Utility of Fractional Excretion of Urea in Diagnosing Etiology of AKI in Cirrhosis

Background: Acute kidney injury is present in a third of hospitalized patients with cirrhosis. AKI in cirrhosis can be functional (Pre renal azotemia and Hepatorenal syndrome) or structural (Acute tubular necrosis). Distinguishing the precise etiology of AKI in cirrhosis remains a clinical challenge. Fractional excretion of sodium as a marker of functional AKI has several limitations. Aim: To diagnose etiology of AKI in patients with cirrhosis admitted in a tertiary care hospital using fractional excretion of urea. Methods: Single centre cross sectional observational study. Forty consecutive patients with cirrhosis and AKI admitted to the hospital were included. AKI was diagnosed as per ICA-AKI/adapted KDIGO criteria. Creatinine and urea in serum and urine were measured within 24 hours of admission. Fractional excretion of urea was calculated. FEUrea >33% ,<21% and between 21% and 33% indicated ATN,HRS and PRA respectively. Patients were classified as having functional AKI or structural AKI Results: Forty patients with cirrhosis and AKI were included in the study. Alcohol was the most common etiology (42.5%). Commonest etiology of AKI was ATN (52.5%) followed by PRA (25%) and HRS (22.5%).ATN was higher in patients of CHILD C cirrhosis and sarcopenia but the association did not reach statistical significance. FEUrea was significantly higher among patients of ATN than HRS & PRA (45.36±11.89 vs 19.71±7.89, P=0.0001). FEUrea > 30 correctly differentiated ATN from HRS and PRA within 24 hours of admission with 100% sensitivity and 78.9% specificity. FEUrea < 13.5 differentiated HRS from non HRS with a sensitivity of 44% and specificity 100%. Conclusion: FEUrea has excellent diagnostic ability in differentiating structural (ATN)from functional AKI.(PRA or HRS). FEUrea may guide therapeutic intervention in patients with cirrhosis and AKI