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

Circulating levels of immunoreactive parathyroid hormone (PTH) were measured in 40 patients with idiopathic hypercalciuria (IH) before and during reversal of hypercalciuria with thiazide, and in four normal subjects before and during induction of hypercalciuria with furosemide. 26 patients with IH had elevated serum PTH levels. The remaining patients had normal levels. Although the correlation was not complete, high PTH levels were generally found in patients who had more severe average urinary calcium losses. When initially elevated. PTH levels fell to normal or nearly normal values during periods of thiazide administration lasting up to 22 months. When initially normal, PTH levels were not altered by thiazide. Reversal of hyperparathyroidism by thiazide could not be ascribed to the induction of hypercalcemia, since serum calcium concentration failed to rise in a majority of patients. Renal hypercalciuria produced by furosemide administration elevated serum PTH to levels equivalent to those observed in patients with IH. The findings in this study help to distinguish between several current alternative views of IH and its relationship to hyperparathyroidism. Alimentary calcium hyperabsorption cannot be the major cause of IH with high PTH levels, because this mechanism could not elevate PTH. Idiopathic hypercalciuria cannot be a variety of primary hyperparathyroidism, as this disease is usually defined, because PTH levels are not elevated in all patients and, when high, are lowered by reversal of hypercalciuria. Primary renal loss of calcium could explain the variable occurrence of reversible hyperparathyroidism in IH, since renal hypercalciuria from furosemide elevates serum PTH in normal subjects. Consequently, a reasonable working hypothesis is that IH is often due to a primary renal defect of calcium handling that leads, by unknown pathways, to secondary hyperparathyroidism.
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PMID:Evidence for secondary hyperparathyroidism in idiopathic hypercalciuria. 468 79

The pathogenesis of renal calculi is reviewed in general terms followed by the results of investigation of 439 patients with renal calculi studied by the author at Toronto General Hospital over a 13-year period. Abnormalities of probable pathogenetic significance were encountered in 76% of patients. Idiopathic hypercalciuria was encountered in 42% of patients, primary hyperparathyroidism in 11%, urinary infection in 8% and miscellaneous disorders in 8%. The incidence of uric acid stones and cystinuria was 5% and 2% respectively. In the remaining 24% of patients in whom no definite abnormalities were encountered the mean urinary magnesium excretion was less than normal. Of 180 patients with idiopathic hypercalciuria, only 24 were females. In the diagnosis of hyperparathyroidism, the importance of detecting minimal degrees of hypercalcemia is stressed; attention is also drawn to the new observation that the upper limit of normal for serum calcium is slightly lower in females than in males. The efficacy of various measures advocated for the prevention of renal calculi is also reviewed. In the author's experience the administration of thiazides has been particularly effective in the prevention of calcium stones. Thiazides cause a sustained reduction in urinary calcium excretion and increase in urinary magnesium excretion. These agents also appear to affect the skeleton by diminishing bone resorption and slowing down bone turnover.
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PMID:Renal calculi. 543 66

Currently, four hypotheses attempt to explain the pathogenesis of idiopathic hypercalciuria. Proposed theories include hypersecretion of parathyroid hormone, hyperabsorption of calcium by the gastrointestinal tract, hyperreabsorption of calcium by the kidney, and hyperexcretion of phosphate by the kidney. These hypotheses are more descriptive than explanatory. A new hypothesis is suggested which encompasses the divergent findings. Idiopathic hypercalciuria may result from hypersecretion of parathyroid hormone which is active at the gastrointestinal and bone target site but is partially defective at its renal site of action.
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PMID:The pathogenesis of idiopathic hypercalciuria: an alternative hypothesis. 629 43

Idiopathic hypercalciuria (IH) was diagnosed in 11 children aged 5 3/12 to 10 6/12. Eight patients investigated 1-12 years later still had hypercalciuria. When compared to a control group of 10 healthy children, 5 patients demonstrated an excessive rise in urinary Ca excretion following an oral Ca load. These patients also demonstrated low urinary cAMP, normal serum iPTH and high normal iTCT levels. The remaining 3 patients responded normally to Ca loading, but otherwise showed similar metabolic findings as the above group. These findings suggest a hyperabsorptive mechanism for all our patients. The finding of relatively low values for TmP/GFR in most IH patients further suggests that here, as in many adult patients, this may be the primary pathogenic mechanism, causing low serum P, increased synthesis of 1,25 dihydroxyvitamin D and, thus, absorption of Ca. We believe this represents a physiologic variant state and not a disease state.
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PMID:Pathophysiologic studies in idiopathic hypercalciuria presenting in childhood. 631 14

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

Idiopathic hypercalciuria is a cause of a variety of urinary tract complaints in clinical pediatrics. These include gross or microscopic hematuria, enuresis, urinary frequency or urgency, dysuria, sterile pyuria, and proteinuria in addition to renal calculi. A random urine calcium-creatinine concentration ratio can be used to initially screen for hypercalciuria. Patients with indeterminate results should have the test repeated, while those with abnormal values should receive a complete metabolic workup to determine the cause of hypercalciuria. Identifiable causes of hypercalciuria should be treated specifically, and thiazide diuretics are the preferred treatment for uncomplicated renal calculi. Pharmacotherapy in children with idiopathic hypercalciuria and symptomatology other than renal stones is controversial and should be limited to patients with severe clinical manifestations.
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PMID:Hypercalciuria in clinical pediatrics. A review. 636 1

