Effects of chlorothiazide on 1,25-dihydroxyvitamin D3, parathyroid hormone, and intestinal calcium absorption in the rat.

Previous studies have shown that thiazide diuretic agents reverse secondary hyperparathyroidism and reduce circulating 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and intestinal calcium absorption rates in patients with idiopathic hypercalciuria of the renal-leak variety. We have investigated whether thiazides can reverse the secondary increase in serum parathyroid hormone (PTH) and 1,25(OH)2D3 levels or intestinal calcium absorption induced by feeding rats a diet low in calcium (LCD, 0.02% calcium) but adequate in phosphorus and vitamin D.

Formation of a single calcium stone of renal origin. Clinical and laboratory characteristics of patients.

Of 859 consecutive patients with calcium renal stones, 182 had formed only one stone before entering our program. Ninety-three (51.1%) had idiopathic hypercalciuria or hyperuricosuria; 36 (19.

Factors that predict relapse of calcium nephrolithiasis during treatment: a prospective study.

We evaluated 522 patients with idiopathic, recurrent calcium nephrolithiasis using a comprehensive clinical and laboratory protocol, and obtained additional laboratory measurements during their subsequent years of treatment in our program. In 57 patients, a new calcium stone ultimately formed during treatment (relapse), whereas 189 others have been free of recurrence during at least two years (average 4.3 +/- 2.

Effects of low-calcium diet on urine calcium excretion, parathyroid function and serum 1,25(OH)2D3 levels in patients with idiopathic hypercalciuria and in normal subjects.

We have used a low-calcium diet providing only 2 mg/kg (body weight) per 24 hours of calcium to distinguish between "renal" and "absorptive" idiopathic hypercalciuria. Sixteen of 27 hypercalciuric subjects excreted calcium in excess of intake during days seven, eight and nine of he diet, suggesting some element of renal hypercalciuria; however, all patients had low or normal serum PTH and urine cAMP levels. In general, fasting urine calcium was elevated in these 16 subjects and normal in the remaining 11, who conserved calcium more normally.

Effects of somatostatin on intestinal calcium transport in the rat.

The addition of somatostatin (SRIF) to rat descending colon in vitro increased the calcium secretory flux from serosa to mucosa (Js leads to m) and reduced tissue short-circuit current (Isc) but did not alter the absorptive flux from mucosa to serosa (Js leads to m). Js leads to m increased by 37% at 10(-9) M SRIF and by 48% at 10(-6) M. The response to SRIF was not altered by 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], and SRIF did not interfere with stimulation of calcium Jm leads to s by 1,25(OH)2D3.

Kinetic characteristics of calcium absorption and secretion by rat colon.

The kinetic characteristics of calcium active transport in rat descending colon were determined by measuring unidirectional transmural calcium fluxes in vitro. The absorptive flux from mucosa to serosa (Jm leads to s) was saturable, with a calculated affinity (Kt) of calcium for the transport system of 1.6 mM and a maximal transport capacity (Vmax) of 133 nmol.

Nephrolithiasis: causes, classification, and management.

The specific biochemical cause of calcium stone formation can now be reliably identified in close to 80% of cases. By permitting treatment to be targeted to the underlying condition, this has, in recent years, resulted in a documented reduction in stone recurrence. Less common types of nephrolithiasis--uric acid, cystine, and struvite stone formation--are also discussed and their management outlined.

Hyperparathyroidism in nephrolithiasis.

We found primary hyperparathyroidism in 56 of 1,132 consecutive patients with nephrolithiasis. We describe 48 of these patients who have undergone curative parathyroidectomy. Thirty of the 48 patients had extremely mild hypercalcemia (serum calcium level, 10.

Acclerated calcium nephrolithiasis.

Of 674 patients with calcium nephrolithiasis, 78 formed their stones in large numbers (average, 22 stones per patient) and at an accelerated rate (average, 172 stones per 100 patient-years). Although their stone disease was unusually severe, these patients had the common metabolic causes of stones and responded well to treatment. Patients with even the most extremely active calcium nephrolithiasis should be evaluated and managed in the same way as those with the common, less active form of the disease.

Uric acid saturation in calcium nephrolithiasis.

Hyperuricosuria appears to cause calcium oxalate nephrolithiasis by promoting the formation of monosodium urate or uric acid crystals, which either act as seed crystals for calcium oxalate or adsorb normally occurring macromolecular inhibitors of calcium oxalate crystallization. Both mechanisms require that hyperuricosuria cause excessive supersaturation of the urine, but this has not yet been studied under conditions of normal lifestyle. We have measured the saturation with respect to sodium hydrogen urate and the concentration of undissociated uric acid in the urine samples of 67 patients with calcium nephrolithiasis, who had idiopathic hypercalciuria, hyperuricosuria, both, or neither disorder.

Effects of diet calcium and 1,25-dihydroxyvitamin D3 on colon calcium active transport.

Unidirectional fluxes of calcium were studied in the absence of electrochemical gradients across rat descending colon segments in vitro. Dietary calcium restriction and 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]enhanced absorption by increasing the mucosal-to-serosal fluxes, whereas secretory (serosal-to-mucosal) fluxes were unchanged. Low-calcium diet also stimulated calcium uptake by everted gut sac segments of ascending as well as descending colon, whereas transverse colon was unresponsive.