Hepatitis C Increases Diabetes Risk in Kidney Transplant Recipients


New data suggest hepatitis C infection, but not hepatitis B infection, increases the prevalence of diabetes in patients who undergo kidney transplants.

Yu Mingxiang, PhD, Fudan University

Yu Mingxiang, PhD

Patients who are infected with hepatitis C virus (HCV) prior to receiving a kidney transplant face a higher risk of being diagnosed with diabetes in the years following the procedure, according to new research.

However, the same study found no such association between preoperative Hepatitis B virus and new-onset diabetes after transplantation (NODAT).

The assessment of a retrospective study involving 557 Chinese patients who underwent transplants between 1993 and 2014. Patients with preoperative HCV were 3.03 times more likely to develop NODAT than the control group, according to investigators.

“An increased incidence of diabetes in HCV-infected subjects was first noted in 1994,” wrote corresponding author Mingxiang Yu, PhD, of Fudan University, and colleagues. “Since then, the association between HCV infection and incident diabetes has been widely examined in different populations.”

Earlier research suggested that liver transplant recipients had significantly higher rates of diabetes if they also had HCV. However, Yu and colleagues said kidney transplant data was less conclusive.

All told, 21.5% of the patients in Yu’s study went on to develop diabetes following their transplants (median follow-up time = 7.5 years). In addition to finding that patients with HCV infection were more likely to develop NODAT, the authors also found that patients co-infected with HBV and HCV faced an increased incidence of NODAT. However, further analysis suggested that it was the presence of HCV infection, rather than the co-infection itself, that appeared to make diabetes more likely.

The authors said the underlying mechanism linking NODAT to HCV in kidney transplant recipients remains a mystery. However, they laid out some theories.

“Insulin resistance was believed to play a central role in the association between HCV infection and NODAT through several pathways, all of which would lead to the degradation or down-regulated expression of the insulin receptor substrate (IRS), and thus, interrupting the metabolic responses to insulin,” investigators wrote.

Further, Yu and colleagues said HCV may have an effect on beta cells that leads to an additional reduction in insulin secretion. They said immunosuppressants may also play a role. However, in contradiction to some earlier research, the authors found no link between the use of the immunosuppressant FK506 and the risk of NODAT.

While the exact cause of the correlation between HCV, kidney transplants, and diabetes remains unknown, Yu writes that the data is sufficient to warrant action on the part of physicians. It is clear, Yu and colleagues argue, is that these patients face particularly steep medical challenges.

“Therefore, it is necessary that [kidney transplant recipients] with previous HCV infection receive rigorous monitoring and screening, so that those with increased risk of NODAT can receive effective diagnosis and timely intervention to improve their long-term survival,” they concluded. “Future studies with viral load and homeostatic model assessments should investigate large populations to further confirm their diabetogenic effects.”

The study, “Effects of preoperative hepatitis B virus infection, hepatitis C virus infection, and co-infection on the development of new-onset diabetes after kidney transplantation,” was published online in the Journal of Diabetes.

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