Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of parathyroidectomy on parathyroid function and calcium (Ca) metabolism were carefully evaluated in 6 patients with primary hyperparathyroidism without symptoms normally attributed to the disease and in 7 with bone disease or nephrolithiasis. Before parathyroidectomy, both groups of patients demonstrated evidence of the sequelae of parathyroid hormone (PTH) excess, since they presented one or more of the following features: low bone density by 125I-photon absorption, hypercalciuria (urinary Ca greater than 200 mg/day on an intake of 400 mg/day), negative Ca balance (absorbed Ca less than urinary Ca), elevated fasting urinary Ca greater than 0.2 mg/mg creatinine for a night-time sample after a 6-hour fast), and decreased renal function (creatinine clearance of less than 65 ml/min). Following parathyroidectomy, most of these deleterious effects were reversed commensurate with the return of immunoreactive serum PTH, serum Ca, and urinary cyclic AMP toward normal. These quantitative non-invasive techniques may be useful for the initial evaluation and follow-up of patients with asymptomatic primary hyperparathyroidism.
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PMID:Metabolic effects of parathyroidectomy in asymptomatic primary hyperparathyroidism. 17 69

There are two alternative mechanisms that might be responsible for idiopathic hypercalciuria in recurrent stone formers: increased intestinal absorption of calcium with parathyroid suppression and overflow hypercalciuria (primary intestinal hyperabsorption) or renal calcium leak with compensatory hyperparathyroidism and intestinal hyperabsorption (primary renal-tubular hypercalciuria). In this study, urinary excretion of cAMP, the intracellular effector substance synthetised under parathyroid hormone stimulation, was found to be in the normal range. This finding would argue against intestinal hyperabsorption of calcium as the primary cause of hypercalciuria.
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PMID:Pathophysiology and therapy of hypercalciuria in patients who form recurrent stones. 18 57

The cuase for the intestinal hyperabsorptionof calcium (Ca) in various forms of hypercalciurias was explored by a careful measurement of plasma 1 alpha, 25-dihydroxycholecalciferol [1 alpha, 25-(OH)I D] and by an assessment of intestinal Ca absorption and of parathyroid function. In 18 cases of primary hyperparathyroidism (PHPT), the mean plasma concentration of 1 alpha, 25-(OH)2D was significantly increased (4.9 +/- 2.2 SD ng/dl vs. 3.4 +/- 0.9 ng/dl for the control group), and was significantly correlated with fractional Ca absorption (alpha) (r = 0.80, P less than 0.001). Plasma 1 alpha, 25-(OH)2D was also correlated with urinary Ca (P less than 0.05), but not with serum Ca or phosphorus (P), P clearance, urinary cyclic AMP, or serum immunoreactive parathyroid hormone. In 21 cases of absorptive hypercalciuria (AH), plasma 1 alpha, 25-(OH)2D was elevated in one-third of cases, and the mean value of 4.5 +/- 1.1 ng/dl was significantly higher than that of the control group (P less than 0.01). Since relative hypoparathyroidism may be present, the normal absolute value of plasma 1 alpha, 25-(OH)2D, found in two-thirds of cases of AH, may be considered to be inappropriately high. Moreover, in the majority of cases of AH, the data points relating plasma 1 alpha, 25-(OH)2D and alpha fell within 95% confidence limits of values found in non-AH groups (including PHPT). The results suggest that the intestinal hyperabsorption of Ca in PHPT aw AH may be vitamin D dependent. However, the disturbance in vitamin D metabolism may not be the sole cause for the high Ca absorption in AH, since in some patients with AH, the intestinal Ca absorption appears to be inapp
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PMID:The role of 1 alpha, 25-dihydroxyvitamin D in the mediation of intestinal hyperabsorption of calcium in primary hyperparathyroidism and absorptive hypercalciuria. 19 63

