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

We evaluated the efficacy of selective treatment in 126 patients with recurrent calcium urolithiasis who were chosen on the basis of ability to correct underlying physiochemical disturbances. Patients with hyperparathyroidism underwent an operation. Patients with renal hypercalciuria were treated with thiazide and those with absorptive hypercalciuria were given a low calcium, low oxalate diet with or without thiazide. The only treatment for normocalciuric patients was high fluid intake, which was suggested also to the other groups. A significant individual mean reduction in stone formation was observed in all groups after 5 years of treatment. However, only 48 per cent of the normocalciuric patients were in remission after 5 years of high fluid intake therapy and 45 per cent of those with absorptive hypercalciuria were free of recurrence with diet only. Thiazide treatment seemed to be effective despite the type of hypercalciuria. The effect of the treatment on stone formation was mediated through reduction of risk factors in the urine. Conversely, a high level of risk factors commonly predicted stone recurrence.
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PMID:Five years of experience with selective therapy in recurrent calcium nephrolithiasis. 608 13

With oral furosemide administration and salt loading, urinary calcium was significantly increased in 8 normal subjects, accompanied by parallel natriuresis. In spite of the excessive calcium loss in the urine, total and ionized serum calcium remained unchanged. All subjects had significant increases in nephrogenous cyclic AMP, suggesting that parathyroid activity is elevated in subjects with furosemide-induced hypercalciuria. With furosemide, fecal calcium was significantly decreased, and resultantly, there was no significant change in the cumulative calcium balance. It is suggested that urinary calcium loss with furosemide is compensated for by secondary hyperparathyroidism via increased intestinal calcium absorption in order to maintain serum calcium at a normal level. The experimental model thus mimics the condition of the renal type of idiopathic hypercalciuria.
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PMID:Effects of oral furosemide and salt loading on parathyroid function in normal subjects. Physiological basis for renal hypercalciuria. 608 14

An increased calcium excretion in 24-hour urine was found in 32 of 42 out-patients with recurrent calcium nephrolithiasis (calcium excretion > 300 mg in males, > 250 mg in females). Subsequent hospitalization of the 32 patients revealed the following diagnosis after a calcium tolerance test: absorptive hypercalciuria in 18, renal hypercalciuria in 4, primary hyperparathyroidism in 2 and dietary hypercalciuria in 7. Normocalciuria in 10 out-patients was confirmed in 6; in one instance there was, however, primary hyperparathyroidism, in 3 there was absorptive hypercalciuria. In one patient it was not possible to classify the hypercalciuria. Total as well as nephrogenic cAMP showed wide scatter and was unsuitable, therefore, in differential diagnosis. In 2 of 3 cases of hyperparathyroidism the serum level of parathormone was distinctly elevated.
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PMID:[Diagnosis of hypercalciuria in calcium nephrolithiasis (author's transl)]. 625 Jul 84

Combined treatment with oral phosphate and 1 alpha (OH)D3 was carried out in nine children with familial hypophosphatemic rickets. All nine had positive responses over a four- to six-year period as judged by healing of rickets, change in growth rate, decrease in alkaline phosphatase activity, and symptomatic improvement. In two patients therapy was stopped for a short time because of hypercalcemia. In one patient in whom therapy was effective there was a significant reduction in creatinine clearance which necessitated cessation of treatment. The results of this study suggest that combined treatment with 1 alpha(OH)D3 and oral phosphate is an effective form of therapy for this condition, but that the balancing of these two modalities of therapy in each patient is essential if hypercalcemia and hypercalciuria, on the one hand, and secondary hyperparathyroidism, on the other, are to be avoided. A simple means of balancing these therapeutic modalities is suggested.
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PMID:Long-term treatment of familial hypophosphatemic rickets with oral phosphate and 1 alpha-hydroxyvitamin D3. 626 14

Calcium metabolism was studied in 37 patients with "idiopathic hypercalciuria" on a home diet and after 10 days of low calcium dietary intake (less than 400 mg/24h). After low calcium intake, urinary calcium excretion returned to within normal limits in 70% of the cases. In the group of patients which failed to respond to calcium restriction, TmPO4/GFR values were reduced and, furthermore, in 20% of them plasma iPTH and urinary cAMP levels were increased. These data seem to indicate that: the incidence of absorptive hypercalciuria is higher than hypercalciuria of renal origin; normocalcemic hyperparathyroidism due to primary calcium leak is present only in a limited number of cases, consequently, hypercalciuria secondary to renal phosphate leak is a rather frequent occurrence.
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PMID:Incidence of normocalcemic hyperparathyroidism in idiopathic hypercalciuria: evaluation by dietary calcium deprivation test. 626 60

