Abstract
A case is reported in which ataxia developed during the course of chronic renal failure.
This case was characterized by basal ganglia calcification in spite of hyperparathyroidism resulting from chronic renal failure, and an increase in T cells and natural killer cells in spite of chronic renal failure.
We postulate that the ataxia may result from neurotoxic effect of parathyroid hormone, or an increase in natural killer cells which have the same antigenicity as oligodendrocytes.
