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

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

Urine calcium excretion is known to be directly correlated with the level of dietary protein intake. In this experiment we examined the persistence of the hypercalciuria induced by the consumption of high protein diets, and the mechanism of the calciuric response. In a 95-day metabolic study, each of six adult male subjects received formula diets supplying 12 g nitrogen or 36 g nitrogen, and approximately 1400 mg calcium per day. Urine calcium increased rapidly and significantly from an average of 191 mg/day on the 12 g nitrogen diet to 277 mg/day on the 36 g nitrogen diet. There was no significant difference in the apparent absorption of calcium, so that overall calcium balance was -37 mg/day on the 12 g nitrogen diet, and significantly lower at -137 mg/day in subjects consuming the high protein diet. Levels of urinary hydroxyproline, serum insulin, and parathyroid hormone were not significantly increased by high intakes of protein. A decrease in the fractional reabsorption of calcium by the kidney seems to be the most likely cause of the protein-induced hypercalciuria. The consumption of high calcium diets is unlikely to prevent the negative calcium balance and probable bone loss induced by the consumption of high protein diets.
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PMID:Protein-induced hypercalciuria: a longer term study. 43 6

Calcium absorption in the jejunum and ileum of patients with absorptive hypercalciuria was studied by in vivo intestinal perfusion. Net calcium absorption in the jejunum was markedly increased at four luminal calcium concentrations (1 to 20 mM) in the patients with absorptive hypercalciuria when compared to that in normal subjects. In the ileum, net calcium absorption was only slightly increased in the patients with absorptive hypercalciuria. Experiments with radioactive calcium (47Ca) revealed increased unidirectional flux out of the jejunal lumen in the patients but no difference in the unidirectional flux into the lumen, when compared to that in normal control subjects. Net magnesium absorption was normal in the patients. These results suggest that hyperabsorption of calcium in patients with absorptive hypercalciuria is mainly due to enhanced calcium transport in the jejunum and that the defect is specific for calcium since magnesium is absorbed normally.
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PMID:Selective jejunal hyperabsorption of calcium in absorptive hypercalciuria. 43 48

Eighty patients with proved calcium urolithiasis participated in an outpatient study designed to define the most likely metabolic problem related to the cause of the stone disease. Diagnostic categories included absorptive hypercalciuria (33 patients), renal leak hypercalciuria (20 patients), hypomagnesiumuria (27 patients), hyperuricemia and hyperuricuria (16 patients), hyperoxaluria (15 patients), normal stone-former (4 patients), renal tubular acidosis (2 patients) and suspicion of hyperparathyroidism (7 patients). Of the 80 patients 40 had more than 1 defect. Patients with a high suspicion of hyperparathyroidism were excluded from the study. Based on these criteria treatment plans incorporating medications, diet or both were instituted. Of 21 patients observed for greater than 2 years 90 per cent have shown no new stone disease.
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PMID:Outpatient evaluation of patients with calcium urolithiasis. 43 49

The authors report on the clinical, biological and radiological anomalies observed in a series of 42 cases of idiopathic hypercalciuria. An histological bone study showed "osteomalacia" type changes (an increase in the osteoid volume and a decrease in the mineralization speed). The Ca45 isotope studies showed that there was an exchangable pool of calcium and a turnover, which was generally low. A study of the kidney functions revealed a decrease in the tubular reabsorption of calcium, while that of phosphorous remained within normal limits. There was no case of hyperparathyroidism in this series. The authors pose the question of whether the failure of calcium to settle on the tissues and the lack of tubular reabsorption of calcium, does not result from the relatively ineffective action of the endogenous circulating parathyroid hormone.
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PMID:[Idiopathic hypercalciuria. Correlative study of bone tissue and phosphocalcium investigations]. 44 70

Urinary saturation with respect to calcium oxalate monohydrate was measured in 111 consecutive patients with calcium nephrolithiasis. Each patient also was evaluated by a detailed conventional metabolic protocol. Patients with idiopathic hypercalciuria produced abnormally oversaturated urine more frequently than normal subjects and normocalciuric patients, but normocalciuric patients had unexpectedly high levels of urine saturation. Measuring levels of calcium concentration, oxalate concentration, or the chemical concentration product of calcium and oxalate in urine did not predict oversaturation. During thiazide treatment, saturation level tended to fall if it was initially elevated, whether the patient was hypercalciuric or not. Patients whose urine was not remarkably oversaturated showed no tendency to elaborate even less saturated urine during thiazide treatment; instead, the average calcium oxalate saturation level remained constant. Direct urine saturation measurements can detect a small but significant number of normocalciuric patients who have marked oversaturation with respect to calcium oxalate and appear to benefit from treatment.
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PMID:Urinary saturation measurements in calcium nephrolithiasis. 44 49

The persistence of hypercalciuria (HCU), despite long-lasting calcium restriction in the diet in patients with absorptive HCU type I gives evidence of an additional endogenous source of calcium contributing to the pathogenesis of this disorder. The role of calcium mobilization from the bone is documented by the effective suppression of enhanced calcium mobilization from the bone, by means of calcitonin load in 5 patients with absorptive HCU type I and comparison with 7 normal controls.
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PMID:Calcitonin load in absorptive hypercalciuria type I. 44 94


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