Recent studies have emphasized the pathophysiological importance of circulating 1,25-dihydroxyvitamin D ((1,25-(OH)2D] in the pathogenesis of hypercalciuria and renal stone formation in primary hyperparathyroidism. Reasoning that phosphate administration might be capable of reducing the plasma concentration of 1,25-(OH)2D in patients with a prominent 1,25-(OH)2D-mediated absorptive component to their disease, 10 carefully selected patients were treated with oral phosphate (1500 mg elemental phosphorus daily) for 1 yr. Phosphate treatment significantly reduced circulating 1,25-(OH)2D levels (84 to 56 pg/ml), the calciuric response to an oral calcium tolerance test (0.30 to 0.21 delta mg calcium/dl GF), and calcium excretion on an unrestricted calcium diet (438-269 mg/day), in essence reversing the absorptive pattern of abnormalities observed before treatment. This response, however, was accompanied by an increase in biochemical hyperparathyroidism, as assessed by circulating immunoreactive PTH and nephrogenous cAMP excretion. In patients with biochemical evidence of an increase in bone resorption before therapy, histomorphometric, radiographic, and biochemical data revealed a trend toward a reduction in bone turnover during phosphorus therapy, with an apparent maintenance of coupled bone resorption and bone formation. This trend, however, was of marginal statistical significance in the patient group as a whole. It is concluded 1) that phosphate therapy represents a viable medical alternative in selected patients with primary hyperparathyroidism, 2) that the net response in treated patients is multifaceted and complex, and 3) that the efficacy of phosphate therapy will ultimately depend upon its long term effects on skeletal homeostasis.
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PMID:A detailed evaluation of oral phosphate therapy in selected patients with primary hyperparathyroidism. 630 Jan 78

Twelve children with urolithiasis or unexplained episodes of gross hematuria, hypercalciuria, and normal serum calcium levels were examined with an oral calcium loading test. Eight patients displayed elevated fasting urinary calcium excretion, consistent with renal hypercalciuria; four exhibited normal fasting calcium excretion, which increased excessively with calcium loading, suggesting hyperabsorption of intestinal calcium. Evidence of secondary hyperparathyroidism was detected in three children with renal hypercalciuria on the basis of urinary cyclic adenosine monophosphate (cAMP) excretion. Serum calcium concentrations obtained four hours after loading increased significantly in children with renal hypercalciuria and were directly correlated with fasting urinary calcium excretion. Among patients with renal hypercalciuria, serum calcium level was higher in patients with normal fasting cAMP excretion. These results suggest that hyperabsorption of intestinal calcium occurs in renal hypercalciuria and may account for the lower-than-predicted incidence of secondary hyperparathyroidism in these patients. Idiopathic hypercalciuria may arise from one fundamental metabolic disturbance with varying degrees of expression, rather than from two separate pathogenic mechanisms.
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PMID:Idiopathic hypercalciuria. Renal and absorptive subtypes in children. 632 Jun 35

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

As a part of a project performed in general practice 93 recurrent urinary stone formers were examined by means of a programme comprising a thorough medical history, clinical examination, serum determinations, a chemical stone analysis, two consecutive 24h urine collections and i.v.-pyelography. The diagnostic information obtained from the different examinations is presented. In 64 (69%) of the patients the probable aetiology of the stone formation was revealed. Twenty seven (29%) of all patients had combined aetiology. Hyperuricosuria and hypercalciuria were groups of equal size, comprising all together 45 patients, and emphasizing the necessity of 24h urine collections. Hyperparathyroidism (surgically verified) was diagnosed in four patients, based on serum calcium. Seven patients had infectious stone. It is stated that an aetiological examination of the recurrent stone former may be adequately carried out in general practice and lead to important therapeutical consequences.
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PMID:Aetiological examination of recurrent urinary stone formers in general practice. 654 32

From 1957 through 1981, 550 cervical explorations for presumed primary hyperparathyroidism were performed in 536 patients at the North Carolina Baptist Hospital. Fifty-one of those patients who did not have persistent hypercalcemia are the basis of this report. Twenty-six patients with hypercalciuria and normal renal function had recurrent passage of calcium-containing renal stones, but never had documented hypercalcemia. Only five patients (19%) had positive findings at exploration: small, hyperplastic glands (n = 3); small adenomas (n = 2). Seventeen of the 23 patients for whom follow-up data were available continued to form and pass renal stones postoperatively, including three of the five patients with "pathologic" glands (follow-up range: 4 months to 21.3 years; mean--7 years, 9 months). Twenty-five patients (also with normal renal function) had chronic calcium nephrolithiasis, hypercalciuria, and isolated or occasional elevations of serum calcium ranging from 10.6 to 10.9 mg/dl. Thirteen of these patients had abnormal parathyroid glands: adenomas (n = 12); hyperplasia (n = 1). All but two of the 13 were cured of their nephrolithiasis, but all ten of the patients with no abnormal glands for whom follow-up data were available continued to pass renal stones (follow-up range--8 months to 18 years; mean--5 years, 7 months). Thus, our experience with treating "normocalcemic" hyperparathyroidism has been disappointing. Although a substantial number of patients with occasional mild hypercalcemia may benefit from cervical exploration, those patients are not, by definition, truly normocalcemic. Metabolic evaluation can separate hypercalciuric recurrent stone formers with autonomous secondary hyperparathyroidism from patients with suppressible secondary hyperparathyroidism, and can thus more accurately identify patients who may benefit from parathyroid exploration.
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PMID:Normocalcemic hyperparathyroidism revisited. 654 87


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