Chronic hepatitis C infection more than doubles the risk of kidney disease for people with HIV

Michael Carter
Published: 18 July 2012

A detectable hepatitis C viral load is associated with an increased risk of chronic kidney disease for people with HIV, European investigators report in the online edition of AIDS.

Patients with ongoing hepatitis C replication were significantly more likely to develop chronic kidney disease, compared to HIV-positive people who were hepatitis C-uninfected or who had cleared hepatitis C.

“The incidence of CKD [chronic kidney disease] was similar between patients with resolved HCV [hepatitis C virus] infection and in anti[body]-HCV negative patients, while patients with chronic HCV infection had a two-fold increased incidence of CKD compared with anti-HCV negative patients,” write the authors.

Kidney disease remains an important cause of serious illness and death in people with HIV. Earlier research has shown that people with antibodies to hepatitis C virus infection are between 50 and 75% more likely to develop chronic kidney disease than HIV-positive people who were not co-infected with hepatitis C.

The impact of ongoing replication of hepatitis C virus on the progression of kidney disease in co-infected patients is uncertain. Therefore, investigators from the EuroSIDA cohort designed a study involving 8235 patients who received care after 2004.

These patients were divided into three groups according to their hepatitis C infection status:

  • Hepatitis C antibody-negative.
  • Hepatitis C antibody-positive/hepatitis C RNA-negative (cleared hepatitis C infection).
  • Hepatitis C antibody-positive/hepatitis C RNA-positive (chronic hepatitis C infection).

Chronic kidney disease was defined as having either an estimated glomerular filtration rate (eGFR) of or below 60 ml/min/1.73 m2 for patients with an eGFR above this level at baseline, or a confirmed 25% decline in eGFR for patients with a baseline measurement of or below 60 ml/min/1.73 m2.

Rates of progression to chronic kidney disease were compared according to the participants’ hepatitis C infection status. The investigators also conducted analyses to see if any other factors were associated with the development of kidney disease.

A quarter of participants were hepatitis C antibody-positive at baseline. Approximately half (48%) of these people were hepatitis C RNA-positive; 9% had cleared their hepatitis C virus infection and 43% had no RNA data available.

During a total of 36,123 person-years of follow-up, a total of 495 patients (6%) progressed to chronic kidney disease. The overall incidence was 13.7 per 1000 person-years of follow-up.

Incidence differed according to hepatitis C infection status.

It was lowest (7.8 per 1000 person-years) in people who had never been infected with hepatitis C. Incidence among patients who had cleared hepatitis C infection was 14.5 per 1000 person-years, and this increased to 18.7 per 1000 person-years for co-infected patients with ongoing hepatitis C replication.

Treatment with the anti-HIV drugs tenofovir (Viread, also in Truvada, Atripla and Eviplera), atazanavir (Reyataz) and lopinavir/ritonavir (Kaletra) were all associated with the development of kidney disease.

“Current guidelines from the European AIDS Clinical Sciety recommend that HIV patients initiating ART that includes one of these drugs should be monitored more frequently for the development of CKD,” emphasise the researchers.

There was also a significant association between diabetes and the development of renal problems (p < 0.0001).

The investigator found that, overall, people with antibodies to hepatitis C (RNA-negative and RNA-positive) were almost twice as likely to progress to chronic kidney disease as hepatitis C uninfected individuals (IRR = 1.85; 95% CI, 1.49-2.30; p < 0.0001).

However, further analysis showed that it was only people with detectable hepatitis C RNA who had an increased risk of kidney disease.

Incidence of kidney disease was comparable between hepatitis C-uninfected participants and the participants who had cleared hepatitis C virus infection.

Compared to these people, a hepatitis C viral load below 500,000 iu/ml increased the risk of progression to chronic kidney disease by 88% (IRR = 1.88; 95% CI, 1.31-2.71; 0 = 0.0006). The risk was even higher for patients with a hepatitis C viral load above 500,000 iu/ml (IRR = 2.10; 95% CI, 1.54-2.87; p < 0.0001).

“These results indicate that the hepatitis C virus itself is a significant risk factor for the development of CKD in HIV co-infected patients,” comment the investigators.

The risk of kidney disease was not affected by hepatitis C genotype.

“If our results are confirmed by others, future larger studies are warranted to explore the reversibility of CKD in patients undergoing anti-HCV therapy,” conclude the investigators. The authors suggest that studies could also “investigate the interaction between HIV/HCV co-infection and certain antiretroviral drugs known to be nephrotoxic”.


Peters L et al. HCV viremia increases the incidence of chronic kidney disease in HIV-infected patients. AIDS, online edition. DOI: 10.1097/QAD.0b013e3283574e71, 2012.

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