Novel approaches to assessing renal function in cirrhotic liver disease

Abstract

Renal dysfunction is common in patients with end-stage liver disease. Etiological factors include conditions as diverse as acute tubular necrosis, immunoglobulin A nephropathy and hepatorenal syndrome. Current standard tests of renal function, such as measurement of serum urea and creatinine levels, are inaccurate as the synthesis of these markers is affected by the native liver pathology. This article reviews novel markers of renal function and their potential use in patients with liver disease.

Hepatorenal Syndrome: Diagnosis and Effect of Terlipressin Therapy in 4 Pediatric Patients

“…Although s-Cr level usually has good specificity for low GFR, it is less useful in patients with liver failure and ascites (12,13). Significant change in renal function may not be reflected in increased s-Cr value because of decreased endogenous creatinine production, poor nutrition, and decreased muscle mass.…”

Bile duct ligation in developing rats: temporal progression of liver, kidney, and brain damage

“…Symmetric dimethylarginine and its isomer, ADMA, are synthesized by different PRMT isoenzymes and released after proteolysis. Renal excretion is the most important disposal method for SDMA, a novel marker of AKI [29], whereas ADMA is primarily metabolized by DDAH. Next, our findings also supported the theory that NGAL is another promising marker of AKI in cirrhosis [30].…”

Macrophage migration inhibitory factor as a potential predictor for requirement of renal replacement therapy after orthotopic liver transplantation

“…Several limitations exist for sCr as a marker of AKI, especially in patients with ESLD. Reduced muscle mass, decreased creatinine biosynthesis, and increased serum bilirubin concentrations might produce false results . Additionally, sCr concentrations increase at a TP when renal injury is already present, and this makes it impossible to detect AKI at very early stages.…”

“…Reduced muscle mass, decreased creatinine biosynthesis, and increased serum bilirubin concentrations might produce false results. 41 Additionally, sCr concentrations increase at a TP when renal injury is already present, and this makes it impossible to detect AKI at very early stages. Despite the drawbacks of sCr as a predictor for AKI, we chose to compare the ability of plasma MIF to potentially predict severe AKI and the requirement of RRT to that of sCr.…”