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)

Bone mineral contents of calcium urolithiasis patients (105 males and 52 females) were measured by the microdensitometry (MD) method, and the patients were divided into the MD normal group and the MD abnormal group. The patients were also divided into the group (21 males and 3 females) treated with thiazides for 1 year or more and the nontreated group to examine various factors in blood and urine. [Nontreated group] The rate of MD abnormality was higher in younger males. The rate tended to increase with age in females. Alkaline phosphatase values were significantly higher in MD abnormal group males than in MD normal group males. Urinary calcium excretion and PTH values were significantly higher in MD abnormal group females than in MD normal group females. Comparison of hypercalciuria and normocalciuria revealed no significant difference between the MD normal rate and the MD abnormal rate. Comparison of single of stone formers and recurrent stone formers also revealed no significant difference between the MD normal rate and the MD abnormal rate. [Treated group] PTH and alkaline phosphatase values were significantly higher in the treated group than in the nontreated group. Alkaline phosphatase values were significantly higher in the MD abnormal group. From the viewpoint of stone recurrence prevention, the monitoring of bones where the majority of calcium in the body is present is considered important besides behavior of calcium in blood and urine.
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PMID:[Calcium urolithiasis and bone change]. 230 17

With 2 groups of 10 patients the influence of an additional therapy with 1 g magnesium sulfate/h during i.v. tocolysis with the betamimetic fenoterol (2 micrograms/min) upon parameters of water and electrolyte balance has been investigated. The whole of the magnesium administered during the 24 hours investigational period has been eliminated via the kidneys. Most probably due to a competition within the distal tubulus hypermagnesemia was associated with hypocalcemia and hypercalciuria, followed by a rise in parathyroid hormone. As PTH is able to compensate hypocalcemia not only by means of bone mobilisation but also by an increase in enteral Ca absorption, estimated losses of calcium are minimal. These may be neglected, as additional therapy with magnesium sulfate--besides the advantages yet known (cardioprotection, saving of betamimetic dosage, reduction of drug tolerance development)--reduces betamimetic induced water retention, thus significantly diminishing lung edema hazard during tocolytic therapy.
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PMID:[Effect of co-medication with magnesium sulfate in beta-mimetic tocolysis on parameters of water-electrolyte balance]. 231 70

Idiopathic hypercalciuria (IH) is a heterogeneous disorder frequently observed in patients with nephrolithiasis. At one extreme of its clinical spectrum is fasting hypercalciuria (FH), a condition characterized by increased bone resorption and turnover. In previous studies we have shown that monocytes from patients with high turnover osteoporosis and from women in early postmenopause elaborate increased amounts of interleukin-1 (IL-1), a cytokine that stimulates bone resorption in vitro and in vivo. Since IL-1 could also mediate the resorptive mechanism of FH and cause a clinically significant bone loss, we have studied the relationship of IH, vertebral mineral density, bone turnover, and monocyte IL-1 activity in 47 patients with absorptive hypercalciuria (AH), 23 with FH, and 38 nonhypercalciuric subjects with recurrent nephrolithiasis (controls). Vertebral mineral density, as measured by quantitative computer tomography, was decreased in each of the three patient groups, but was significantly lower in FH patients than in AH patients or control subjects. Twenty-four-hour total urinary hydroxyproline excretion was increased in FH patients compared to that in AH patients or controls, but blood levels of osteocalcin were not. Monocytes from FH subjects yielded significantly more IL-1 (alpha + beta) activity than those from AH patients or controls; levels of IL-1 activity in monocytes of AH and control patients were similar. In IH subjects, significant correlations were found between IL-1 and hydroxyproline (r = 0.70; P less than 0.0001), IL-1 and quantitative computer tomography values (r = -0.49; P less than 0.005), and IL-1 and urinary calcium (r = -0.36; P less than 0.05). Serum PTH levels were within normal limits in all subjects and were similar in the three study groups, 1,25-Dihydroxyvitamin D3 levels, although higher in IH patients than in controls, were not significantly different in FH and AH subjects. Increased IL-1 activity and decreased vertebral mineral density are features of a subset of patients with IH. Although a cause-effect relationship remains to be established, increased monocytic IL-1 activity, rather than elevated PTH or 1,25-dihydroxyvitamin D3 levels, could underlie the resorptive component of FH.
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PMID:Increased monocyte interleukin-1 activity and decreased vertebral bone density in patients with fasting idiopathic hypercalciuria. 237 Feb 92

