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

We have investigated and treated 176 patients who were suffering from renal calculi. The stones contained calcium in 87% of patients, predominantly urate in 11%, and rarely contained magnesium ammonium phosphate or cystine. Of the patients with calcium stones, hypercalciuria was present in 75% and was identified in 57% by the measurement of the 24-hour urinary calcium excretion, and in a further 18% by a standardization calcium "fast-and-load" test. Nine patients were found to have primary hyperparathyroidism and were treated surgically. A further 21% were suspected to have normocalcaemic hyperparathyroidism, and metabolic studies are being developed to clarify this. The treatment of hypercalciuria included a low-calcium diet, and various combinations of a thiazide diuretic, phosphate supplements and sodium cellulose phosphate. Hypercalciuria was controlled in all compliant patients, and only two developed further stones. Hyperuricosuria was rarely the sole metabolic abnormality in patients with calcium stones, though this might reflect the referral pattern of the Unit. Uric acid stones were frequently, but not invariably, associated with hyperuricosuria and acid urine, and even large uric acid calculi dissolved with a combined therapy of high fluid intake, allopurinol and an alkalinizing agent. Surgical treatment was rarely required in these patients. A stone in the renal pelvis of one patient was removed percutaneously and did not require ultrasonic fragmentation. Modern methods of investigation and treatment have greatly improved the outlook for patients with recurrent renal calculi.
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PMID:Investigation and treatment of renal calculi. 404 15

A 26-year-old woman was admitted to the Institute of Endocrinology in Bucharest for evaluation of primary hyperparathyroidism (P-HPT). Anamnesis revealed a 10-year history of nephrolithiasis; peptic ulcer, chronic pancreatitis, cholelithiasis. Eight months previously, she had given birth to a child who had neonatal hypocalcaemic tetany. Investigations revealed the presence of moderate hypercalcaemia, hypercalciuria, hypo-phosphoremia; serum chloride level was above 100 mEq/1, and the chloride phosphate ratio was greater than 33. X-ray films of the abdomen revealed the presence of nephrolithiasis and right nephrocalcinosis. Selenium methyonine scanning, ultrasonography and computerized tomography were negative. On surgical exploration a 2-3 cm parathyroid adenoma was removed from between the trachea and the esophagus.
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PMID:Primary hyperparathyroidism. Report of a clinical case without bone lesions. 404 20

The highest degree of urinary supersaturation with respect to calcium oxalate monohydrate (COM) and brushite at which secondary nucleation and growth of small amounts of COM and hydroxyapatite (HAP) are inhibited was determined by new and simple methods. There were 39 subjects who produced 24 h-urine collections (11 idiopathic stone formers (ISF), 12 patients suffering from primary hyperparathyroidism (HPT) and 16 healthy controls (HC). These subjects had a moderate calcium and low oxalate intake. The results obtained were compared with the state of urinary saturation and with urine chemistry. The measurements of crystallization conditions with respect to COM were repeated in 26 subjects (11 ISF, 5 HPT, 10 HC) after a dietary oxalate load. In 24 h-urines of HC diluted to 2.4 1/24 h the degree of supersaturation necessary to induce crystallization of COM and HAP was 2-5 times higher than the state of urinary saturation measured under the same test conditions. ISF showed a decreased pyrophosphate concentration and a decreased inhibitory activity to HAP crystallization in their 24 h-urine. The urinary inhibitory activity towards crystallization of HAP showed a positive correlation to urinary pyrophosphate concentration. In the 24 h-urine of HPT hypercalciuria and increased saturation with respect to brushite which reached values to induce HAP crystallization were found. After a dietary oxalate load urinary supersaturation with respect to COM reached values to induce COM crystallization in ISF and HPT but not in HC.
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PMID:Crystallization conditions in urine of patients with idiopathic recurrent calcium nephrolithiasis and with hyperparathyroidism. 404 2

