Therapeutic strategies in the management of secondary hyperparathyroid
ism consist of prophylactic calcitriol therapy. It increases calcium s
ensitivity of the gland, diminishes the biosynthesis of mRNA for pre-p
ro-PTHi and inhibits parathyroid cell proliferation. An early calcitri
ol therapy is preferred. Long-time studies for several years are rare.
In a long-time study for 6 years the progression of secondary hyperpa
rathyroidism and of renal osteopathy were examined in 41 patients on h
emodialysis without (n = 17) and with (n = 24) intermittent oral low-d
ose calcitriol therapy (0.25 mu g calcitriol p.o. 3 times a week). In
contrast to prior studies, patients with aluminum-containing phosphate
binders and/or diabetes mellitus were excluded, because of their lowe
r PTHi concentration. Under comparable conditions (hemodialysis parame
ter, aluminum-free phosphate binder, calcium, phosphate, creatinine, u
rea, alcaline phosphatase) patients without calcitriol therapy showed
a significant rise in PTHi concentration beginning in the third year.
Low-dose calcitriol therapy inhibited the progression of secondary hyp
erparathyroidism with no major side effects, e.g. hypercalcemia and hy
perphosphatemia. Radiological signs of renal osteopathy were more rare
than without calcitriol therapy. Conclusion. Low-dose intermittend or
al calcitriol therapy prevents progression of secondary hyperparathyro
idism without major side effects for 6 years.