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Kidney Week

Abstract: PO0456

Hypophosphatemia as a Surrogate Marker of Renal Outcome in Chronic Hepatitis B Patients Receiving Antiviral Therapy

Session Information

Category: CKD (Non-Dialysis)

  • 2101 CKD (Non-Dialysis): Epidemiology, Risk Factors, and Prevention

Authors

  • Park, Mee yeon, Samsung Medical Center, Gangnam-gu, Seoul, Korea (the Republic of)
  • Jeon, Junseok, Samsung Medical Center, Gangnam-gu, Seoul, Korea (the Republic of)
  • Lee, Jung eun, Samsung Medical Center, Gangnam-gu, Seoul, Korea (the Republic of)
  • Huh, Wooseong, Samsung Medical Center, Gangnam-gu, Seoul, Korea (the Republic of)
  • Kim, Yoon-Goo, Samsung Medical Center, Gangnam-gu, Seoul, Korea (the Republic of)
  • Kim, Dae joong, Samsung Medical Center, Gangnam-gu, Seoul, Korea (the Republic of)
  • Lee, Hyun Suk, Samsung Medical Center, Gangnam-gu, Seoul, Korea (the Republic of)
  • Jang, Hye Ryoun, Samsung Medical Center, Gangnam-gu, Seoul, Korea (the Republic of)

Group or Team Name

  • Division of Nephrology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
Background

Antiviral therapy is crucial for the treatment of chronic hepatitis B (CHB). Although hypophosphatemia has been known to be an important adverse effect of antiviral agents, the clinical significance is yet to be revealed. In this study using a large cohort of CHB patients, the incidence and clinical significant of hypophosphatemia was investigated.

Methods

CHB patients who started antiviral therapy between 2005 and 2015, and had received at least one year of therapy, were included after excluding liver cirrhosis, diabetes mellitus, hypertension, concomitant administration of diuretics, and ESRD. Hypophosphatemia was defined as serum phosphorous level ≤ 2.5mg/dL. The primary outcome was changes in renal function. Secondary outcomes included the incidence of infection and changes in serum potassium, uric acid, and total carbon dioxide (tCO2)

Results

Of the 4,335 patients, hypophosphatemia developed in 75 patients (1.7%). When patients were categorized depending on the change of serum phosphate level, median phosphate level of 728 patients (16%) decreased by more than 0.5mg/dL from the baseline. During the 2-year follow-up period, patients with hypophosphatemia showed lower eGFR compared to the control group. Also, patients whose serum phosphate level decreased by more than 0.5mg/dL showed significantly lower eGFR compared to the control group at all time points. The incidence of infection and changes in serum potassium, uric acid, and tCO2 were similar between groups.

Conclusion

Hypophosphatemia was associated with renal function decline in CHB patients receiving antiviral therapy. Although the incidence of hypophosphatemia during antiviral therapy was relatively low, our results support the clinical significance of hypophosphatemia as a surrogate marker of adverse renal outcome in CHB patients.