The causes for the hypercalciuria and diagnostic criteria for the various forms of hypercalciuria were sought in 56 patients with hypercalcemia or nephrolithiasis (Ca stones), by a careful assessment of parathyroid function and calcium metabolism. A study protocol for the evaluation of hypercalciuria, based on a constant liquid synthetic diet, was developed. In 26 cases of primary hyperparathyroidism, characteristic features were: hypercalcemia, high urinary cyclic AMP (cAMP, 8.58+/-3.63 SD mumol/g creatinine; normal, 4.02+/-0.70 mumol/g creatinine), high immunoreactive serum parathyroid hormone (PTH), hypercalciuria, the urinary Ca exceeding absorbed Ca from intestinal tract (Ca(A)), high fasting urinary Ca (0.2 mg/mg creatinine or greater), and low bone density by (125)I photon absorption. The results suggest that hypercalciuria is partly secondary to an excessive skeletal resorption (resorptive hypercalciuria). The 22 cases with renal stones had normocalcemia, hypercalciuria, intestinal hyperabsorption of calcium, normal or low serum PTH and urinary cAMP, normal fasting urinary Ca, and normal bone density. Since their Ca(A) exceeded urinary Ca, the hypercalciuria probably resulted from an intestinal hyperabsorption of Ca (absorptive hypercalciuria). The primacy of intestinal Ca hyperabsorption was confirmed by responses to Ca load and deprivation under a metabolic dietary regimen. During a Ca load of 1,700 mg/day, there was an exaggerated increase in the renal excretion of Ca and a suppression of cAMP excretion. The urinary Ca of 453+/-154 SD mg/day was significantly higher than the control group's 211+/-42 mg/day. The urinary cAMP of 2.26+/-0.56 mumol/g creatinine was significantly lower than in the control group. In contrast, when the intestinal absorption of calcium was limited by cellulose phosphate, the hypercalciuria was corrected and the suppressed renal excretion of cAMP returned towards normal. Two cases with renal stones had normocalcemia, hypercalciuria, and high urinary cAMP or serum PTH. Since Ca(A) was less than urinary Ca, the hypercalciuria may have been secondary to an impaired renal tubular reabsorption of Ca (renal hypercalciuria). Six cases with renal stones had normal values of serum Ca, urinary Ca, urinary cAMP, and serum PTH (normocalciuric nephrolithiasis). Their Ca(A) exceeded urinary Ca, and fasting urinary Ca and bone density were normal. The results support the proposed mechanisms for the hypercalciuria and provide reliable diagnostic criteria for the various forms of hypercalciuria.
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PMID:The hypercalciurias. Causes, parathyroid functions, and diagnostic criteria. 436 91

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

Urine specimens were collected from 26 normal subjects, 10 patients with proven primary hyperparathyroidism, and eight patients with hypercalcaemia due to other causes. After overnight urine concentration, an oral water load was given to induce a diuresis and provide urine specimens with a relatively wide range of creatinine concentration for each subject. In normal subjects the urinary calcium/creatinine ratio was found to be independent of urine concentration. In eight out of 10 patients with primary hyperparathyroidism and in two out of eight patients with hyper-calcaemia due to other causes, the urinary calcium/creatinine ratio was found to be high when the creatinine concentration was low, but usually normal when the creatinine concentration was high. The results suggest that if the urinary calcium/creatinine ratio of random urine specimens is used as a ;screening' procedure to detect hypercalciuria the latter cannot be excluded if the urinary creatinine concentration is more than 40 mg per 100 ml.
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PMID:The urinary calcium-creatinine ratio as a measure of urinary calcium excretion. 578 80

