Diabetes is a frequent cause of end stage renal disease (ESRD) in the dialysis population. It is known that the diabetic patients with ESRD on maintenance haemodialysis have lower values of parathyroid hormone (PTH) than non-diabetics. DM involves multiple pathological manifestations. The most familiar laboratory finding is hyperglycaemia in the presence or absence of hypoinsulinaemia. Therefore Sugimoto and his colleagues sought to clarify whether high glucose and/or lack of insulin modulate PTH secretion. Patients with DM usually have hypomagnesaemia, a factor which known to interfere with PTH synthesis. The effect of hypomagnesaemia on PTH is controversial. In vitro studies showed that a reduction in extracellular magnesium concentration stimulated the secretion of PTH in the absence of changes in calcium concentration Severe hypomagnesaemia impairs the secretion and biologic action of PTH and increases metabolism of PTH. Magnesium depletion may also cause decreases in both osteoblast and osteoclast activity and lead to a form of adynamic bone disease.Also, studies with bovine parathyroid cell cultures have shown PTH inhibition with an excess glucose or deficit of insulin. Thus, it appears that both factors are independent. Other studies have reached the conclusion that DM may result in a state of resistance to action of PTH in addition to down regulation of receptors of PTH.