P-22 URINARY BIOMARKER NEUTROPHIL GELATINASE-ASSOCIATED LIPOCALIN (NGAL) FOR IDENTIFYING ACUTE KIDNEY INJURY IN PATIENTS WITH SEVERE ALCOHOLIC HEPATITIS AND CIRRHOSIS

Conflict of interest

No

Introduction and Objectives

Patients with hepatic cirrhosis (HC) and severe alcoholic hepatitis (AH) are at risk of developing acute kidney injury (AKI) due to multiple factors. The main phenotypes of AKI include hypovolemic, acute tubular necrosis (ATN), hepatorenal syndrome (HRS), and miscellaneous types. The urinary biomarker Neutrophil Gelatinase-Associated Lipocalin (NGAL) may be useful for differential diagnosis, as it is an early-produced protein at the renal tubular level.

The objective of this study is to establish the correlation between urinary biomarker NGAL levels and the phenotype of acute kidney injury in cirrhotic patients with severe alcoholic hepatitis.

Patients / Materials and Methods

Descriptive, retrospective, and analytical study of patients with a diagnosis of severe alcoholic hepatitis with cirrhosis, acute kidney injury classified by AKI-ICA (Acute Kidney Injury Criteria-International Club of Ascites), and urinary NGAL values. Three groups were compared: one with hypovolemic AKI, the second group with ATN-type AKI, and a control group of 55 patients with non-alcoholic cirrhosis and ATN-type AKI. Statistical analysis: Data are presented as Mean ± SD or Median (IQR 25-75). Univariate analysis was conducted to compare AKI phenotypes (hypovolemic, ATN, and non-alcoholic etiology ATN with a cohort of 55 patients) with MELD and Child-Pugh as cofactors; significance was considered at ≤ 0.05.

Results and Discussion

A total of 102 patients were included with an average age of 45 (39.7-51) years; 93 (91.17%) were men and 9 (8.82%) were women. Cirrhosis was classified as Child-Pugh A: 4 (3.92%), B: 5 (4.9%), and C: 93 (91.17%). Severe Alcoholic Hepatitis had a MELD score of 32 (26-39) points, a modified Maddrey score of 58.9 (44.9-102.2) points, an ABIC (Age-Bilirubin-INR-Creatinine) score of 8.5 ± 1.4 points, and a Glasgow score of 9 (8-10) points. Acute kidney injury was present in 74.5% (n=76) of cases with the following AKI-ICA grades: 1A: 9 (8.82%), 1B: 9 (8.82%), 2: 17 (16.66%), and 3: 41 (40.19%). The phenotypes were: Hypovolemic AKI: 50 (65.78%), Acute Tubular Necrosis (ATN): 23 (30.26%), and Hepatorenal Syndrome: 3 (3.94%).

The mean NGAL levels for the acute kidney injury phenotypes were hypovolemic 79.64 ± 61.73, ATN 857.79 ± 914.95, and non-alcoholic etiology ATN 743.09 ± 971.39. Significant differences were found between groups F(74,1)=30.54 p≤.001; comparisons between groups were important for hypovolemic acute kidney injury vs. ATN p≤.001; hypovolemic acute kidney injury vs. non-alcoholic ATN p≤.001, and not significant between ATN groups p=0.806 (Figure 1).

Conclusions

There is a relationship between urinary biomarker NGAL values and the hypovolemic acute kidney injury phenotype compared to ATN in cirrhotic patients with severe alcoholic hepatitis and ATN of other etiologies; it is an early biomarker of renal damage useful for establishing severity and prognosis.

Figure 1. Univariate analysis of AKI phenotypes (hypovolemic, ATN, and Non-alcoholic ATN etiology) with NGAL values.