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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined parathyroid gland function in 47 patients with idiopathic hypercalciuria in an effort to determine whether serum levels of parathyroid hormone (PTH) and/or urinary excretion of cyclic adenosine monophosphate (cyclic AMP) can discriminate between the various forms of hypercalciuria. Although we could separate our 47 patients into two groups, 21 patients with renal hypercalciuria (RH) and 15 patients with absorptive hypercalciuria (AH), there remained a group of 11 patients who did not exactly correspond to either group. Basal serum PTH was normal in the two groups: for RH, 10.32 +/- 0.93; for AH, 11.43 +/- 1.10 microliter Eq/ml. Similarly, urinary cyclic AMP did not differ between the two groups: for RH, 4.88 +/- 0.5; for AH, 4.87 +/- 0.55 nmoles/dl/min GFR. Moreover, the response of the parathyroid glands to acute hypocalcemia produced by intravenous infusion of EDTA was not different among patients with AH, RH, and control subjects. Only one patient showed a marked increase of serum PTH in response to acute hypocalcemia, and the bone biopsy revealed increased osteoclastic resorption. In conclusion, our data show that serum levels of PTH and urinary cyclic AMP do not differentiate between the various forms of idiopathic hypercalciuria. The EDTA test demonstrated that secondary hyperparathyroidism is very uncommon in these patients.
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PMID:Absence of secondary hyperparathyroidism in most patients with renal hypercalciuria. 633 Apr 24

In hypoparathyroidism the absence of parathyroid hormone leads to a reduction in the absorption of calcium by renal tubular cells. In spite of treatment with vitamin D, hypercalciuria persists and normocalcaemia can only be maintained by providing the kidney with a large load of calcium. Thiazide diuretics enhance tubular calcium reabsorption and it has been suggested that they can be used as an alternative to vitamin D. Bendrofluazide in a dose of 10 mg daily was given to 9 patients with severe hypoparathyroidism in addition to their usual treatment with calcium and vitamin D. Following the introduction of Bendrofluazide the calculated renal threshold for calcium reabsorption (TmCa/GFR) increased by a mean value of 0.14 mmol/l, and the mean rise in serum calcium was 0.13 mmol/l. This increase was due to a direct effect of the drug and was not caused by salt restriction or changes in glomerular filtration rate. The rise in serum calcium is modest compared to the rise following the introduction of vitamin D and except for patients with mild hypoparathyroidism, thiazides are not an alternative to vitamin D. They may however reduce the oral calcium load required to maintain normocalcaemia.
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PMID:Effect of bendrofluazide on calcium reabsorption in hypoparathyroidism. 648 26

A group of 121 patients with a history of multiple or complicated calcium urolithiasis were divided into three subgroups: normal, absorptive and renal/resorptive calciuria by means of a calcium-loading test. Patients with renal hypercalciuria had lower bone mineral content (BMC) than the other groups but did not differ in amount of bone or TmPO4/GFR. The 24-hour urine calcium excretion was elevated in patients with renal and absorptive type of hypercalciuria but not in patients with normal calcium-loading test and there was no correlation to BMC. The c-AMP/creatinine seemed to discriminate patients with resorptive calciuria from patients with renal calciuria. It is suggested that only patients with renal hypercalciuria should be treated with calcium-retaining drugs such as thiazides.
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PMID:Calcium-loading test and bone disease in patients with urolithiasis. 665 69

A 50-year-old Latin American man with tumoral calcinosis presented with hyperphosphatemia (6.62 +/- 1.04 SD mg/dl), elevated renal threshold phosphorus concentration (TmP) (7.3 mg/GFR), and 1,25-dihydroxyvitamin D [1,25-(OH)2D] (69 pg/ml) hypercalciuria (239 mg/day), and a high fractional intestinal calcium (Ca) absorption (0.74). Sodium cellulose phosphate therapy (20 g/day) lowered urinary Ca, and partially reduced serum phosphorus (P) and TmP to 5.91 +/- 0.63 mg/dl and 6.2 mg/GFR, respectively. Serum 1,25-(OH)2D remained elevated at 58-64 pg/ml. Amphojel therapy (4 oz/day) decreased urinary P to 23 +/- 21 mg/day and lowered serum P to 5.75 +/- 0.36 mg/dl (P < 0.05). TmP increased to a value of 8.0 mg/GFR while serum 1,25-(OH)2D continued to remain elevated at 53 pg/ml. This case illustrates the probable operation of dual abnormalities in tumoral calcinosis represented by augmented renal conservation of P and an elevation in the circulating concentration of 1,25-(OH)2D.
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PMID:Tumoral calcinosis: evidence for concurrent defects in renal tubular phosphorus transport and in 1 alpha,25-dihydroxycholecalciferol synthesis. 677 76

In ten male hypophosphataemic hypercalciuric recurrent renal stone formers with absorptive hypercalciuria and ten male normophosphataemic normocalciuric control persons, fasting plasma and urine chemistry was studied throughout the day under basal conditions and following an oral phosphorus load. After overnight fasting, plasma phosphorus and TMP/GFR were lower and urinary calcium higher in patients than in controls. Both in patients and controls, plasma phosphorus rose throughout the morning hours. In the afternoon, plasma phosphorus was almost equal in patients and controls. The circadian rise of plasma phosphorus despite no increase of urinary phosphorus argues against the presence of a fixed renal tubular phosphorus leak in absorptive hypercalciuria, at least in the fasting state. Patients differed from controls not only with respect to urinary calcium, but also with respect to fasting absolute and fractional urinary excretion of sodium and chloride. Increased fractional urinary sodium was found both in normotensive and hypertensive patients. Since tubular reabsorption of phosphorus and the setting of fasting plasma phosphorus depend, among other factors, on tubular handling of sodium, the finding may be relevant for the genesis of transient fasting hypophosphataemia in absorptive hypercalciuria.
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PMID:Is there a renal phosphorus leak in recurrent renal stone formers with absorptive hypercalciuria? 677 72

