Why do some kidney transplant patients develop diabetes? Inflammation, researchers say

By John Murphy, MDLinx
Published June 22, 2016

Key Takeaways

A new study may explain why certain kidney disease patients develop diabetes after organ transplantation but others don’t. Researchers have found that patients who have higher levels of the inflammatory cytokine TNFα before transplantation are more likely to develop diabetes after transplantation, according to a study published online in CardioRenal Medicine.

Between 15% and 50% of kidney transplant recipients develop post-transplant diabetes mellitus (PTDM), typically in their first year after transplantation, the researchers noted.

“For patients who have received a new lease on life from a donated kidney, developing diabetes can be a major blow,” said the studys first author Maria Martinez Cantarin, MD, Assistant Professor in the Division of Nephrology at the Sidney Kimmel Medical College at Thomas Jefferson University, in Philadelphia, PA. “We hadn’t had a good sense of how diabetes could be avoided for these patients.”

To investigate the association between diabetes and organ transplantation, the researchers obtained samples of blood and visceral adipose tissue from 32 kidney transplant recipients as well as from 36 kidney donors for comparison. Of the 32 kidney recipients, 11 developed diabetes within 1 year of follow up. 

Several months after transplantation, the researchers compared plasma cytokine levels between transplant recipients and donor control subjects. They found that transplant recipients who developed PTDM had higher levels of TNFα before transplantation than transplant recipients who didn’t develop diabetes.

After the researchers adjusted for age and other confounding factors, their analysis showed that for each 25% increase in TNFα, the transplant recipients’ odds of developing PTDM doubled.

“These results suggest that elevated TNFα prior to transplant could be a predictor of subsequent PTDM,” the authors wrote.

The researchers also compared the adipose tissue samples from the transplant recipients and the donors. They found that the recipients who developed diabetes had 40% higher production of TNFα than those who didn’t. This indicated that in some patients whose fat produced high levels of the inflammatory cytokine, the fat was not protective and instead increased their chances of developing diabetes.

“These data suggest that adipose tissue inflammation contributes to the chronic inflammatory state seen in chronic kidney disease and end-stage renal disease patients,” the authors noted.

These findings are important because they change how clinicians take care of these patients, Dr. Martinez Cantarin said.

“Before, diabetes seemed like an inevitable side effect of the transplantation process,” she explained. “This study points to the idea that we may be able help the patient alter or control inflammation prior to transplantation in order to reduce the risk of developing diabetes.”

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