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Hepatitis B virus infection and development of chronic kidney disease: a cohort study
Yun Soo Hong1, Seungho Ryu2,3,4, Yoosoo Chang2,3,4
1Departments of Epidemiology and Medicine, and Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA.
Insights
Chronic hepatitis B virus (HBV) infection, indicated by hepatitis B surface antigen (HBsAg) positivity, is linked to an increased risk of developing chronic kidney disease (CKD), primarily due to higher rates of proteinuria.
Area of Science:
- Nephrology
- Hepatology
- Epidemiology
Background:
- The association between chronic hepatitis B virus (HBV) infection and chronic kidney disease (CKD) risk remains debated.
- Hepatitis B surface antigen (HBsAg) serology is a key indicator of HBV infection.
Purpose of the Study:
- To investigate the prospective relationship between HBsAg serology status and the incidence of CKD.
- To clarify the impact of chronic HBV infection on kidney disease development.
Main Methods:
- A large cohort study involving 299,913 adults in South Korea without pre-existing CKD.
- Incident CKD was defined by reduced estimated glomerular filtration rate (eGFR < 60 mL/min/1.73m²) and/or proteinuria.
- Follow-up spanned January 2002 to December 2016, accumulating over 1.67 million person-years.
Main Results:
- HBsAg-positive individuals showed a significantly higher hazard ratio (HR) for incident CKD (1.11; P=0.01).
- The increased CKD risk was driven by a higher incidence of proteinuria (HR=1.23; P<0.001), not by a reduced eGFR.
- Associations remained consistent across different baseline liver enzyme levels.
Conclusions:
- HBsAg positivity is associated with an elevated risk of incident CKD, specifically linked to proteinuria.
- Chronic HBV infection may be a contributing factor to the rising prevalence of CKD.
Background:
The effect of chronic hepatitis B virus (HBV) infection on the risk of chronic kidney disease (CKD) is controversial. We examined the prospective association between hepatitis B surface antigen (HBsAg) serology status and incident CKD in a large cohort of men and women.
Methods:
Cohort study of 299,913 adults free of CKD at baseline who underwent health screening exams between January 2002 and December 2016 in South Korea. Incident CKD was defined as the development of an estimated glomerular filtration rate (eGFR) < 60 ml/min/1.73m2 and/or proteinuria.
Results:
Over 1,673,701 person-years of follow-up, we observed 13,924 incident cases of CKD (3225 cases of eGFR < 60 ml/min/1.73m2 and 11,072 cases of proteinuria). In fully adjusted models comparing positive to negative HBsAg participants, the hazard ratio (HR, 95% confidence interval) for incident CKD was 1.11 (1.03-1.21; P = 0.01). The corresponding HR for incident proteinuria and for eGFR < 60 ml/min/1.73m2 were 1.23 (1.12-1.35; P < 0.001) and 0.89 (0.73-1.07; P = 0.21), respectively. The associations were similar across categories of liver enzyme levels at baseline.
Conclusion:
In this large cohort, HBsAg positive serology was associated with higher risk of incident CKD, and we provide novel evidence that this association was due to a higher incidence of proteinuria in HBsAg positive participants. Our study adds to the growing body of evidence suggesting that chronic HBV infection may be a contributor to the increasing incidence of CKD.
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