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

Effects of oral sodium cellulose phosphate therapy (5 g three times a day with meals for 4 days) on renal excretion of oxalate and on the crystallization of calcium oxalate in urine were examined in six patients with absorptive hypercalciuria on a constant metabolic dietary regimen. During treatment, urinary oxalate increased by 9-50 mg/day. However, urinary calcium decreased by 138-225 mg/day (50%-70%). Thus, the state of saturation of urine with respect to calcium oxalate decreased or did not change significantly. There was no consistent or significant change in the formation product ratio (limit of metastability) or in the crystal growth of calcium oxalate in urine.
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PMID:Effect of sodium cellulose phosphate therapy on crystallization of calcium oxalate in urine. 24 92

A longitudinal 9-year retrospective study of 24-hour urinary calcium values has been made in a metabolic stone clinic amongst patients with idiopathic hypercalciuria. No seasonal variations could be observed in contrast ot a previous study from Leeds, A prospective longitudinal study was made of 24-hour urinary calcium values in a small group of normal subjects. No seasonal variation could be ovserved. In the prospective study no seasonal variations in urinary oxalate could be observed. In a 2-year longitudinal study of stone patients with idiopathic hypercalciuria, urinary oxalate was found to be higher in the summer than in the winter. This was attributed to the combination of a higher intake of oxalate-rich foods in the summer, and the low calcium diet with which they were treated.
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PMID:Seasonal variations in urinary excretion of calcium and oxalate in normal subjects in patients with idiopathic hyperclaciuria. 31 63

Catecholamines induce bone resorption and hypercalcaemia by the beta-adrenergic effect in bone and hypercalciuria by the alpha adrenergic effect in kidney. The interplay between the alpha-adrenergic hypercalciuria and beta-adrenergic hypercalcaemia explains why in some, but not all, phaeochromocytomas hypercalcaemia occurs. The hypothesis predicts hypercalciuria in both phaeochromocytoma and neuroblastoma. In hyperthyroidism, negative calcium balance and hypercalcaemia cannot be attributed to the direct effect of thyroid hormones on the bone but can be explained by augmentation of the catecholamine effects on bone and kidney by thyroid hormones. The hypothesis offers a solution for an apparent paradox in hyperthyroidism of increased urinary cAMP while nephrogenous cAMP is decreased. It also explains why propranolol corrects hypercalcaemia without influencing renal calcium loss.
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PMID:Catecholamines cause the hypercalciuria and hypercalcaemia in phaeochromocytoma and in hyperthyroidism. 33 Oct 32

The calciuric response to an oral glucose load (100 g) was determined in 16 patients with calcium oxalate urolithiasis (seven with renal hypercalciuria and nine with absorptive hypercalciuria) and seven normal subjects. The rates of renal calcium excretion increased significantly after glucose ingestion in all three groups. The calciuric response in patients with absorptive hypercalciuria and intestinal hyperabsorption of calcium was indistinguishable from that of normal subjects. However, the calcium excretions were significantly higher during 1 hr preceding and 3 hr after glucose ingestion in patients with renal hypercalciuria (with presumed "renal leak" of calcium) than in normal subjects. The increment in the calcium excretion rate was also higher in patients with renal hyperacalciuria, particularly during the 2nd hour of glucose ingestion. The results provide a further support for the concept of different etiologies of renal and absorptive hypercalciurias.
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PMID:An exaggerated augmentation of renal calcium excretion after oral glucose ingestion in patients with renal hypercalciuria. 34 35

The biplot technique is a very useful graphical method to display the relationships between row and column characteristics in two-way tables. This method is applicable as long as the rank-2 approximation explains a large part (e.g. 95%) of the whole variability. However, since in large tables only a rank-3 approximation will yield such a high degree of explanation, a three-dimensional biplot technique has been introduced, using a 3d-screen as a matter of presentation of clinical laboratory data. The value of such a procedure is illustrated using as a clinical example a patient population with recurrent renal stone formation due either to primary hyperparathyroidism or to idiopathic hypercalciuria.
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PMID:Analysis of clinical laboratory data by biplot methods using a three-dimensional display: discrimination of renal stone-patients with idiopathic hypercalciuria and primary hyperparathyroidism. 38 10

