Evaluation of Long-Term Outcomes of Direct Acting Antiviral Agents in Chronic Kidney Disease Subjects: A Single Center Cohort Study

Abstract

Background: The chronic kidney disease (CKD) population, including kidney transplant recipients (KTRs) and subjects on renal replacement therapy, is particularly vulnerable to unfavorable outcomes from chronic hepatitis C (CHC). Currently, there are oral direct-acting antiviral agents (DAAs) available to eradicate the virus with favorable short-term outcomes; however, their long-term effects are lacking. The aim of the study is to assess the long-term efficacy and safety of DAA therapy in the CKD population.

Methods: An observational, cohort single-center study was performed. Fifty-nine CHC subjects with CKD, treated with DAAs between 2016 and 2018, were enrolled in the study. Safety and efficacy profiles were assessed, including sustained virologic response (SVR), occult hepatitis C infection (OCI) incidence, and liver fibrosis.

Results: SVR was achieved in 96% of cases (n = 57). OCI was diagnosed only in one subject following SVR. Significant liver stiffness regression was observed 4 years after SVR compared to baseline values (Mdn = 6.1 kPa, IQR = 3.75 kPa; 4.9 kPa, IQR = 2.9 kPa), p < 0.001. The most common adverse events were anemia, weakness, and urinary tract infection.

Conclusion: DAAs provide a safe and effective cure for CHC in both CKD patients and KTRs with a favorable safety profile in the long-term follow-up.

Keywords: chronic infection; direct-acting antiviral agents (DAA); hemodialysis; hepatitis C infection (HCV); kidney transplantation; liver fibrosis; occult hepatitis C infection; treatment efficacy.

Scheme 1

Study population.

Figure 1

Distribution of serum creatinine concertation (mg/dL) at baseline, EOT (end of treatment), and 1, 2, and 4 years following sustained virologic response (SVR).

Figure 2

Distribution of the estimated glomerular filtration rate (eGFR, mL/min/1.73 m²) at baseline, end of treatment (EOT), and 1, 2, and 4 years following sustained virologic response (SVR).

Figure 3

Distribution of LS (kPa) parameters at baseline and 4 years after the end of treatment (EOT).

Figure 4

Distribution of the Fibrosis Index Based on 4 Factors (FIB-4) score at baseline, end of treatment (EOT), and 1, 2, and 4 years following sustained virologic response (SVR).

Figure 5

Distribution of the aspartate aminotransferase-to-platelet ratio (APRI) score at baseline, end of treatment (EOT), and 1, 2, and 4 years following sustained virologic response (SVR).

Figure 6

Predictions of ΔE values from the fitted regression model based on baseline LS concentration and patient’s treatment-experienced factor.

Figure 7

Fibrosis distribution at baseline and at 4 years after end of treatment (EOT).