Abstract

Restless leg syndrome occurs frequently among patients with end-stage renal disease. Although the etiopathogenesis of restless leg syndrome has not been fully elucidated, advanced age, female gender, positive family history, chronic renal failure, pregnancy and folic acid and iron deficiency have all been implicated. Recent studies found a diminished ability of D2 receptors to bind ligands and reduced 18F-dopa uptake in the putamen and striatum in patients with restless leg syndrome. A marked increase in the plasma concentrations of glycation end-products was observed in uremic patients. Methylglyoxal is a major end-product of glycolysis. Methylglyoxal is a reactive carbonyl species that is formed during glucose metabolism. Methylglyoxal may increase the dopamine concentration and other toxic metabolites such as salsolinol in dopaminergic neurons and dopamine-mediated oxidative stress could contribute to damage of dopaminergic neurons.

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