Farnolith (a dietary fibre preparation) was given to normal patients (n = 6) with absorptive hypercalciuria type I (n = 6) and to one patient with renal hypercalciuria. Farnolith binds calcium and reduces calcium absorption in the intestines. In normal subjects, the urine and serum parameters of calcium metabolism (total and ionized calcium, 1.25-dihydroxy-vitamin D) were unchanged. In absorptive hypercalciuria type I, a significant decrease in calcium excretion was achieved; oxalate excretion decreased as well. Low PTH values normalized; vitamin-D metabolites were not affected. In renal hypercalciuria, PTH and 1.25 DHCC were increased, whereas hypercalciuria persisted. Our investigations show that Farnolith is a reasonable treatment for absorptive hypercalciuria. Calcium homeostasis is rendered normal by Farnolith without producing secondary hyperoxaluria as sodium cellulose phosphate. Patients with primary renal calcium leakage and secondary hyperparathyroidism should not be treated with Farnolith.
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PMID:[Studies of calcium metabolism in normal persons and patients with hypercalciuria in relation to therapy with the dietary fiber preparation Farnolith]. 253 20

Various studies have shown that a high protein (HP) diet, compared to a low protein (LP) diet, leads to hypercalciuria and alterations in renal and systemic hemodynamics. The authors compared the effects of HP diet to those of normal protein diet (NP) to determine the possible mechanisms by which changes in systemic hemodynamics and hypercalciuria occurred. The studies were conducted in awake rats; the effects of dietary sodium content on the changes induced by HP also were evaluated. The relationship of prostaglandins (PG), renin (PRA), and aldosterone (PA) to changes in blood pressure (BP) was assessed. Two weeks after HP and normal sodium feeding (40%), glomerular filtration rate (GFR) and urine flow (V) were not different from the same values in a group on an NP diet (23%). When HP was fed with low sodium, there was a rise in V as a consequence of greater fluid intake. Although plasma calcium remained constant, the hypercalciuria correlated with high protein and sodium content. Alterations in 1,25(OH)2 vitamin D3 or PTH (cyclic AMP excretion) function did not explain the hypercalciuria induced by HP. This suggests that HP leads to inhibition of tubular calcium reabsorption by mechanism(s) yet to be elucidated. Although HP did not alter GFR, it led to an increase in BP, a fall in renal vascular resistance, and an increase in RPF, regardless of sodium intake. PRA and urine PGE2 excretion were significantly higher in the rats on HP diet, whereas PA remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal and systemic effects of short-term high protein feeding in normal rats. 254 89

Aminoaciduria and secondary hyperparathyroidism accompany vitamin D deficiency. However, the degree of aminoaciduria and PTH elevation have not been studied relative to different calcium and phosphorus dietary intakes. Weanling rats were fed 5 vitamin D deficient diets for 4-6 weeks: very low Ca (VLC) 0.02% Ca, 0.3% P; VLC + 1,25-dihydroxyvitamin D [1,25(OH)2D3], same + 500 pmol i.p. for 2 days; low Ca (LC) 0.45% Ca, 0.3% P; very low P (VLP) 1.2% Ca, 0.1% P; high Ca (HC) 2.5% Ca, 0.3% P, and control 1.2% Ca, 0.70% P + 2.5 micrograms% vitamin D. Amino acids, serum 25-hydroxyvitamin D [25(OH)D3], 1,25(OH)2D3, and PTH, using a specific antirat PTH antibody, were measured. A significant generalized aminoaciduria (11 amino acids) was found in all vitamin D-deficient groups. Furthermore, it was independent of plasma Ca and PTH, and urinary cAMP excretion irrespective of diet. Serum 25(OH)D and 1,25(OH)2D were significantly reduced in all vitamin D-deficient groups. VLC and VLC + 1,25(OH)2D3 were associated with the highest PTH levels (10- and 13-fold increase, respectively) and urinary cAMP (2.3-fold increase in each) and the lowest serum Ca. LC rats had an 8.8- and a 1.7-fold increase in PTH and urinary cAMP, respectively. Phosphate depletion was found in VLP rats documented by insignificantly elevated PTH, normal urinary cAMP, hypercalciuria, and percent tubular reabsorption of phosphate of greater than 99%. While dietary Ca and P affect plasma and urinary Ca and P plasma PTH and urinary cAMP, it appears that dietary P affects the aminoaciduria observed in this study via mechanisms that remain unclear. The possibility that the mechanism for the tubulopathy is multifactorial should be entertained.
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PMID:Aminoaciduria of vitamin D deficiency is independent of PTH levels and urinary cyclic AMP. 254 72

