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)

Oral sodium cellulose phosphate, an inhibitor of intestinal calcium absorption, may reduce urinary magnesium, increase urinary oxalate, and have a limited hypocalciuric action or cause negative calcium balance in the absence of increased calcium absorption or in the presence of renal calcium "leak". To overcome these potential complications, we have taken the following precautions: oral magnesium supplements were given, a moderate oxalate restriction was imposed, a modest dose of sodium cellulose phosphate was used (usually 10 g per day), and only patients with documented absorptive hypercalciuria were treated. During a cumulative treatment period of 42.8 years, 18 patients with recurrent calcium nephrolithiasis showed a sustained reduction in urinary calcium, without developing consistent or substantial reduction in urinary magnesium, hyperoxaluria, hyperparathyroidism, or reduced bone density, Urinary saturation (relative saturation ratio) of calcium oxalate and brushite typically decreased. Remission of stone disease was found in 78 per cent of patients. We conclude that sodium cellulose phosphate is a useful drug for absorptive hypercalciuria when used appropriately.
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PMID:A cautious use of sodium cellulose phosphate in the management of calcium nephrolithiasis. 729 89

In 25 cases of spasmophilia the parathyroid function was assessed by complete exploration of the P-Ca metabolism and radioimmunoassay (RIA) of parathormone (PTH). Concomitantly the bone mineralization status was assessed by induced hypercalciuria tests and administration of 30 mg vitamin D2. RIA of PTH revealed increased values in 50% of the cases. The values fall within the range of secondary hyperparathyroidism, but this percentage varies with the values of the parathyroid function obtained by P-Ca metabolism explorations. The increased PTH values do no correlate with the level of plasma total calcium, ionic calcium, and magnesemia. Nor do they correlate with the bone mineralization disorders or the duration of the disease and the age of the patients.
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PMID:The functional status of the parathyroid in adult spasmophilia patients estimated by plasma parathormone assay. 732 51

The effect of long-term thiazide therapy (hydrochlorothiazide, 50 mg twice/day) on intestinal calcium (Ca) absorption and serum 1 alpha,25-dihydroxyvitamin D [1 alpha,25-(OH)2D] concentration was examined in 10 patients with renal hypercalciuria (RH), many of whom had hyperabsorption of Ca, and in 11 cases of absorptive hypercalciuria (AH), all of whom had intestinal hyperabsorption of Ca. In patients with RH, the intestinal Ca absorption decreased significantly during thiazide therapy (mean treatment period of 15 mo) from 0.68 +/- 0.09 SD to 0.56 +/- 0.10 (p less than 0.01), commensurate with the "correction" of the renal leak of Ca and secondary hyperparathyroidism. Furthermore, serum 1 alpha,25-(OH)2D decreased significantly from 5.2 +/- 2.2 SD ng/dl to 3.7 +/- 0.8 ng/dl (p less than 0.025) during thiazide therapy. In patients with AH, the intestinal hyperabsorption of calcium persisted during thiazide treatment (0.69 +/- 0.07 versus 0.69 +/- 0.06), despite restoration of normal urinary Ca. Serum 1 alpha,25-(OH)2D was virtually unchanged during treatment (4.5 +/- 1.4 ng/dl versus 4.7 +/- 0.9 ng/dl). The results support the hypothesis that the intestinal hyperabsorption of Ca in RH is a result of increased serum concentration of 1 alpha,25-(OH)2D secondary to the hyperparathyroid state, while that in AH may not be totally dependent on increased concentrations of 1 alpha,25-(OH)2D.
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PMID:Selective effects of thiazide therapy on serum 1 alpha,25-dihydroxyvitamin D and intestinal calcium absorption in renal and absorptive hypercalciurias. 735 72

Disorders of calcium metabolism are not generally considered important either clinically or pathophysiologically in essential hypertension. Recent reports, though, suggest that increased parathyroid gland function may be one of the more common endocrine disturbances associated with hypertension. We measured serum parathyroid hormone (PTH) concentrations as well as routine blood and urine chemistries in 34 hypertensives. Their mean PTH, 79.1 +/- 3.1 muliter Eq/muliter, was significantly higher (p less than 0.025) than the mean PTH, 66.9 +/- 3.3, of an age- and sex-matched normotensive control population. The mean serum calcium, 9.5 +/- 0.1 mg%, was identical in the two populations. Compared to a second age- and sex-matched normotensive population, the hypertensives demonstrated a significant (p less than 0.005) relative hypercalciuria. For any level of urinary sodium, hypertensives excreted more calcium. These preliminary data suggest that parathyroid gland function may be enhanced in essential hypertension. This increased gland activity appears, in part, to be an appropriate, physiologic response to a previously unrecognized relative hypercalciuria, or renal calcium leak, associated with essential hypertension. We conclude that the increased prevalence of hypertension in subjects with hyperparathyroidism probably represents the final event in a continuum that begins with obligatory urinary calcium losses in hypertensives, but whose pathological presentation is hyperparathyroidism. The results of this pilot study indicate a need for derivative experiments directed at defining the importance of our preliminary findings in the pathogenesis of human and experimental hypertension.
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PMID:Enhanced parathyroid function in essential hypertension: a homeostatic response to a urinary calcium leak. 738 May 20

Hypophosphatemia either as a consequence of secondary hyperparathyroidism or as a consequence of a primary defect in phosphate metabolism appears to be a well established abnormality among subsets of patients with idiopathic hypercalciuria and nephrolithiasis. The detailed biochemical events that lead to hypophosphatemia in those patients who exhibit a primary abnormality of phosphate metabolism remain to be clarified.
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PMID:Is there a disorder of phosphate metabolism in idiopathic hypercalciuria? 742 89

