Among the variegate interrelationships which link PTH secretion and nephrolithiasis, the present paper deals first with the problem of stone formation in patients suffering from primary hyperparathyroidism (PHP) and secondly with the troublesome issue of parathyroid secretion in stone formers with hypercalciuria. As regards the first problem, the conclusion is that no definite difference has been as yet described between PHP patients with and without stones, which could explain why some of these patients form stones and others do not. So it might be arguable that increased urinary excretion of lithogenetic promotors (namely calcium and oxalate) might simply unmask an underlying (inherited?) defect which is the real cause of the urolithiasis. Addressing the second problem, the paradoxical tale of secondary hyperparathyroidism accompanying hypercalciuria which, as studies continue, changes into hypoparathyroidism, is briefly traced. In fact, most of the recent data concur in defining the presence of reduced PTH levels, together with fasting hypercalciuria and reduced mineral bone density. However, the real cause of these findings is still a matter of debate.
|Number of pages||5|
|Journal||Italian Journal of Mineral and Electrolyte Metabolism|
|Publication status||Published - Jun 1996|
- parathyroid hormones
ASJC Scopus subject areas