Uremia is one of the most common causes of secondary restless leg syndrome (RLS), but its mechanism has not been fully elucidated so far. Functional impairment caused by diencephalic dopaminergic neuron damage, direct regulation of dyskinesia by iron deficiency and indirect regulation through the dopaminergic system, resting state caused by continuous hemodialysis, and influence on ammonium sulfate metabolism play an important role in the pathogenesis of RLS in uremia. In addition, factors such as peripheral neuropathy, calcium-phosphorus imbalance, gene, and toxin stimulation may also be involved in the development and progression of RLS in uremia.