Chronic renal failure is characterized by abnormalities in
glucose metabolism. In fact there are present a normal fasting plasma
glucose level )or mild
hyperglycemia) in the presence of
hyperinsulinemia, blunted decrease in the plasma
glucose concentration in response to exogenous
insulin administration, and diminished effect of intravenous
insulin on
glucose uptake in forearm perfusion studies. The
glucose intolerance is not the result of reduced insulin secretion, or circulating
insulin antagonists, and does not correlate with the coexisting
metabolic acidosis.
Glucose intolerance exists because the peripheral
insulin-sensitive tissue (muscle, adipose tissue, liver) of the patients with
chronic renal failure are
insulin resistant. However there are two subgroups of uremic patients with regard to
glucose tolerance: about half of uremic patients can augment their insulin secretion sufficiently to maintain normal
glucose tolerance despite
glucose intolerance. In the other half, insulin secretion following
glucose loads is not different from normal values, so that
glucose intolerance results. The cause of the peripheral
insulin resistance remain unclear. Besides deranged renal function can result in the development of
hypoglycemia. The most important predisposing mechanism to
hypoglycemia is diminished
glucose availability due to substrate limitation; the second important mechanism (alcohol,
insulin,
propranolol, etc.). Finally, in
chronic renal failure persistent
hyperinsulinemia can contribute
hyperlipemia and to high incidence of
cardiovascular disease.