Profile, risk factors and outcome of acute kidney injury in paediatric acute‐on‐chronic liver failure. (12th February 2018)

• Record Type: Journal Article
• Authors: Lal, Bikrant B.; Alam, Seema; Sood, Vikrant; Rawat, Dinesh; Khanna, Rajeev
• Is Part Of: Liver international. Volume 38:Number 10(2018)
• Page Start: 1777
• Page End: 1784
• Publication Date: 2018-02-12
• Subjects: hepatorenal syndrome -- outcome -- paediatric ACLF -- wilson disease; Liver -- Periodicals; Liver -- Diseases -- Periodicals; 616.362
• DOI: 10.1111/liv.13693
• Languages: English
• ISSNs: 1478-3223

Abstract

Abstract: Background & Aims: There are no studies on acute kidney injury in paediatric acute‐on‐chronic liver failure. This study was planned with aim to describe the clinical presentation and outcome of acute kidney injury among paediatric acute‐on‐chronic liver failure patients. Methods: Data of all children 1‐18 years of age presenting with acute chronic liver failure (Asia pacific association for the study of the liver definition) was reviewed. Acute kidney injury was defined as per Kidney Diseases—Improving Global Outcomes guidelines. Poor outcome was defined as death or need for liver transplant within 3 months of development of acute kidney injury. Results: A total of 84 children with acute‐on‐chronic liver failure were presented to us in the study period. Acute kidney injury developed in 22.6% of patients with acute‐on‐chronic liver failure. The median duration from acute‐on‐chronic liver failure to development of acute kidney injury was 4 weeks (Range: 2‐10 weeks). The causes of acute kidney injury were hepatorenal syndrome (31.6%), sepsis (31.6%), nephrotoxic drugs (21%), dehydration (10.5%) and bile pigment related acute tubular necrosis in one patient. On univariate analysis, higher baseline bilirubin, higher international normalized ratio, higher paediatric end stage liver disease, presence of systemic inflammatory response syndrome and presence of spontaneous bacterial peritonitis had significant association with presence of acute kidney injury. On logistic regression analysis, presence of systemic inflammatory response syndrome (adjusted OR: 8.659, 95% CI: 2.18‐34.37, P = .002) and higher baseline bilirubin (adjusted OR: 1.07, 95% CI: 1.008‐1.135, P = .025) were independently associated with presence of acute kidney injury. Of the patients with acute kidney injury, 5(26.3%) survived with native liver, 10(52.6%) died and 4 (21.1%) underwent liver transplantation. Conclusion: Acute kidney injury developed in 22.6% of children with acute‐on‐chronic liver failure. Bilirubin more than 17.7 mg/dL and presence of systemic inflammatory response syndrome were high risk factors for acute kidney injury. Development of acute kidney injury in a child with acute‐on‐chronic liver failure suggests poor outcome and need for early intervention.