Pancreatic Beta-cell Function in CAPD

Pancreatic beta-cell function was evaluated in uraemic patientsby measuring beta-cell peptides in the peripheral blood afterintravenous glucagon (1 mg) stimulation. Patients in chronicrenal failure, patients on haemodialysis, and both new and establishedsubjects on continuous ambulatory peritoneal dialysis (CAPD)(10in each group) were studied and compared to 8 healthy controls.Fasting glucose (3.6–4.4 mmol/1) and insulin concentrations(9.5–11.7 mU/1) were normal and did not differ betweenthe uraemic groups, but c-peptide concentrations were markedlyincreased in uraemia (1.84–2.38 nmol/1) compared to controls(0.48 nmol/1). Following glucagon stimulation an exaggeratedblood glucose response with delayed glucose peak was observed,while the peak insulin response to glucagon was normal; however,the return to basal concentrations was delayed in uraemia. Thec-peptide response was also exaggerated and peak concentrationsin uraemic subjects (3.0–4.3 nmol/1) were significantlygreater than controls (1.5 nmol/1). The response of CAPD patientswas similar to those on haemodialysis and non-dialysed uraemicpatients. The abnormalities seen were due to uraemia, and CAPDtreatment had no specific adverse effect on beta-cell function.Thus, from this data there was no evidence that CAPD per seis detrimental to beta-cell integrity.