1. Administration of an aqueous extract of the dried leaves of Solanum malacoxylon (DLSM) to rats causes a rapid hyperphosphataemia and a decrease in plasma alkaline phosphatase activity; the two effects are typical of 1,25(OH)2D3, the hormonally active metabolite of vitamin D3. 2. DLSM, like both vitamin D3 and parathyroid hormone, increases plasma calcium and citrate levels in rats. The effect of DLSM in influencing plasma citrate, and the role of this important metabolite in mineral metabolism is discussed. 3. A decrease of plasma magnesium levels occurs in rats following treatment with DLSM. This decrease, which is associated with a renal loss of this cation, is remarkably similar to that produced by hypervitaminosis D3. 4. Prolonged administration of DLSM to vitamin D deficient rats causes a polyuria, hypercalciuria, hyperphosphaturia, hypermagnesuria, an increase in urinary total hydroxyproline, an increase in plasma total hexosamines, and a corresponding decrease in the bone total hexosamines. These effects, some of which can also be produced by hyperparathyroidism, or following the administration of parathyroid extract (PTE), large doses of vitamin D3, or 1,25(OH)2D3, suggest that DLSM, like the latter compounds, is capable of causing bone mineral mobilization, and the dissolution of bone organic matrix.
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PMID:The vitamin D3 metabolite-type activity of Solanum malacoxylon. 21 24

We have investigated an 18-yr-old hypercalciuric female with features of both renal hypercalciuria and pseudohypoparathyroidism. She had increased circulating parathyroid hormone levels, which are common to both diseases. She also had a modest hypocalcemia and low normal basal cAMP excretion, both of which are more likely to occur in pseudohypoparathyroidism. She also had Albright's osteodystrophy, which is frequent in patients with pseudohypoparathyroidism and has never been reported in patients with renal hypercalciuria. In contrast to patients with pseudohypoparathyroidism, her serum 1,25-dihydroxycholecalciferol level was increased and her renal responses to parathyroid hormone infusion, including renal calcium reabsorption, were normal. This patient, therefore, raises the possibility that some patients with renal hyperalciuria may have a forme fruste of pseudohypoparathyroidism.
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PMID:Albright's osteodystrophy in a patient with renal hypercalciuria. 22 62

Idiopathic hypercalciuria constitutes two major variants-absorptive hypercalciuria, characterized by a primary intestinal hyperabsorption of calcium, and renal hypercalciuria, in which renal tubular reabsorption of calcium is primarily impaired. The two forms of hypercalciuria may be distinguished from each other, since a) parathyroid function is stimualted in renal hypercalciuria, but normal or suppressed in absorptive hypercalciuria, b) the renal leak of calcium is present in renal hypercalciuria, but not in absorptive hypercalciuria, c) intestinal calcium absorption is probably increased primarily in absorptive hypercalciuria, and secondarily in renal hypercalciuria (from parathyroid hormone excess), d) the increased calcium absorption in renal hypercalciuria probably results from the parathyroid hormone-dependent stimulation of 1,25-dihydroxyvitamin D synthesis, whereas that in absorptive hypercalciuria may be vitamin D-independent, e) the response of the two conditions to certain treatments is unique, and f) the sequelae of parathyroid hormone excess, such as low bone density and negative calcium balance, may be present in renal hypercalciuria, but not in absorptive hypercalciuria. These findings provide a physiological basis for the consideration of absorptive and renal hypercalciurias as distinct and separate entities.
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PMID:Physiological basis for absorptive and renal hypercalciurias. 22 36

