It is common knowledge that diabetes is the leading cause of chronic kidney disease (CKD). In fact, 44% of patients in need of dialysis had diabetes, according to a CDC (Centers for Disease Control) report in 1999. The 2016 report published in the Journal of the American Medical Association also showed that 1 in 4 diabetic adults have kidney disease.
Recent studies, however, revealed that the opposite is also true. That is, chronic kidney disease may also cause diabetes.
Dr. Vincent Poitout, Director of the University of Montreal Hospital Research Centre (CRCHUM), principal investigator, and researcher of the study conducted by a team from the CRCHUM said that “We identified molecular mechanisms that may be responsible for increased blood glucose levels in patients with non-diabetic chronic kidney disease. Our observations in mice and in human samples show that the disease can cause secondary diabetes.”
His colleague and postdoctoral fellow, nephrologist Laetitia Koppe backed the statement with proof of abnormal blood sugar levels in test subjects (mice). Experiments were conducted to find answers as to why half of the people affected by chronic kidney disease show abnormal levels of blood sugars.
It was observed that impaired insulin secretion from pancreatic beta cells was found in the mice. The same observations that were seen in diabetic patients. When samples of pancreatic cells were taken from patients with chronic kidney disease, the same abnormalities were discovered.
Dr. Koppe explained, “We conducted experiments in mice and found impaired insulin secretion from pancreatic beta cells, as observed in diabetes. We observed the same abnormalities in samples of pancreatic cells from patients with chronic kidney disease.”
Understanding the Link Between CKD and Diabetes
The study showed that urea is directly to blame for impaired secretion of insulin among CKD patients. While urea is presented in nephrology textbooks as harmless, the inability of a kidney to filter and eliminate in CKD increases the risk of impaired insulin secretion.
Drs. Koppe and Poitout also identified phosphofructokinase 1, a particular protein that is found at the heart of pancreatic beta cells and which function is affected by increased urea in blood, a common occurrence for patients with chronic kidney disease.
According to them, “Increased urea causes impaired insulin secretion from the pancreatic beta cells. This creates oxidative stress and excessive glycosylation of phosphofructokinase 1, which causes an imbalance of blood glucose and may progress to diabetes.”
Why Establishing the Link Matters
The study reveals a link between CKD and diabetes instead of just a novel mechanism.
Although further studies need to be conducted to ensure that the findings are valid in humans, earlier data and observations highlight the need for patients with non-diabetic chronic kidney disease to take preventive measures against developing secondary diabetes.
As what Dr. Poitout pointed out, “If our observations are confirmed, it will mean that patients with non-diabetic chronic kidney disease are at risk of developing diabetes. One might then suggest therapeutic approaches, such as taking antioxidants, which may protect pancreatic beta cells and reduce the risk of developing diabetes.”
People with CKD who are aware of the study will be encouraged to seek treatment for kidney disease as well. By keeping urea under control, diabetes may be kept at bay.
Some of the treatments include keeping a tight control on blood pressure and blood glucose, and following a low-protein diet to mitigate macroalbuminuria or having huge amounts of protein in the urine.
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