Abstract
Hypoparathyroidism is known to be one of the causes of aplastic bone disease in patients on chronic hemodialysis (HD). However, little is known about the precise mechanism and clinical characteristics of hypoparathyroidism. We investigated the clinical characteristics of hypoparathyroidism in HD patients employing a cross-sectional and retrospective longitudinal study. Eighty HD patients were divided into 3 groups according to the levels of serum intact-PTH; low PTH group (<50pg/ml, 34 cases), medium PTH group (50-150pg/ml, 23 cases), and high PTH group (>50pg/ml, 23 cases). There were no differences in age or gender among the 3 groups. The duration of HD was shorter in the low PTH group than in the high PTH group (p<0.01). There were no differences in the doses of calcium carbonate, vitamin D therapy, serum Ca, or P among the 3 groups. Serum 1, 25-dihydroxyvitamin D in the low PTH group was not different from those of the other 2 groups. Serum aluminum in the low PTH group was lower than those of the other 2 groups (p<0.05). The bone mineral density at the distal radius measured by DXA was similarly decreased after the start of HD in all 3 groups, based on cross-sectional study. The retrospective longitudinal study of microdensitometry of thehand demonstrated progressive decreases and there were no differences among the 3 groups. The retrospective longitudinal study of c-terminal PTH demonstrated that there were no differences in c-PTH among the 3 groups until 5 years after the start of HD. These data demonstrated that hypoparathyroidism does not differ in terms of clinical characteristics, other than a briefer duration of HD and a lower serum level of aluminum, and that hypoparathyroidism in HD patients does not affect bone mineral density. Furthermore, we cannot discriminate hypoparathyroidism from potential secondary hyperparathyroidism until 5 years after the start of HD. The pathogenesis of hypoparathyroidism remains unkown, but these observations suggest that undefined factors, of which the effects manifest 5 years after the start of HD, play some role in the development of this disorder.
