Dysglycaemia is under-recognised amongst patients with chronic kidney disease (CKD) and may contribute to the high cardiovascular morbidity and mortality of this patient population. Insulin resistance and impaired beta cell function contribute to dysglycaemia. The incretin effect has not been studied in CKD.
We aim to determine the prevalence of dysglycaemia in non-diabetic patients with stage 5 chronic kidney disease and end stage renal failure and calculate the incretin effect.
Non-diabetic patients with Stage 5 chronic kidney disease (CKD), end-stage renal failure on peritoneal dialysis (PD) and hemodialysis (HD) were recruited from a tertiary hospital. A comprehensive beta-cell assessment was performed, using intravenous and oral glucose testing and the incretin effect calculated. Metabolic parameters were collected and compared to healthy controls.
Baseline characteristics were similar between groups, including age, fasting glucose and BMI. There was a trend for increased impaired glucose tolerance (IGT) comparing patients with CKD (Stage 5 CKD, PD and HD, n=23) with controls (n=9) but this was not statistically significant (32% IGT in Stage 5 CKD, PD and HD vs 22% in controls, p-value from Fisher’s exact, 0.69). The incretin effect calculated via the homeostasis model assessment was not statistically significant between groups; however, comparing patients with CKD with controls, fasting cholesterol levels were higher in controls (median 4.3 in CKD vs 5.5 in controls; p-value based on Wilcoxan rank-sum test, 0.01).
In this study, there was a trend for increased impaired glucose tolerance in non-diabetic patients with different stages of chronic kidney disease, compared to controls. Further studies are needed to assess the incretin response in this cohort.