In a clinical study of 275 idiopathic stone formers the GFR was significantly raised in hypercalciuric patients compared with normal controls P less than 0.001). The possibility that the mechanism underlying hypercalciuria and raised GFR may be prostaglandin-mediated was considered because it is now well established that prostaglandins regulate intra-renal haemodynamics and influence tubular electrolyte excretion. Experiments were performed in conscious Sprague Dawley rats to determine the changes in calcium and sodium excretion following prostaglandin synthetase inhibition with indomethacin. Both calcium and sodium excretion together with urine flow were significantly reduced (P less than 0.002). Further experiments were performed in anaesthetised monkeys (Macacca fascicularis) to see if the inhibitory effect of indomethacin was reversible. Exogenous prostaglandin (PGE2) infusion resulted in a marked calciuretic response without producing changes in GFR or blood pressure. Selected hypercalciuric patients were treated with indomethacin, which resulted in a significant fall in urinary calcium excretion (P less than 0.001). This clinical and experimental study suggests that PGE2 is the hormone which determines the renal handling of calcium by controlling renal tubular function.
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PMID:The influence of renal prostaglandins on glomerular filtration rate (GFR) and calcium excretion in urolithiasis. 679

Bone mineral content (BMC) was measured with the Norland Cameron apparatus in 120 renal stone formers (RSF) with idiopathic stone disease and in 41 patients with primary hyperparathyroidism. RSF were classified, according to an oral calcium load test, into three groups: no hypercalciuria (HC; 41 cases); absorptive HC (53 cases), and resorptive or renal HC (25 cases). BMC values in RSF as a group were significantly lower than normal (p less than 0.001, Mann-Whitney test) though higher than in hyperparathyroid patients. There was a trend for BMC to decrease from male RSF without HC to patients with renal or resorptive HC. No statistical difference was found between the groups, however, BMC values in absorptive HC were different from normal (p less than 0.001). Why patients with HC are demineralized is unclear since no correlation was found between BMC and basal values of serum phosphate, TRP, calculated TmP/GFR, urinary calcium or hydroxyproline. Nevertheless our results indicate that urolithiasis, and possibly its treatment, is not a benign condition for the skeleton.
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PMID:Bone mineral content in idiopathic renal stone disease and in primary hyperparathyroidism. 682 40

Of 100 consecutive patients with recurrent renal calculi, 43 had idiopathic hypercalciuria (IH) on outpatient evaluation. Hypercalciuria was classified as diet-dependent or fasting; all patients had normal serum iPTH and urinary cyclic AMP, and serum phosphate and TmPO4/GFR were reduced in IH compared to normocalciuric stone formers. In 16 patients with IH, clearance studies revealed an elevated urine flow are factored for GFR (V/GFR) as compared with normal controls (p less than 0.05). In 12 patients, serum PTH was normally suppressed by calcium infusion but TmPO4/GFR was persistently reduced. Acute and chronic phosphate administration significantly reduced urine calcium excretion but did not correct the abnormal V/GFR. We conclude that in IH of both the fasting and the diet-dependent type, there is a defect in the proximal tubular reabsorption of sodium and fluid as well as PTH-independent tubular phosphate wasting. The proximal tubular defect is not a consequence of hypercalciuria nor of phosphate depletion but may be a cause of these abnormalities.
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PMID:Proximal tubular defects in idiopathic hypercalciuria: resistance to phosphate administration. 716 88

The patient, a 30-year-old woman, was admitted to Itoh Hospital in February, 1979 for hyperthyroidism. She had a history of pyelonephritis and recurrent urinary tract infection. Laboratory data on admission revealed overt hyperthyroidism (T3: 405 ng/dl, T4: 22.5 micrograms/dl and T3U: 57.--%), severe hypercalcemia of 12.6 mg/dl and hypercalciuria. The PSP excretion and GFR were both decreased. Serum c-PTH was nondetectable. As the thyroid function improved, there was a gradual decrease and later normalization of plasma calcium, phosphate and urinary calcium excretion. When subtotal thyroidectomy was performed on October 19, 1979, hypertrophy of the parathyroid gland was not demonstrated. In comparison with 98 other hyperthyroid patients, the pathogenesis of hypercalcemia was discussed. In conclusion, hypercalcemia in the patient, T. Y., was regarded as a kind of disequilibrium hypercalcemia which resulted from a combination of increased bone turnover and decreased calcium excretion by the kidney.
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PMID:A case report on disequilibrium hypercalcemia in hyperthyroidism. Comparison of calcium metabolism with other patients with hyperthyroidism. 717 16

Fifty-six consecutive patients with sarcoidosis, 31 subacute and 25 chronic, were investigated for abnormalities of calcium and phosphate metabolism with particular reference to parathyroid function. No abnormality of serum calcium, phosphate, creatinine or alkaline phosphatase was found. Serum levels of 25-OH cholecalciferol were normal and parathyroid hormone levels were normal in all but one patient. Maximum renal tubular reabsorption capacities for calcium and phosphate (TmCa/GFR, TmP/GFR) in relation to glomerular filtration rate in the fasting state, were abnormal in some patients but this did not correlate with any other abnormality in parathyroid function. There was significant hypercalciuria (greater than 10 mmol calcium per 24 hours) in 7.5% of our patients and this is believed to be due to increased calcium flow.
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PMID:Calcium and phosphate metabolism in sarcoidosis with particular reference to parathyroid function. 725 66


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