Biochemical evidence of mild hepatic dysfunction identifies decompensated heart failure patients with reversible renal dysfunction

Abstract

Background Differentiation of HF-induced renal dysfunction (RD) from irreversible intrinsic kidney disease is challenging, likely related to the multifactorial pathophysiology underlying HF-induced RD. In contrast, HF-induced liver dysfunction results in characteristic laboratory abnormalities. Given that similar pathophysiologic factors are thought to underlie both conditions, and that the liver and kidneys share a common circulatory environment, patients with laboratory evidence of HF-induced liver dysfunction may also have a high incidence of potentially reversible HF-induced RD. Methods and Results Hospitalized patients with a discharge diagnosis of HF were reviewed (n = 823). Improvement in renal function (IRF) was defined as a 20% improvement in estimated glomerular filtration rate (eGFR). An elevated international normalized ratio (INR; odds ratio [OR] 2.8; P <001), bilirubin (BIL; OR 2.2; P <001), aspartate aminotransferase (AST; OR 1.8; P =.004), and alanine aminotransferase (ALT; OR 2.1; P =.001) were all significantly associated with IRF. Among patients with baseline RD (eGFR ≤45 mL min-1 1.73 m-2), associations between liver dysfunction and IRF were particularly strong (INR: OR 5.7 [P <001]; BIL: OR 5.1 [P <001]; AST: OR 2.9 [P =.005]; ALT: OR 4.8 [P <001]). Conclusions Biochemical evidence of mild liver dysfunction is associated with reversible RD in decompensated HF patients. In the absence of methodology to directly identify HF-induced RD, signs of HF-induced dysfunction of other organs may serve as an accessible method by which HF-induced RD is recognized. © 2013 Elsevier Inc. All rights reserved.