<prompt> Hypercalciuria is seen in -HyperparathyroidismVitD intoxicationSarcoidosisAll  <response>: 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 25OHD rather than merely increased levels of the active metabolite 1,25OH 2 D the latter may not be elevated in vitamin D intoxication. 25OHD has definite, if low, biologic activity in the intestine and bone. The production of 25OHD is less tightly regulated than is the production of 1,25OH 2 D. Hence concentrations of 25OHD are elevated severalfold in patients with excess vitamin D intakeIn patients with sarcoidosis and other granulomatous diseases, such as tuberculosis and fungal infections, excess 1,25OH 2 D is synthesized in macrophages or other cells in the granulomas.Indeed, increased 1,25OH 2 D levels have been repoed in anephric patients with sarcoidosis and hypercalcemia. Macrophages obtained from granulomatous tissue conve 25OHD to 1,25OH 2 D at an increased rate. There is a positive correlation in patients with sarcoidosis between 25OHD levels reflecting vitamin D intake and the circulating concentrations of 1,25OH 2 D, whereas normally there is no increase in 1,25OH 2 D with increasing 25OH D levels due to multiple feedback controls on renal 1a-hydroxylaseharrison 18 pg 3108 