Acute kidney injury in hospitalized cirrhotic patients: Risk factors, type of kidney injury, and survival

Abstract

Background and aim: Acute kidney injury (AKI) is a common complication of chronic liver disease (CLD). We performed a prospective study to evaluate the risk factors and spectrum of AKI among decompensated cirrhosis (DC) patients and the impact of AKI on survival.

Methods: This study was conducted in consecutive DC patients hospitalized in SCB Medical College between December 2016 and October 2018. AKI was defined as per ICA criteria. Demographic, clinical, and laboratory parameters and outcomes were compared between patients with and without AKI.

Results: A total of 576 DC subjects were enrolled, 315 (54.69%) of whom had AKI; 34% (n = 106) had stage 1A, 28% (n = 90) stage 1B, 21% (n = 65) stage 2, and 17% (n = 54) stage 3 AKI. Alcohol was the predominant cause of CLD (66.7%). In 207 (65.7%) patients, diuretic/lactulose/nonsteroidal anti-inflammatory drugs use was noted, and infection was present in 190 (60.3%) patients. Compared to those without AKI, patients with AKI had higher leucocyte count, higher serum urea and creatinine, higher Child-Turcotte-Pugh, higher Model of End-Stage Liver Disease (MELD) scores (P < 0.001), longer hospital stay, and lower survival at 28 days and 90 days (P < 0.001). Besides, in patients with stages 1A to 3 AKI, there were differences in overall survival at 28 days (P < 0.001) and 90 days (P < 0.001).

Conclusions: Over half of DC patients had AKI, and alcohol was the most common cause of cirrhosis in them. Use of AKI-precipitating medications was the most common cause of AKI, followed by bacterial infection. AKI patients had increased prevalence of acute-on-chronic liver failure and had prolonged hospitalization and lower survival both at 28 days and 90 days.

Keywords: acute kidney injury; acute‐on‐chronic liver failure; chronic liver disease; decompensated cirrhosis.

Figure 1

(a) Etiology of cirrhosis with and without acute kidney injury. (), Alcohol; (), HBV/HCV infection; (), NASH/NAFLD; (), others. (b) Precipitants of acute kidney injury (AKI) for stages AKI 1A, 1B, 2, and 3. (), Variceal bleeding; (), diarrhoea and/or vomitting; (), infection; (), drug precipitant.

Figure 2

(a) Kaplan–Meier survival curves showed significant differences in survival between patients with acute kidney injury (AKI) 1A, AKI 1B, AKI 2, and AKI 3 and those without acute kidney injury at 28 days (log‐rank P value <0.001). () without AKI; () AKI 1A; () AKI 1B; () AKI 2; () AKI 3. (b) Kaplan–Meier survival curves showed significant differences in survival between patients with acute kidney injury (AKI) 1A, AKI 1B, AKI 2, and AKI 3 and those without acute kidney injury at 90 days (log‐rank P value <0.001). () without AKI; () AKI 1A; () AKI 1B; () AKI 2; (), AKI 3. (c) Receiver operating characteristic curves (AUROC) for prognostic parameters for 28‐day survival in patients with AKI. (), Admission serum urea; (), admission serum creatinine; (), infection; (), variceal bleeding; (), diarrhoea/vomiting; (), normal creatinine/reversal of AKI; (), reference line. (d) Receiver operating characteristic curves (AUROC) for prognostic parameters for 90‐day survival in patients with AKI.