Serum cystatin C in advanced liver cirrhosis and different stages of the hepatorenal syndrome

Abstract

Background and study aims The hepatorenal syndrome (HRS) is classified into two types (HRS-2 and HRS-1) based on mild or high serum creatinine elevations. Although it has been identified as an early marker of renal dysfunction, data are lacking about cystatin C across the wide range of renal changes in end-stage liver disease. This study investigates serum cystatin C and creatinine in patients with advanced liver cirrhosis and classic HRS throughout its whole spectrum. Patients and methods Serum cystatin C immunonephelometric measurements were obtained from 65 Child–Pugh C patients: 32 with normal creatinine, 17 with HRS-2 and 16 with HRS-1. The glomerular filtration rate (GFR) was estimated according to modification of diet in renal disease (MDRD) and the Hoek formulae (creatinine- and cystatin C-based, respectively) with staging of renal dysfunction severity into an increasing order from 1 to 5. Results Early HRS was identified by the raised cystatin C in 56.3% of patients having normal creatinine. Cystatin C correlated significantly with creatinine in HRS-2 ( r = 0.74; p < 0.001) and showed a significantly lower multiplication ratio (folds of rise) compared to creatinine in HRS-1 patients ( p < 0.01). There was no satisfactory agreement between MDRD and Hoek GFR staging ( k = 0.29). Conclusions The ‘early’ HRS identified by a rise in cystatin C in cases with advanced cirrhosis was found to be common and can be added to the already classified two types, as type-3 HRS. Compared to creatinine, cystatin C provides no better information in HRS-2, and underestimates the renal deterioration in HRS-1. Further studies are required to determine the course of the early HRS.