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

Malignancy is the most common cause of hypercalcemia, which may result from direct involvement of bone or from local or distant production of substances that enhance bone resorption. The recognized incidence of primary hyperparathyroidism has increased greatly since the advent of automated biochemical screening. A single parathyroid adenoma is most frequently the cause. Sarcoidosis commonly results in hypercalciuria but seldom causes sustained hypercalcemia. Increased production of 1,25-dihydroxycholecalciferol leads to hyperabsorption of calcium and enhanced bone resorption.
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PMID:Evaluation of the hypercalcemic patient. 721 54

10 patients with normocalcemic secondary hyperparathyroidism due to renal hypercalciuria and 1 patient with normocalcemic primary hyperparathyroidism are presented. The diagnostic criteria of both manifestations of disturbed calcium metabolism are outlined. Successful therapeutic approach depends on the exact discrimination between each form of normocalcemic hyperparathyroidism.
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PMID:Normocalcemic hyperparathyroidism. 728

Fifty patients with primary hyperparathyroidism were studied with an oral calcium-tolerance test, measurements of plasma levels of vitamin D metabolites, and determination of calcium excretion on both a low-normal (400 mg) and high-normal (1000 mg) calcium intake. There were strong positive correlations between plasma levels of 1,25-dihydroxyvitamin D (1,25(OH)2D) and both the calciuric response to the calcium-tolerance test (r = +0.75, P less than 0.001) and calcium excretion on the 1000-mg calcium diet (r = +0.65, P less than 0.001). The patients were classified into two subpopulations: 30 patients showed hyperabsorption with the calcium-tolerance test, striking hypercalciuria, marked elevations in plasma 1,25(OH)2D, and a high incidence (19 of 30 patients) of renal stones; 20 patients had a normal response to the tolerance test, normocalciuria, normal or high-normal plasma 1,25(OH)2D, and a low incidence of stones (three of 20 patients). The findings emphasize the importance of circulating 1,25(OH)2D in the pathogenesis of hypercalciuria and stone formation in primary hyperparathyroidism.
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PMID:The importance of circulating 1,25-dihydroxyvitamin D in the pathogenesis of hypercalciuria and renal-stone formation in primary hyperparathyroidism. 735 50

A standard oral calcium loading test has been employed in a group of idiopathic hypercalciuria (IH) subjects and in a group of marginally hypercalcaemic subjects with primary hyperparathyroidism (PHPT) in whom the diagnosis was revealed by careful combined measurements of serum ionized calcium and immuno-reactive parathyroid hormone (iPTH). Initial values for serum ionized calcium and creatinine clearance were similar in IH and in a control group of normal subjects, whereas iPTH levels were normal or low. Following oral loading, serum ionized calcium rose to similar levels in both IH and control subjects, with no suggestion of relative hypercalcaemia due to a postulated intestinal hyperabsorption in the IH group. A renal tubular calcium 'leak' was however clearly evident in the IH group, in both the fasting and post-absorptive phase. In the marginally hypercalcaemic PHPT subjects on the other hand, a relative post-absorptive hypercalcaemia was clearly apparent, as well as a gross renal tubular calcium leakage. Thus careful preliminary separation of masked PHPT from IH subjects is an essential step before evaluation of response to oral calcium challenge in stone-forming subjects. When this is done, no evidence of a relative post-absorptive hypercalcaemia can be seen in the residual IH group, and hypercalciuria appears to be 'renal' rather than 'absorptive' in origin.
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PMID:The pathogenesis of idiopathic hypercalciuria: evidence for renal tubular calcium leak. 743 29

A 51-year-old man has had absorptive hypercalciuria and corticosteroid-responsive hypercalcemia for at least 12 years. There has been no clinical or laboratory proof of primary hyperparathyroidism, hypervitaminosis D, or other known causes of hypercalcemia and absorptive hypercalciuria. Hypercalciuria as well as the elevated serum level of calcium and 1 alpha, 25(OH)2D fell to normal during treatment with corticosteroids. The disturbed calcium metabolism in this patient is characteristic of that observed in sarcoidosis, but extensive studies have failed to uncover evidence of this condition.
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PMID:Corticosteroid-responsive hypercalcemia with elevated serum 1-alpha, 25 dihydroxyvitamin D. 743 65

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, 10.15 to 10.95 mg/dL), often accompanied by very substantial hypercalciuria. Stone disease was of equal severity in these 30 patients and in the 18 with more pronounced hypercalcemia (serum calcium level above 11 mg/dL). In all 48 patients, recurrent stone formation was virtually abolished by parathyroidectomy.
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PMID:Hyperparathyroidism in nephrolithiasis. 743 44

