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)

In order to study further the adaptation of inorganic phsophate (Pi) reabsorption during phosphorus depletion, Pi transport was measured at three perfusate Pi concentrations in isolated perfused rat kidney preparations, utilizing synthetic albumin-containing cell-free perfusate. With elevation of the perfusate Pi, phosphaturia was significantly less, and absolute Pi reabsorption was significantly greater in kidneys derived from phosphorus-deprived rats than in organs from nondeprived counterparts. Prior parathyroidectomy did not affect the transport of Pi by the isolated kidney preparation. Increasing the perfusate Pi did not diminish hypercalciuria in kidneys from phosphorus-deprived rats. The results indicate that the adaptive response in Pi reabsorption during phosphorus deprivation can be demonstrated independently of the composition of fluid perfusing the kidney. The mechanism underlying the adaptation, however, remains unclarified.
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PMID:Renal response to phosphorus deprivation in the isolated rat kidney. 71 74

This study was undertaken to examine whether patients with non-insulin-dependent diabetes (NIDDM) are hypercalciuric and whether there is a pathophysiologic relationship between urinary calcium excretion (UCE) and the degree of diabetic nephropathy. Although UCE did not parallel the increase of urinary albumin excretion rate (AER) and the presence of hematuria was not corrected with the degree of UCE, we confirmed that 36% of diabetic patients have hypercalciuria and that the prevalence of hypercalciuria is more frequent in diabetic patients with normo- or microalbuminuria than in the controls. In 6 months, the AER of two hypercalciuric patients increased. However, the blood pressure and HbA1c of these two patients increased during the same 6 months. Therefore, it remains unclear whether hypercalciuria induced an increase in the AER of these patients.
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PMID:Hypercalciuria and hematuria in non-insulin-dependent diabetes mellitus. 177 27

Concentrations of total calcium and albumin were measured in serum specimens from 41 women at intervals before, during, and after 42 pregnancies. The albumin concentration decreased but the calcium decreased more slowly, so that the albumin-adjusted calcium concentration increased from conception to term. These findings, taken in conjunction with published observations of hypercalciuria, increased concentrations of 1,25-dihydroxycholecalciferol and calcitonin in serum, and decreased concentrations of intact parathyrin in serum, strongly suggest that maternal ionized calcium increases throughout normal pregnancy.
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PMID:Albumin-adjusted calcium concentration in serum increases during normal pregnancy. 229 7

33 normocalcemic patients (22 males and 11 females) aged 20-68 years with recurrent renal stone formation and idiopathic hypercalciuria were compared to 33 approximately sex- and age-matched normal controls. Quantitative histomorphometric analysis of iliac crest biopsies were performed after intravital tetracycline double labeling in the patients and in 30 sex- and age-matched normal controls. No difference was found between patients and controls in albumin adjusted serum calcium levels. Serum phosphorus was significantly reduced (p less than 0.01) in the patient group whereas the urinary phosphorus/creatinine ratio was increased (p less than 0.01). The serum calcium phosphate product (S-CaxS-P) was significantly reduced in the patients (p less than 0.05). As expected, the urinary calcium/creatinine ratio was higher in the patient group than in the controls (p less than 0.001). Serum parathyroid hormone was normal. The histomorphometric analysis revealed signs of a moderate mineralization defect (reduced adjusted appositional rate (p less than 0.05), prolonged mineralization lag time (p less than 0.05) and prolonged formation (p less than 0.05)), and an increased extension of eroded surfaces (P less than 0.05) in the patients. The amount of trabecular bone and the balance between the thickness of bone resorbed and later formed per remodeling cycle and all other histomorphometric parameters were found normal in the patients. The combined histomorphometric and biochemical data are best explained by a primary renal phosphate leak leading to hypophosphataemia and a slight mineralization defect. The hypercalciuria may be explained by an enhanced renal production of 1.25-dihydroxyvitamin D secondary to the reduced serum levels of phosphorus. No signs of secondary or primary hyperparathyroidism were observed.
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PMID:A histomorphometric determination of iliac bone remodeling in patients with recurrent renal stone formation and idiopathic hypercalciuria. 271 52

