Chronic kidney disease in children is an irreversible process that may lead to
end-stage renal disease. The mortality rate in children with
end-stage renal disease who receive dialysis increased dramatically in the last decade, and it is significantly higher compared with the general pediatric population. Furthermore, dialysis and transplant patients, who have developed
end-stage renal disease during childhood, live respectively far less as compared with age/race-matched populations. Different reports show that
cardiovascular disease is the leading cause of death in children with
end-stage renal disease and in adults with childhood-onset
chronic kidney disease, and that children with
chronic kidney disease are in the highest risk group for the development of
cardiovascular disease.
Urea, which is generated in the liver during catabolism of
amino acids and other nitrogenous metabolites, is normally excreted into the urine by the kidneys as rapidly as it is produced. When renal function is impaired, increasing concentrations of blood
urea will steadily accumulate. For a long time,
urea has been considered to have negligible toxicity. However, the finding that plasma
urea is the only significant predictor of aortic plaque area fraction in an animal model of
chronic renal failure -accelerated
atherosclerosis, suggests that the high levels of
urea found in chronic dialysis patients might play an important role in accelerated
atherosclerosis in this group of patients. The aim of this review was to provide novel insights into the role played by
urea in the pathogenesis of accelerated
cardiovascular disease in
renal failure.