Among 52 patients with recurrent renal calcium stones submitted for neck exploration 12 had adenomas, 23 hyperplasia and only 17 histologically normal parathyroid glands. These patients were selected for surgery despite a normal mean value of the total serum calcium concentration because they had, in most cases, indirect evidence of parathyroid hyperfunction such as intermittent hypercalcaemia (in 25 of the patients), hypercalciuria or a pathological response to calcium infusion. It is suggested that the patients with adenomas suffered from primary hyperparathyroidism (HPT), which however did not cause persisting hypercalcaemia. It seems likely that parathyroid hyperplasia either was a mild or an early form of primary HPT or secondary to increased calcium losses. In this study, no single laboratory feature could clearly separate the different groups. None of the patients with adenomas formed any new stone during follow-up (2-7 years) and also 40% of those with hyperplasia appeared to experience benefit from surgery. This benefit was more common in those with occasionally raised serum calcium values. In cases with borderline hypercalcaemia HPT is common and is cured by parathyroidectomy. However, in clinical practice the differential diagnosis may be difficult. In cases without firm evidence of HPT a conservative approach is favoured. Thiazides appear to reduce the stone recurrence rate in most euparathyroid patients and will probably help to unmask borderline HPT in recurrent renal stone formers.
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PMID:Clinical effects of parathyroid surgery in normocalcaemic patients with recurrent renal stones. 746 37

The aetiology of nephrolithiasis was investigated in 32 north Indian children (25 boys, 7 girls, mean age 7.9 +/- 3.3 years). An underlying disorder was detected in 16 (50%) patients and included idiopathic hypercalciuria (8 patients), hyperoxaluria (3 patients) and renal tubular acidosis, primary hyperparathyroidism and hyperuricosuria (1 patient each). Magnesium ammonium phosphate calculi were found in 2 patients with recurrent urinary tract infections, 1 of whom had a duplex pelvic collecting system. In 16 patients (50%) a cause for renal calculi was not identified. Our findings suggest that an underlying disorder is present in a large proportion of children with nephrolithiasis where appropriate treatment may be beneficial.
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PMID:Aetiology of nephrolithiasis in north Indian children. 757 12

Primary hyperparathyroidism often presents with minimal symptoms. Surgery has been advocated for those patients who are severely hypercalcemic, are young, have reduced bone density or reduced renal function, and have marked hypercalciuria. The natural history of primary hyperparathyroidism and the basis for these recommendations are discussed.
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PMID:Indications for surgery in patients with minimally symptomatic primary hyperparathyroidism. 774 51

Evaluations of 1,270 patients with recurrent nephrolithiasis in an outpatient setting were analyzed for the purpose of updating the classification of nephrolithiasis. All but 4% had abnormal urinary biochemistry that placed them into one or more of 20 etiologic categories. A single diagnosis was documented in 41.3% of patients. The remaining 58.7% had more than one diagnosis. Hypercalciuric calcium (Ca) nephrolithiasis, encountered in 60.9% of patients, comprised six variants--absorptive hypercalciuria Type I and II, renal hypercalciuria, primary hyperparathyroidism, and unclassified hypercalciuria (renal phosphate leak and fasting hypercalciuria). Hyperuricosuria Ca nephrolithiasis (HUCN) and gouty diathesis (GD) accounted for 35.8% and 10.0% of patients, respectively. Distinguishing features were hyperuricosuria and normal urinary pH in HUCN, and normal urinary uric acid and low urinary pH (< 5.5) in GD. Hyperoxaluric Ca nephrolithiasis, occurring in 8.1% of patients, was subdivided into enteric, primary, and dietary variants. Hypocitraturic Ca nephrolithiasis affected 28% of patients in its idiopathic variant. Many of these patients' problems were probably dietary in origin, while some could have had incomplete renal tubular acidosis. Hypocitraturia due to renal tubular acidosis or chronic diarrheal syndrome affected only 3.3% of patients. Hypomagnesiuric Ca nephrolithiasis, infection stones, and cystinuria were uncommon, accounting for 6.8%, 5.9%, and 0.9% of patients, respectively. The acquired problem of low urine volume (< 1 L/d) was found in 15.3% of patients. The remaining 3.5% of patients were difficult to classify despite the presence of abnormal urinary biochemistry.
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PMID:Ambulatory evaluation of nephrolithiasis: an update of a 1980 protocol. 782 19


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