[Calcium lithiasis II. Idiopathic or hypophosphatemic hypercalciuria? Vitamin D - metabolism and othophosphate therapy]

Hypophosphateamia in patients with Ca lithiasis leads to the activation of the vitamin D endocrine system: the plasma 1.25(OH)2-D3 concentration is raised. The raised 1,25(OH)2-D3 biosynthesis causes an increase in intestinal Ca absorption, which in its turn explains the hypercalciuria. The syndrome originally presented by Albright and his pupils as "idiopathic hypercalciuria" in fact corresponds to a secondary, reactive D hypervitaminosis. According to the present findings the often wrongly used term "so-called idiopathic calciuria" should be replaced by the pathogenetically correcter term "hypophosphataemic calciuria". Efficient treatment of this syndrome consists in sufficient oral orthophosphate substitution. In the interests of a better understanding as a requirement for suitable treatment of this metabolic disorder, the vitamin D metabolites and their renal key enzymes, 25-OH-Vitamin-D3-1-Hydroxylase and 25-OH-Vitamin -D3-24-Hydroxylase, are described. The hormonal control add the activation and inactivation of the vitamin D endocrine system are explained independently of the individual Ca and phosphate requirement of the organism. The dependence of renal Ca excretion on the rate of glomerular filtration is pointed out once again. The clinical-diagnostic term hypercalciuria must not be applied globally but individually. Indications, counter-indications, dosage, duration and side-effects of the orthophosphate therapy are discussed.