The authors analyze clinical and laboratorial features of 13 patients with surgically confirmed primary hyperparathyroidism (HPT). Among them, 8 presented renal lithiasis, 7 had bone disease, and 2 had both. All patients were hypercalcemic and had elevated serum carboxyterminal levels of PTH. The aminoterminal portion of the PTH was above the normal range in 9 patients and inappropriately high for the level of serum calcium in other two. The c'AMP was elevated in 7/8 patients. Hypophosphatemia was detected in 8/11 patients. Among the lithiasic patients, hypercalciuria was found in only 3. Five patients were submitted to an oral calcium load test which detected no intestinal hyperabsorption of calcium (IH) secondary to HPT in any of them. The rate of elimination of stones/patient/year was 1.7 before the establishment of HPT diagnosis. Despite the presence of renal lithiasis, hypercalciuria and IH were not common findings in HPT patients. Serum calcium and urinary c'AMP were the best screening tests for the diagnosis of HPT in this series. The diagnosis should be further confirmed determining the PTH.
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PMID:[Primary hyperparathyroidism: clinical and laboratory spectrum]. 264 May 6

In a female patient with primary hyperparathyroidism and disturbances of cardiovascular function clinical, biochemical and electrocardiographic as well as bone scintigraphic parameters were analyzed before and during therapy with verapamil (Falicard) for 7 month. Verapamil therapy resulted in decrease of the frequency of the supraventricular tachycardia, and, in higher doses (4 X 120 mg), also reduction of blood pressure, however, with dose limiting bradycardia and prolongation of PQ-time. Both the normalization of serum phosphate level, diminution of hypercalcemia of the ionized calcium and the decrease of hypercalciuria and increase of scintigraphic index as an expression of the decrease of high activity of bone metabolism suggest alterations of the calcium homeostasis. Under oral calcium load the constantly increased PTH values markedly could be suppressed indicating an alteration of intracellular parathyroid calcium set point. Discussion is performed with respect to possible protective metabolic and cardiovascular effects of calcium antagonists in this endocrine functional disorder.
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PMID:[Verapamil in primary hyperparathyroidism]. 276 97

A familial observation of hypophosphatemic rickets with unusual inheritance and evolution, different from that of X linked hypophosphatemia, is reported. The mode of inheritance was autosomal dominant, a father and his son being affected. Severe early signs of rickets and delayed growth were present in both cases. Plasma 1,25 dihydroxyvitamin D and PTH levels were normal. There was no hypercalciuria. Complete cure of rickets and catch-up growth were obtained with the only treatment of vitamin D (40,000 U/day) in the father and of 1 alpha hydroxyvitamin D (1 microgram/day) in the son. This observation is quite similar to the 'autosomal hypophosphatemic bone disease' described by Scriver et al. It illustrates the heterogeneity of familial hypophosphatemia which presently includes 4 different physiopathological entities.
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PMID:[Scriver type autosomal hypophosphatemic rachitis: a family case]. 283 21

The "syndrome of inappropriate calcitriol secretion" may be observed in diseases with disseminated granulomas. The main examples are sarcoidosis and tuberculosis, but it can also be observed in fungal infections, in granulomas due to foreign bodies and in lymphomas. The syndrome is due to autonomous production of 1 alpha hydroxylase by granulomas. The insuing synthesis of calcitriol escapes normal regulation by serum calcium and phosphate levels. The syndrome includes hypercalcemia, hypercalciuria, high 1,25(OH)2D3 serum levels and reduced PTH secretion. It can supervene in anephric or hypoparathyroid patients. The notion that calcitriol may be secreted extrarenally is new. It could have important bearings on several issues in nephrology, immunology and oncology.
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PMID:[Inappropriate calcitriol secretion syndrome]. 295 94


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