5 mg/dL in less than 2 weeks and failure of renal function to improve following diuretic withdrawal and plasma volume expansion (IAC criteria) [9]

SIRS : Evidence of a systemic response to infection defined by the presence of two or more of the following signs within the previous 24 hours: fever (temperature >38.3°C) or hypothermia (rectal temperature < 35.6°C); tachycardia (heart rate of >90 beats/min); tachypnea (respiratory rate >20 breaths/min, PaCO2 <32 mm Hg) or need for invasive mechanical ventilation; alteration of the white cell count >12,000 cells/mm3, <4,000 cells/mm3 or >10% immature neutrophils (bands) [10]

Bacterial Infections were defined as proven infection based on microbiologic cultures [10]

Management of renal failure: The patients with AKI were assessed with serial creatinine till improvement and discharge or death. Baseline creatinine at the day of admission was considered for all patients for development of AKI. In the presence of AKI, attempt was made to identify the precipitating factor for AKI through a structured proforma and the hospital records. Special emphasis was given to prerenal causes i.e secondary to the use of diuretics, gastrointestinal bleed, large volume paracentesis, presence of bacterial infection, and hepatorenal syndrome. Patients were managed according to standard guidelines and in all patients with symptoms and signs suggestive of volume depletion, diuretics were withheld and plasma expansion with intravenous albumin was done with specific therapy directed to the underlying insult. Patients with hepatorenal syndrome were treated with intravenous terlipressin which was administered at a dose of 1-2mg IVq 6 h as bolus doses which was increased upto a max of 12 mg/day if baseline serum creatinine level did not improve by 25% at day 3 of therapy. Treatment with terlipressin was continued in responders (as described) until the serum creatinine level fell to <1.5 mg/dl or a maximum of 14 days.Terlipressin non-responsewas defined as failure to decrease serum creatinine to less than 50% of baseline at day 7 or no decrease at day 3 or requirement of RRT or discontinuation due to side-effects. Terlipressin was discontinued in case of severe adverse effects and patients were switched to alternative therapy with noradrenaline or renal replacement therapy. RRT was used for patients withsevere volume overload, metabolic acidosis, or hyperkalemia unresponsive to goal directed standard medical therapy as described.