The role of 1,25-dihydroxyvitamin D (1,25(OH)2D) in the pathogenesis of idiopathic hypercalciuria was studied in 37 renal stone formers who, during two 10-day periods, followed first a normal and then a low calcium diet. The following samples were taken during each diet; 24 h urine; fasting blood and urine; blood and urine following a 1 g oral calcium load. Patients were divided according to serum calcium level, 24 h urinary calcium excretion on the first diet and fasting calcium excretion on the second diet. Eight patients were found to be normocalciuric (NSF), 16 had absorptive hypercalciuria (AH), five renal hypercalciuria (RH) and eight primary hyperparathyroidism. In NSF and AH, a positive correlation was found between the fasting and the 24 hour urinary calcium (r = 0.787, P less than 0.001), while negative correlations were found between the fasting urinary calcium and the serum parathyroid hormone (r = -0.703, P less than 0.001) or the fasting urinary cyclic AMP (r = -0.434, P less than 0.01). Patients with RH had higher serum PTH and urinary cAMP levels for a given degree of fasting calciuria mainly on the low calcium diet. Mean serum 1,25(OH)2D was similar in NSF (43.6 +/- 4.5 pg/ml), AH (43.6 +/- 2.3 pg/ml) and RH (40.4 +/- 4.8 pg/ml) on the first diet; increases were similar in all groups after 10 d of calcium restriction. A positive correlation was found between the serum 1,25(OH)2D concentrations and the 24 h urinary calcium excretion on the first diet in NSF (r = 0.889, P less than 0.001) but not in AH or RH. There was no evidence of such correlation with the low calcium diet. No correlation between the calciuric response to calcium loading and the serum concentrations of 1,25(OH)2D was found. The results suggest that serum concentrations of 1,25(OH)2D may be related to urinary calcium excretion in NSF more than in AH or RH. The factors responsible for the hyperabsorption of calcium in the latter patients remain to be elucidated.
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PMID:Influence of dietary calcium on serum 1,25-dihydroxyvitamin D concentrations in renal stone formers. 609 46

Clodronate disodium (dichloromethylene diphosphonate), a specific inhibitor of bone resorption, was given by mouth (1.0-3.2 g daily) to nine patients with primary hyperparathyroidism for two to 32 weeks so that its clinical and metabolic effects could be evaluated. Bone resorption decreased in all patients as judged by a fall in the fasting urinary calcium to creatinine and hydroxyproline to creatinine ratios. Serum calcium concentration was increased in all patients before treatment and fell in response to treatment to values near the upper end of the normal range. Hypercalcaemia and hypercalciuria recurred when treatment was stopped. In three patients treated for longer than 19 weeks clodronate failed to sustain the reduction in serum calcium concentration but the concentration remained below pretreatment values. These results suggest that clodronate may be of use in the medical management of primary hyperparathyroidism, particularly in patients in whom suppression of bone disease is desirable before surgery or in whom surgery is contraindicated.
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PMID:Drug treatment of primary hyperparathyroidism: use of clodronate disodium. 621 61

The availability of accurate and inexpensive methods for measuring serum calcium levels has resulted in a rapid increase in the number of diagnoses of primary hyperparathyroidism, notably in its asymptomatic hypercalcemic forms. In addition, the development of a radioimmunoassay of the parathyroid hormone and, more recently, measurements of nephrogenous cyclic AMP during fasting and after calcium loading have led to the recognition of clinical variants of the disease, such as intermittent or borderline hypercalcemia and pure hypercalciuria with normal calcemia. The degree of hypercalcemia in stable primary hyperparathyroidism depends on renal tubular reabsorption of calcium rather than on bone resorption. The poor correlation observed between calcium tubular reabsorption rate and magnitude of parathyroid hormone hypersecretion suggests that as yet undetermined factors interfere with the effects of parathyroid hormone on renal tubules and probably account for the fluctuations in calcemia reported during serial determinations in patients. The sigmoid relationship between parathyroid hormone release and extracellular calcium concentrations has been analyzed from recent in vitro studies with dispersed parathyroid cells. In primary hyperplasia of the parathyroid glands hypersecretion of parathyroid hormone seems to depend principally upon the increase in tissue mass with normal sensitivity to calcium at cellular levels, whereas in adenoma the primary abnormality responsible for hypersecretion of parathyroid hormone would be an alteration in cell sensitivity to calcium, as indicated by an elevated "set point". Finally, while complicated primary hyperthyroidism requires surgery, our limited knowledge of the natural history of asymptomatic forms makes it impossible to decide which of these patients will ultimately need to be operated upon.
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PMID:[Present status of primary hyperparathyroidism]. 623 8


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