THE advent of long-term hemodialysis and renal transplantation has focused attention upon the peripheral neuropathy associated with chronic renal insufficiency.1 2 3 4 Although the initial clinical manifestations of this generally symmetrical neuropathy usually consist in painful paresthesia of the feet, progression of the neuropathy may lead to sensory deficit, loss of deep tendon reflexes and severe muscular weakness. The pathophysiology of this neuropathy is unknown; however, histologic studies have shown destruction of myelin and axon cylinders, predominantly in the distal segments of the peripheral nerve trunks.2 Prevalence of clinical neuropathy among patients managed conservatively (excluding dialysis and transplantation) has been reported as . . .
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Jebsen et al. (1967) studied this question.
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