Twenty-one unselected patients with recurrent nephrolithiasis and normocalcemic hypercalciuria with or without hypophosphatemia and 18 normal subjects were studied with an oral calcium tolerance test and for 3- to 5-day periods while consuming a low normal (400 mg) and high-normal (1000 mg) calcium intake. The oral calcium tolerance test consisted of the measurement of the calcemic, calciuric, and parathyroid (assessed by determinations of serum immunoreactive parathyroid hormone and nephrogenous cAMP) responses to acute 1000- or 350-mg doses of calcium. Nineteen patients displayed normal results for basal serum calcium, parathyroid function, and fasting calcium excretion, and striking calcemic (mean increase in serum calcium, 0.9 vs. 0.2 mg/dl in the normal subjects) and calciuric (mean increase in urinary calcium, 0.33 vs. 0.15 mg calcium/100 ml GF in the normal subjects) responses to the 1000-mg calcium tolerance test, associated with a mean 54% suppression in nephrogenous cAMP. These patients were operationally defined as having "absorptive" hypercalciuria. The variable occurrence of hypophosphatemia in this group suggested that the pathogenesis of "absorptive" hypercalciuria may be complex and/or multifactorial. There were strong positive correlations between the calciuric response to the calcium tolerance test and fractional isotopic calcium absorption (r = 0.75, P less than 0.00), the calcemic responses to the test (r = 0.71, P less than 0.001) and the calciuric responses noted on the 1000- vs. the 400-mg daily calcium intake (r = 0.78, P less than 0.001). Two patients displayed low or low normal basal serum calcium, increased parathyroid function, increased fasting calcium excretion, and a striking calciuric but minimal calcemic response to the 1000-mg calcium tolerance test, associated with a moderate suppression in nephrogenous cAMP. These patients were operationally defined as having "renal" hypercalciuria. Several lines of evidence indicated that the hyperparathyroidism in these patients was physiological or secondary, including the near normalization of parathyroid function on the daily 1000-mg calcium intake. A steep slope of calcium excretion on calcium intake (due to increased calcium absorption) was noted in all hypercalciuric patients and accounted for the significantly improved diagnostic accuracy of screening patients for hypercalciuria on the high-normal calcium intake. The simple measurement of total cAMP excretion (nanomoles per 100 ml GF) and urinary calcium on the 1000-mg daily calcium intake seemed to provide reliable separation of patients with "renal" from those with "absorptive" hypercalciuria. A physiological (350 mg) dose of oral calcium produced a 30% suppression of nephrogenous cAMP in normal subjects; this suggests that dietary calcium exerts an important control of parathyroid function under physiological circumstances.
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PMID:Pathophysiological studies in idiopathic hypercalciuria: use of an oral calcium tolerance test to characterize distinctive hypercalciuric subgroups. 23 82

Three indices of circulating parathyroid hormone (PTH) activity were compared between two groups: the first a group of 23 patients from three large kindreds with autosomal dominant hypercalcemia without hypercalciuria [familial hypocalciuric hypercalcemia (FHH)] and the second a group of 64 patients with typical primary hyperparathyroidism (1HPT) manifesting comparable hypercalcemia. The group with 1HPT differed from normal with respect to plasma PTH 1HPT concentration (normal, less 0.2 ng/ml), urinary cAMP excretion per 100 ml glomerular filtrate (U cAMP/GF) (normal, 2.3 x/divided by 0.6 nmol/100 ml glomerular filtrate; mean, x/divided 1 SD), and renal tubular maximum of phosphate transport corrected for glomerular filtration rate (TMP/GFR; normal, 3.4 +/- 0.4 mg/dl; mean, +/- 1 SD). The group with 1HPT also diverged significantly from the group with FHH for all three indices: for PTH, 0.37 x/divided by .48 vs. 0.25 x/divided .46 (P less than 0.05); for UcAMP/GF, 4.3 x/divided by .53 vs. 2.6 x/divided .60 (P less than 0.0005); and for TMP/GFR, 2.0 +/- 0.6 vs. 2.6 +/- 0.7 (P less than 0.01). The between-group differences for all three indices were also significant after adjustment for their variation with serum calcium. However, only the difference in TMP/GFR remained significant after adjustment for covariance attributable to serum calcium concentration, age, and creatinine clearance. The group with FHH differed from normal for TMP/GFR but not for UcAMP/GF. However, analysis of changes in UcAMP/GF and serum calcium concentration around the time of parathyroidectomy in three patients with FHH suggested that the parathyroid glands contributed to the abnormalities of mineral homeostasis in at least one. It was concluded that higher serum concentrations of PTH do not account for the lower renal clearance of calcium and magnesium in FHH calcium concentration, the group with FHH showed indices suggesting lower circulating PTH activity than the group with 1HPT.
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PMID:Circulating parathyroid hormone activity: familial hypocalciuric hypercalcemia versus typical primary hyperparathyroidism. 23 92

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


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