Three types of hypercalciuria are described; their existence and frequent association with calcium urolithiasis in humans are accepted. Various dietary factors such as minerals, electrolytes, fluids, vitamin D, carbohydrates, proteins are discussed with regard to their ability to alter the nature and the degree of calcium excretion following their ingestion. It is emphasised that at present we have only limited knowledge on the chain of events linking calorie intake and the response of the kidney.
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PMID:A survey of calcium urolithiasis in normocalcemic hypercalciuria: possible role of nutrients and diet-mediated factors. 38 96

FActors predisposing to renal stone formation have been studied in 309 patients. Dehydration before diagnosis of urolithiasis was due in 12% of the cases to frequent diarrhea and in 36% to bad working conditions. Daily fluid intake was less than 1 liter in 25% of the patients before stone formation and was persistently low in 11% after stone discovery. 41% of the patients drank irregularly over the day, before stone formation, and 11% continued to do so after its detection. Immobilization was present in the patient's history in over 20% of the cases. Normocalcemic hypercalciuria was found in 26% of the patients. 24% of the patients drank water with a calcium concentration of 100--500 mg/l before the lithiasis was diagnosed; 21% continued to do so after stone discovery or paradoxically even drank harder water than before stone detection.
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PMID:High fluid-low calcium intake: not all renal stone formers adhere to this simple treatment. 42 10

The clinical peculiarities, and the etiological and pathogenetic factors of urolithiasis in 296 patients suffering from spontaneous stone elimination were studied. It was established that 209 patients eliminated stones consisting of uric acid, sodium salts and ammonium salts. Moderate hypocalcemia and hyperphosphatemia and also hyperuricemia and hyperuricuria were present. There were 39 'eliminators' of calcium stones. Their blood calcium content was higher, hypercalciuria, inorganic phosphorus and normal uric acid, were noted. Compound stones were present in 48 observations. When carrying out additional biochemical tests in 57 patients with calcium and compound stones, primary hyperparathyroidism was diagnosed in 34 observations; and parathyroidectomy was successfully performed.
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PMID:On the pathogenesis of stone formation in stone-eliminating patients. 42 6

Patients with recurrent stone disease and hypercalciuria were cleared up according to Nordin's schedule. In cases of absorptive hypercalciuria, an ion exchanger operating in the intestine, sodium cellulose phosphate (SCP), is applied under strict control of oxalate, calcium and magnesium excretion as well as ionized calcium in serum. Under treatment with SCP (27 patients), we found a reduction in the renal excretion of calcium and magnesium, and, as a side effect, a significant augmentation of the renal oxalate excretion. In cases of resorptive or resorptive/absorptive hypercalciuria, except in patients with primary HPT, 23 patients were mediated by thiazides (Esidrix). This drug effects a marked decrease of urinary calcium based on a higher rate of reabsorption of calcium in the distal tubule. No severe side effects especially primary HPT were observed.
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PMID:Resorptive and absorptive hypercalciuria. Therapy with sodium cellulose phosphate or thiazides. 42 8

The pathogenesis of the association of medullary sponge kidney and hyperparathyroidism from parathyroid adenoma remains obscure. This unusual case of medullary sponge kidney and secondary hyperparathyroidism due to renal-leak hypercalciuria gives insight into a possible mechanism for the occurrence of medullary sponge kidney with parathyroid adenoma. Suppressible hyperparathyroidism due to renal calcium wasting could represent an intermediate stage in the development of unsuppressible parathyroid hormone secretion. Thus, parathyroid adenoma occurring with medullary sponge kidney may represent a consequence of disordered renal calcium excretion rather than a primary abnormality.
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PMID:Medullary sponge kidney and renal-leak hypercalciuria. A link to the development of parathyroid adenoma? 43 Jun 89


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