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PTU-109 Plasma Heat Shock Protein-32 Levels in Patients with Hepatitis C Virus-Related Cirrhosis: Relation to Renal Function and Hemodynamics
  1. H A El Aggan1,
  2. M I Reda2,
  3. M M Rizk3
  1. 1Department of Medicine
  2. 2Department of Radiodiagnosis
  3. 3Department of Clinical Pathology, Faculty of Medicine, University of Alexandria, Alexandria, Egypt

Abstract

Introduction Heat shock protein-32 (HSP-32) is a microsomal enzyme that has hemodynamic effects and may play a role in the pathogenesis of renal diseases. Therefore, the present work was designed to study the plasma levels of HSP-32 and its product carbon monoxide (CO) in patients with hepatitis C virus (HCV)-related cirrhosis in relation to renal function and hemodynamics.

Methods Thirty patients with HCV-related cirrhosis and 15 healthy subjects were included in the study. The severity of liver disease was assessed using Child-Pugh classification and The Model for End-Stage Liver Disease (MELD) score. Renal function was evaluated by serum creatinine (sCr) level, estimated glomerular filtration rate (eGFR) and urine sodium (UNa)concentration. Plasma HSP-32 levels were measured using commercially available enzyme-linked immunosorbant assay. Blood carboxyhemoglobin (COHB) concentration, an index of CO production, was assayed by spectrophotometry. Renal hemodynamics including renal artery peak systolic velocity (PSV), end-diastolic velocity (EDV), mean velocity (MnV), resistive index (RI) and pulsatility index (PI) and renal blood flow (RBF), were measured using Doppler ultrasonography.

Results Patients with HCV-related cirrhosis showed significant increases in plasma HSP-32 levels, blood COHB concentration and renal artery RI and PI and significant decreases in RBF and renal artery EDV and MnV compared with healthy subjects (P < 0.001) The plasma HSP-32 levels and blood COHB concentration showed positive correlations with Child-Pugh and MELD scores, sCr and renal artery RI and PI and negative correlations with eGFR, UNa concentration, RBF and renal artery EDV and MnV (P < 0.05). No correlations were found between plasma HSP-32 levels and blood COHB concentration on one hand and age of the patient, apparent duration of HCV infection and serum HCV RNA levels on the other hand (P > 0.05).

Conclusion The increased HSP-32 activity with enhanced endogenous CO generation may play an important role in renal dysfunction in HCV-related cirrhosis and could be a potential therapeutic target.

Disclosure of Interest None Declared

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