Hypercalciuria is seen in -
<p>Primary hyperparathyroidism is a generalized disorder of calcium, phosphate, and bone metabolism due to an increased secretion of PTH. The elevation of circulating hormone usually leads to hypercalcemia and hypophosphatemia. There is great variation in the manifestations. Patients may present with multiple signs and symptoms, including recurrent nephrolithiasis, peptic ulcers, mental changes, and, less frequently, extensive bone resorptionHypercalcemia in vitamin D intoxication is due to an excessive biologic action of the vitamin, perhaps the consequence of increased levels of 25(OH)D rather than merely increased levels of the active metabolite 1,25(OH) 2 D (the latter may not be elevated in vitamin D intoxication). 25(OH)D has definite, if low, biologic activity in the intestine and bone. The production of 25(OH)D is less tightly regulated than is the production of 1,25(OH) 2 D. Hence concentrations of 25(OH)D are elevated severalfold in patients with excess vitamin D intakeIn patients with sarcoidosis and other granulomatous diseases, such as tuberculosis and fungal infections, excess 1,25(OH) 2 D is synthesized in macrophages or other cells in the granulomas.Indeed, increased 1,25(OH) 2 D levels have been repoed in anephric patients with sarcoidosis and hypercalcemia. Macrophages obtained from granulomatous tissue conve 25(OH)D to 1,25(OH) 2 D at an increased rate. There is a positive correlation in patients with sarcoidosis between 25(OH)D levels (reflecting vitamin D intake) and the circulating concentrations of 1,25(OH) 2 D, whereas normally there is no increase in 1,25(OH) 2 D with increasing 25(OH) D levels due to multiple feedback controls on renal 1a-hydroxylase(harrison 18 pg 3108)</p>
Hyperparathyroidism
VitD intoxication
Sarcoidosis
All
Endocrinology