An oral calcium loading test was performed on 55 patients with upper urinary tract stones to find absorptive or renal hypercalciuria. The mean urinary calcium excretion level of this patient group was significantly greater than that of a control group of 10 patients without abnormal upper urinary tract. Idiopathic hypercalciuria defined as more than 250 mg per day in males and more than 200 mg per day in females was observed in 13 patients; 4 patients with absorptive hypercalciuria, 6 patients with renal hypercalciuria and 3 patients of origin-unknown hypercalciuria. Five of the 6 patients with renal hypercalciuria had recurrent and/or multiple urolithiasis. From these results, this test was considered to be useful in the discrimination between absorptive and renal hypercalciuria.
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PMID:[Studies on an oral calcium loading test in upper urinary tract stone formers]. 648 63

Seven children with asymptomatic gross hematuria are described. Six had recurrent hematuria; one had a single episode. Occasional global glomerulosclerosis and/or mesangial electron dense deposits were present in the three patients in whom renal biopsy was performed; the changes were felt to be insufficient to account for the hematuria. None of the patients had urolithiasis or any significant urinary tract abnormality. One was an adopted child; a family history of urolithiasis was obtained in the other six. Idiopathic hypercalciuria was documented in six patients; the seventh subsequently passed a calcium oxalate calculus. One patient is 10 weeks of age at the time of this submission. Of the remainder, three patients received no specific therapy; renal calculi developed six months, six years, and eight years later. Three patients were treated with a thiazide diuretic soon after onset of hematuria and confirmation of idiopathic hypercalciuria; there was complete cessation of hematuria within five days with no recurrence as long as therapy was continued. We suggested that measurement of urinary calcium excretion as part of the initial evaluation of a child with gross hematuria may, in some cases, obviate invasive investigations and allow for effective therapy.
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PMID:The association of idiopathic hypercalciuria and asymptomatic gross hematuria in children. 729 44

Calcium oxalate nephrolithiasis is a common syndrome that recurs and may be complicated by infection, obstruction, bleeding, and rarely, impairment in renal function. The formation of Ca oxalate stones depends on the state of urinary supersaturation with respect to Ca and oxalate and the action of urinary inhibitors of crystal nucleation, aggregation, and growth. Idiopathic hypercalciuria is the most common cause of Ca oxalate stones and is characterized by hypercalciuria, normocalcemia, and intestinal Ca hyperabsorption with or without elevated serum 1,25(OH)2D3 levels in the absence of other known causes of hypercalciuria. Current diagnostic evaluation of recurrent Ca oxalate nephrolithiasis should be conducted while the patients follow their usual diets and includes the following: 1. Analysis of stone composition by polarization microscopy. 2. Measurement of serum Ca, phosphate, uric acid, 1,25(OH)2D3, and creatinine. 3. Twenty-four-hour urine collection for an analysis of volume, pH, and excretion of Ca, phosphorus, magnesium, uric acid, citrate, sodium, oxalate, and creatinine. Therapy to prevent stone recurrence is designed to reduce urinary supersaturation of Ca oxalate by increasing urine volume, reducing urine Ca to below 200 mg/24 hr with thiazide, maintaining dietary Ca intake at 600 to 800 mg/day, and adding potassium citrate if urine citrate levels are reduced. If elevated, urine oxalate excretion can be reduced by dietary oxalate restriction. Stones less than 2 cm in diameter located in the renal parenchyma or upper urinary tract can be fragmented with ESWL, whereas larger stones or those in the lower urinary tract should be removed by either percutaneous nephrolithotomy or ureteroscopic procedures.
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PMID:Diagnosis and treatment of calcium kidney stones. 767 Oct 93

We report the results of an oral tolerance test performed in 317 patients with kidney stones. In order to avoid PTH or AMPc measurements, and therefore to reduce costs and time to get the results, we measured the tubular maxima of phosphate per glomerular filtration rate (TmP04/GFR, the phosphate threshold). Urine collections from 7 to 9 h and from 9 to 13 h were obtained. The samples were analyzed for calcium, creatinine and phosphorus content. All patients ingested 1 g of calcium mixed in a meal at 9 o'clock. Venous blood samples were obtained for calcium, creatinine and phosphorus measurements, previous to the calcium ingestion. Urinary calcium to creatinine ratio, before and after the calcium-load, as well as TmP04/GFR were calculated. In 97 subjects (30.8%) there were no calcium metabolism abnormalities. Idiopathic hypercalciuria was present in 183 (57%) and primary hyperparathyroidism in 37 (11.7%). Idiopathic hypercalciuria was classified in four subgroups: absorptive hypercalciuria with normal serum phosphorus, absorptive hypercalciuria with low serum phosphorus (renal phosphate leak), renal hypercalciuria with normal phosphorus and renal hypercalciuria with low serum phosphorus.
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PMID:[Usefulness of oral calcium test in renal lithiasis]. 792 97


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