Normocalcaemic male stone formers, 31-51 years old (n = 108) on a free diet, were divided into a hypercalciuric group (n = 47) with calcium excretion rates higher than 8.0 mmol/24 h, a normocalciuric group (n = 32) with calcium excretion rates below 6.1 mmol/24 h and an intermediate group (n = 29). There were no statistically significant differences between the hypercalciuric and the normocalciuric groups with respect to serum levels of calcium, phosphate, creatinine, urate, ALAT, albumin, PTH, 1,25-dihydroxyvitamin D or urinary excretion of cAMP. The group of patients with high calcium excretion had significantly higher serum levels of 25-hydroxyvitamin D3 (75 +/- 4 nmol/l) than the group with low calcium excretion (57 +/- 4 nmol/l) (p less than 0.002), while the group of patients with intermediate calcium excretion had 25-hydroxyvitamin D3 levels between the other two groups (69 +/- 4 nmol/l). A highly accurate method based on isotope dilution-mass spectrometry was used to assay 25-hydroxyvitamin D3. Of the patients with hypercalciuria (n = 47), seven were classified as hyperabsorbers on the basis of calcium load tests. These patients were found to have even higher serum levels of 25-hydroxyvitamin D3 (108 +/- 10 nmol/l)--significantly higher than that of the hypercalciuric patients as a whole. The above study was carried out in March 1983. In September, the group of patients with high urinary calcium excretion also had significantly higher levels of 25-hydroxyvitamin D3 than the group of patients with low calcium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High circulating levels of 25-hydroxyvitamin D3 in renal stone formers with hyperabsorptive hypercalciuria. 352 38

Fourteen very low birthweight infants (mean +/- SD 1,070 +/- 180 g and 29.3 +/- 1.9 weeks gestation) fed their own mother's milk were clinically followed until 3-4 months of age with frequent measurements of serum calcium, phosphorus, magnesium, 25-hydroxyvitamin D (25-OHD), parathyroid hormone, alkaline phosphatase, and albumin, and urine calcium, phosphorus, and magnesium. These infants were matched for birthweight and gestation with 14 infants (1,075 +/- 152 g and 29.0 +/- 1.7 weeks) who had been similarly followed during concomitant studies of infants fed standard formula (Similac 20 cal/oz). Urine phosphorus was markedly lower in the breast milk-fed group from initiation of feedings, and serum phosphorus became significantly lower at and after 6 weeks of age. The fall in serum phosphorus was accompanied by a marked calciuria. Parathyroid hormone was suppressed in the breast milk-fed group, although serum calcium was not elevated and did not differ from formula-fed infants. A high incidence of moderate-severe hypomineralization on radiographs was seen in both breast milk- and formula-fed groups. Six of 14 breast-fed infants required phosphorus supplementation at 8-10 weeks of age because of significant hypophosphatemia, hypercalciuria, and hypomineralization. These infants differed from those not requiring phosphorus supplements by being smaller at birth but not of lower gestation, and having persistently low serum 25-OHD at and after 6 weeks of age.
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PMID:Serial serum 25-hydroxyvitamin D and mineral homeostasis in very premature infants fed preterm human milk. 387 19

We studied the effect of calcium deprivation and loading in 17 healthy subjects and 76 patients with renal calculi. Five had primary hyperparathyroidism with an elevated plasma ionised calcium and detectable plasma parathyroid hormone. Forty-nine had idiopathic hypercalciuria, defined by a urine calcium greater than 7 mmol/day on a free diet. Twenty-two were normocalciuric. Fasting plasma calcium, corrected for albumin, was higher in the patients with idiopathic hypercalciuria (2.40 +/- 0.10 mmol/l) than in controls (2.28 +/- 0.05 mmol/l, p less than 0.005). Plasma calcium was intermediate in the normocalciuric stone formers (2.35 +/- 0.08 mmol/l) and elevated in the patients with primary hyperparathyroidism (2.62 +/- 0.07 mmol/l). Nephrogenous cyclic adenosine monophosphate (cAMP) and parathyroid hormone levels were highest in the primary hyperparathyroid group and did not differ significantly within the other groups. Nephrogenous cAMP correlated positively with plasma calcium in the patients with primary hyperparathyroidism and negatively in controls; there was no correlation in the idiopathic hypercalciuria group. Following an oral calcium load, plasma calcium rose and nephrogenous cAMP fell similarly in all groups. Fasting urinary calcium and its increase after load were greatest in the idiopathic hypercalciuria and primary hyperparathyroid groups, with intermediate results in the normocalciuric patients. Neither the initial metabolic patterns nor the response to thiazide fitted with the previously described patterns of absorptive and renal hypercalciuria. Increased parathyroid gland activity is the most probable cause of idiopathic hypercalciuria.
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PMID:The pathogenesis of idiopathic hypercalciuria: evidence for parathyroid hyperfunction. 632 69

