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Decrease of Serum Angiotensin Converting Enzyme Levels Upon Telbivudine Treatment for Chronic Hepatitis B Virus Infection and Negative Correlations Between the Enzyme Levels and Estimated Glumerular Filtration Rates

Author(s):
Kung-Hao LiangKung-Hao Liang1,*, Yi-Cheng ChenYi-Cheng Chen1, Chao-Wei HsuChao-Wei Hsu1, Ming-Ling ChangMing-Ling Chang1, Chau-Ting YehChau-Ting Yeh2,*
1Liver Research Center, Chang Gung Memorial Hospital, Taipei, Taiwan
2Molecular Medicine Research Center, Chang Gung University, Taoyuan, Taiwan
Corresponding Authors:


Hepatitis Monthly:Vol. 14, issue 1; 15074
Published online:Jan 30, 2014
Article type:Research Article
Received:Sep 26, 2013
Accepted:Oct 31, 2013
How to Cite:Kung-Hao LiangYi-Cheng ChenChao-Wei HsuMing-Ling ChangChau-Ting YehDecrease of Serum Angiotensin Converting Enzyme Levels Upon Telbivudine Treatment for Chronic Hepatitis B Virus Infection and Negative Correlations Between the Enzyme Levels and Estimated Glumerular Filtration Rates.Hepat Mon.14(1):15074.https://doi.org/10.5812/hepatmon.15074.

Abstract

Background:

During antiviral therapy for chronic hepatitis B, renal function impairment could be a critical concern when oral nucleot(s)ide analogues were used. Paradoxically, long-term telbivudine treatment was associated with an increase of estimated glomerular filtration rate (eGFR) through unknown mechanisms.

Objectives:

We aimed to investigate changes in serum protein abundances associated with renal function in response to antiviral treatments.

Materials and Methods:

Primarily, a transcriptomic assay was performed to identify differentially expressed genes in peripheral blood cells caused by the telbivudine treatment. Two genes coding angiotensin converting enzyme (ACE) and complement factor H (CFH) were screened from 14 candidate renal function-related genes. ACE and CFH production were further investigated using enzyme-linked immunoassays.

Results:

Verification studies showed no significant change of serum CFH levels, but there was a significant reduction of serum ACE levels by continuous telbivudine treatment for 330.00 0.85 days (34 patients; paired t-test, P = 0.022). Serum HBV DNA and ALT levels also decreased (P = 0.008 and < 0.001, respectively). A significant increase in eGFR was found (33 patients, paired t-test, P = 0.002) at 708.64 31.63 days. Patients eGFRs were negatively correlated with serum ACE levels (r = -0.375, P = 0.002) but not with serum HBV DNA and ALT levels (P = 0.241 and 0.088 respectively). Significant decreases of the ACE levels were also observed upon entecavir treatment (20 patients; paired t-test, P = 0.020) at 412.88 36.92 days. No significant correlation was found between serum ACE levels and eGFRs (r = -0.239, P = 0.138) in entecavir-treated patients.

Conclusions:

We discovered a consistent reduction of serum ACE levels by two oral antiviral monotherapies, entecavir and telbivudine. Serum ACE levels were negatively correlated with eGFRs in telbivudine treated patients.

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