Curing hepatitis C may help reduce kidney disease progression

People who achieved sustained virological response to interferon-based hepatitis C treatment experienced significantly less decline in kidney function, especially if they had liver cirrhosis, according to study findings presented at the 2016 AASLD Liver Meeting last month in Boston.

People with chronic hepatitis C have an increased risk of chronic kidney disease and experience more rapid kidney disease progression, though the reasons for this effect are not well understood.

Carla Rodriguez of Kaiser Permanente and colleagues compared changes in kidney function over time, and time to development of end-stage renal disease (ESRD), in people who did or did not achieve sustained response to hepatitis C treatment using interferon.

The researchers analysed changes in estimated glomerular filtration rate (eGFR), a method of estimating creatinine clearance. Levels above 90 ml/min/1.73m² are considered normal, chronic kidney disease was defined as below 60, less than 30 indicates severe kidney impairment and below 15 indicates ESRD.

The analysis included 3258 Kaiser Permanent Southern California and Mid-Atlantic members diagnosed with chronic hepatitis C between January 2004 and December 2014 who completed at least 4 weeks of treatment with interferon-based therapy, which could include the first-generation direct-acting antivirals boceprevir (Victrelis) or telaprevir (Incivo or Incivek).

About 60% of people in the cohort were men and the mean age was approximately 52 years. Nearly half were white, 29% were Hispanic and 15% were black (a group known to be at higher risk for kidney disease). Over half had hepatitis C virus (HCV) genotype 1, 19% had genotype 2 and 13% had genotype 3. About a quarter had liver cirrhosis, 13% had diabetes, 2% had co-infection with HIV and 1% also had hepatitis B.

A total of 2383 people with an assessment of sustained virological response at 24 weeks post-treatment (SVR24) were included in the ESRD analysis, and 2127 people with at least two measurements were included in the eGFR change analysis. The average follow-up period was about four years for both people who were cured and non-responders.

Overall, 63% of treated people achieved SVR using interferon-based therapy. People who achieved SVR had a significantly smaller average annual decline in eGFR compared to those who were not cured (-1.11 vs -2.32 ml/min, respectively).

This effect was especially pronounced for people with liver cirrhosis. Among people without cirrhosis, annual eGFR declines were -0.96 ml/min for those with SVR and -1.46 ml/min for those without. Among people with cirrhosis, eGFR declines were -1.58 vs -3.55 ml/min, respectively.

During follow-up 23.2% of people without cirrhosis and 27.7% of people with cirrhosis had at least a 25% decline in eGFR if they achieved SVR, compared to 27.2% and 41.9%, respectively, if they were not cured. No individuals without cirrhosis and 1.1% of people with cirrhosis progressed to ESRD if they achieved SVR, compared to 2.0% and 3.1%, respectively, without SVR. Adjusted hazard ratios for a 25% or greater decline in eGFR among people with SVR were 0.13 overall and 0.21 for those with cirrhosis.

Adjusted hazard ratios for progression to ESRD were 0.85 overall and 0.53 for people without cirrhosis.

"SVR reduced the average annual rate of renal decline by half and the risk of ESRD by almost 87%," Dr Rodriguez and colleagues concluded. "This study provides additional evidence that achieving cure of HCV infection with an interferon-based therapy results in extrahepatic benefits."

The researchers noted as a limitation that these results might not be generalisable to people cured with interferon-free direct-acting antiviral therapy, but there is little reason to think these people would not benefit as well.