In a woman with bilateral recurrent calcium nephrolithiasis and hypercalciuria, hypercalcemia developed and she underwent parathyroid surgery, which led to excision of a histologically-confirmed adenoma. The patient became normocalcemic but remained hypercalciuric despite reduction of dietary calcium intake. Several calculi recurred in both kidneys. Four to six years after parathyroidectomy, hypercalcemia recurred and the patient underwent a new surgical exploration; a parathyroid gland with diffuse adenomatous aspects and another gland with pure hyperplasia were excised. Once again, after surgery the patient became normocalcemic but remained hypercalciuric. Evidence for a "renal calcium leak" hypercalciuria was obtained, and thiazide administration led to normalization of urinary calcium excretion. In calcium nephrolithiasis, persistent hypercalciuria may lead to recurrence of autonomous hyperparathyroidism.
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PMID:Recurrence of autonomous hyperparathyroidism in calcium nephrolithiasis. 742 48

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

To clarify the pathogenesis of calcium-containing urinary stone, calcium metabolism of the 113 patients with calcium-containing stone was studied by fasting and oral calcium loading test. The stone patients were classified into four groups. Those were normocalciuria (NC, n = 60), absorptive hypercalciuria-1 (AH-1, n = 26), absorptive hypercalciuria-2 (AH-2, n = 16) and renal hypercalciuria (RH, n = 11). In the AH-1 group, hypercalciuria resulted from enhancement of intestinal calcium (Ca) absorption. The increase in serum Ca from absorbed Ca increased renal filtered load of Ca. Urinary excretion of Ca was correlated to that of sodium (Na) in fasting and Ca load, and both increments were also correlated in Ca load. As of this fact, the increase in Na excretion was responsible for a cause of hypercalciuria in the AH-1 group. In the RH group, the serum ionized Ca level and % tubular reabsorption of Ca were significantly lower than those of other groups. Urinary excretion of Ca and Na ratio was significantly higher than that of the NC and AH-1 groups. This condition was due to an impaired renal tubular reabsorption of Ca and the resulting secondary hyperparathyroidism. These findings suggested was response disorder of distal tubular to parathyroid hormone. Urinary excretion of phosphorus (P) was correlated to that of Na in fasting and Ca load, and both increments were also correlated in Ca load in the AH-1 group. The increase in urinary excretion of P resulted from the secondary hyperparathyroidism in the RH group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A study of calcium metabolism in calcium-containing stone formers]. 747 14

Bone involvement in idiopathic calcium nephrolithiasis is characterized by the following abnormalities: a) the bone density is decreased, the severity of bone loss being dependent upon the existence of hypercalciuria and upon the pathophysiology of this latter: it is inconsistent in the absence of hypercalciuria or when hypercalciuria is of the absorptive type I or II, whereas it is almost constant in fasting hypercalciuria without secondary hyperparathyroidism and constant and severe in the rare true renal hypercalciuria. b) The bone histology (which has been evaluated only in idiopathic hypercalciuric patients) mainly shows a defect in bone formation at the exception of the rare renal hypercalciuria. Osteoclastic hyperresorption is only seen in this latter type of hypercalciuria whereas in the other types of hypercalciuria only an increase of the total or inactive resorption surface is observed. This phenomenon is possibly explained only by a delayed refilling of the resorption lacunae secondary to the decreased bone formation. The osteoid thickness is either normal or decreased despite decrease in mineralization apposition rate which seems therefore to be secondary to the decreased bone formation. c) Symptomatic bone disease in hypercalciuric stone formers is exceptional and always related to a severe long term calcium restriction. d) The biochemical markers of bone resorption tend to be increased in idiopathic hypercalciuria. Hydroxyprolinuria is more often elevated than pyridinolinuria. However pyridinolinuria is negatively correlated to bone density. The contrast between the increase of these bone resorption markers and the usual normality of plasma PTH and of the osteoclastic resorptive surfaces, suggest the role of meat induced acid load which may favor inactive resorption by dissolution of bone buffers. A disturbed profile synthesis of cytokines which induce differentiation and proliferation of the osteoclasts and which modulate the osteoblastic proliferation and function (IL-1, IL-6, TNF-alpha, GM-CSF...) may play a role in the bone loss of calcium stone formers but further studies are necessary to precise its transient or permanent involvement in their bone disease. e) The decrease of bone formation may be explained by the suppressed PTH secretion which may be explained by hypercalcitriolemia. This excess of calcitriol synthesis may be secondary either to monocyte increased synthesis of IL-1 which stimulates the renal 1 alpha-hydroxylase by the mean of an increased PGE2 synthesis or to the relative hypophosphatemia of the calcium stone formers comparatively to healthy controls. Hypercalcitriolemia may originate from the activated monocyte itself. The decrease in bone formation may also be secondary to the action of monokines on the osteoblast differentiation and/or function.
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PMID:[Bone involvement in idiopathic calcium lithiasis]. 756 25

In order to clarify the risk-factors for men with vertebral fractures due to osteoporosis, we carried out a study of 51 cases. Twenty-five percent of patients had an endocrine disorder (hyperparathyroidism, hypogonadism, hyperthyroidism) or had received corticosteroids. These patients were compared with 26 age-matched controls. Eleven patients compared with 2 of the 26 control subjects had arteriopathy of the lower limbs; 11 patients had hypercalciuria or hyperphosphaturia compared with 3 of the control subjects. Arteriopathy appears to be associated with osteoporosis in older patients (mean age 71 years), whereas renal tubular disorders were found in younger patients (mean age 45 years).
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PMID:Renal tubular disorders and arteriopathy of the lower limbs: risk factors for osteoporosis in men? 769 23


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