Mild hypocalcemia was observed in 6 out of 12 patients with SIADH associated hyponatremia, this was in fact related to low albumin levels resulting partly from body fluid dilution. In the 7 SIADH patients where it was measured, we observed an increased fractional calcium excretion (3.2 +/- 1.7%) as long as the patients were hyponatremic. This was corrected by water restriction (0.73 +/- 0.4%, p less than 0.01). We suggest that volume expansion was responsible for the increased calcium clearance, and not hyponatremia by itself, since in volume depletion hyponatremia, calcium clearance was within the normal range. Mild hypocalcemia and hypercalciuria is a common finding in SIADH-associated hyponatremia.
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PMID:Hypercalciuria in the syndrome of inappropriate secretion of antidiuretic hormone. 716 85

Burn patients are at risk for bone disease due to aluminum (Al) exposure from use of antacids and albumin, partial immobilization, and increased production of endogenous glucocorticoids. Moreover, severely burned children are growth impaired up to 3 years after the burn. To determine the extent of bone disease, we studied nine men and three women, ages 18-41 years, with greater than 50% body surface area burn. Seven patients underwent iliac crest bone biopsy following double tetracycline labeling, one additional patient expired after a single label, and three others had postmortem specimens obtained for quantitative Al only. Serial serum and urine samples were obtained weekly until biopsy or death. All biopsied patients had reduced bone formation and osteoid area, surface, and width, with mineral apposition rate, osteoblast surface, and osteoclast number with normal eroded surfaces compared to age- and sex-matched normal ambulatory volunteers. Burn patients also had reduced bone formation, mineral apposition rate, osteoid area, and surface compared to age-matched volunteers at short-term bed rest. Serum levels of osteocalcin were low. Most patients had mild hypercalcemia but only a third had hypercalciuria. All patients had elevated Al in blood or urine; urine Al correlated inversely with serum osteocalcin. In 60% significant bone Al was detectable by stain or quantitation. Our data are compatible with burn patients having markedly reduced bone turnover. Al loading, partial immobilization, endogenous corticosteroids, and cytokine production may be among the etiologic factors.
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PMID:Bone disease in burn patients. 845 88

The relationships between dietary protein and sulfur amino acid (methionine and cystine or taurine) intakes and urinary calcium excretion were examined both in animals and in young men. Thirty-two adult Wistar rats were divided into 4 groups, i.e., basal diet (group I), supplemented with albumin (II), methionine and cystine (III), or taurine (IV). During the 5-week feeding period, food consumption was recorded and 48 h urine samples were collected 4 times for each rat. Urinary calcium, creatinine and sulfate were measured. The results showed that the calcium and sulfate excretion in rats in group II and III were significantly higher than rats in the basal diet group. In contrast, supplementing a basal diet with taurine did not increase sulfate excretion and failed to induce hypercalciuria. The same result was also observed in the study carried out in Chinese young men. An increase in protein intake from 67 g to 107 g caused an increase in urinary calcium and sulfate. Supplementation with methionine and cystine in an amount to simulate those in the high protein diet had a similar effect. Adding taurine to the diet had no effect on urinary calcium and sulfate excretion. About 60 percent of the supplemented taurine in the diet was detected in the urine.
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PMID:The effect of dietary sulfur-containing amino acids on calcium excretion. 963 66


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