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)

Calcium metabolism and renal acidification ability were examined in renal stone patients. On a random diet 33 of 52 patients excreted more than 4 mg. per kg. body weight per day of urinary calcium and were entered into a second study on a 300 mg. calcium diet. Absorptive and renal hypercalciuria was differentiated by fasting urinary calcium (mg. per 100 ml. glomerular filtration). Every absorptive hypercalciuria patient tested and 5 renal hypercalciuria patients had a normal renal acidification ability, and the serum parathyroid hormone and urinary cyclic adenosine monophosphate levels were normal. By calcium restriction urinary calcium decreased more in absorptive hypercalciuria than in renal hypercalciuria (2.48 +/- 0.14 versus 3.34 +/- 0.27 mg. per kg. body weight per day, p less than 0.05). However, urinary calcium remained high in 76 per cent of the patients with absorptive hypercalciuria. Nine patients had a defect in renal tubular acidification and the calcium metabolism was similar to those with renal hypercalciuria. Present studies show that renal hypercalciuria and renal tubular acidification defect cannot be differentiated without an ammonium chloride test.
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PMID:Renal hypercalciuria and acidification defect in kidney stone patients. 292 70

We studied a new hereditary syndrome of hypophosphatemic rickets and hypercalciuria in six affected members of one kindred. In all patients, the manifestations of disease began in early childhood. The characteristic features are rickets, short stature, increased renal phosphate clearance (the ratio between the maximal tubular reabsorption rate for phosphorus and the glomerular filtration rate [TmP/GFR] is 2 to 4 S.D. below the age-related mean), hypercalciuria (8.6 mg of urinary calcium per kilogram of body weight per 24 hours vs. the upper normal value of 4.0), normal serum calcium levels, increased gastrointestinal absorption of calcium and phosphorus, an elevated serum concentration of 1,25-dihydroxyvitamin D (390 +/- 99 pg per milliliter vs. the upper normal value of 110), and suppressed parathyroid function (an immunoreactive parathyroid hormone level of 0.33 +/- 0.1 ng per milliliter and a cyclic AMP level of 1.39 +/- 0.12 nmol per deciliter of glomerular filtrate vs. the lower normal values of 0.3 and 1.5, respectively). Long-term phosphate supplementation as the sole therapy resulted in reversal of all clinical and biochemical abnormalities except the decreased TmP/GFR. We propose that the pivotal defect in this syndrome is a renal phosphate leak resulting in hypophosphatemia with an appropriate elevation of 1,25-dihydroxyvitamin D levels, which causes increased calcium absorption, parathyroid suppression, and hypercalciuria. This syndrome may represent one end of a spectrum of hereditary absorptive hypercalciuria. Our observations support the importance of phosphate as a mediator in controlling 1,25-dihydroxyvitamin D production in human beings.
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PMID:Hereditary hypophosphatemic rickets with hypercalciuria. 298 3

Extensive metabolic studies were performed in a 14-year-old boy suffering from the rare clinical entity known as childhood idiopathic hypercalciuria associated with dwarfism, renal tubular abnormalities and bone lesions. The salient features were: hyperphosphaturia with hypophosphatemia, hypercalciuria with normocalcemia, elevated serum 1,25-dihydroxycholecalciferol[1,25(OH)2D3] levels, marked intestinal hyperabsorption of calcium and phosphorus, with low serum parathyroid hormone (PTH) and urinary adenosine 3':5'-cyclic monophosphate (c-AMP). Bone biopsy confirmed the clinical and radiological diagnosis of rickets. It appears that the following pathophysiological sequence is operating: primary renal phosphate leak with hypophosphatemia, increased 1,25(OH)2D3 synthesis, enhanced intestinal calcium absorption which in turn inhibits release of PTH and c-AMP. Hypercalciuria is seen to be secondary to both avid intestinal calcium absorption and depressed PTH activity, and rickets the result of phosphate depletion. Treatment with oral phosphorus only resulted in an acceleration of growth rate, cure of rickets, and return of urinary calcium excretion to normal values.
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PMID:Hypercalciuric rickets: metabolic studies and pathophysiological considerations. 298 52

The circadian rhythm of urinary total hydroxyproline (THP) excretion was determined in matched groups of ten male idiopathic calcium stoneformers and ten normal subjects in order to determine whether enhanced resorption of bone might contribute to hypercalciuria in these patients. THP increased progressively in normal subjects in successive eight-hour urine collections from period 1 (8 AM to 4 PM) to period 3 (12 midnight to 8 AM), the nocturnal high level in period 3 being significantly greater than in period 1 (P less than 0.01) and in period 2 (P less than 0.05). By contrast, no significant circadian rhythm was observed in THP excretion in the stoneformers. Their THP excretion was similar to that of normal subjects in period 3, but was significantly higher than that of normal subjects in period 1 (THP/creatinine ratio(mg/mg): 0.026 +/- 0.003 v 0.017 +/- 0.001; P less than 0.05. Indices of parathyroid hormone activity were not significantly different between stoneformers and normal subjects; mean serum 1,25(OH)2 vitamin D levels were higher in the stoneformers than the normal subjects (44 v 37 pg/mL) but the difference was not significant (P greater than 0.05). These studies suggest that increased bone turnover may contribute to hypercalciuria in these calcium stoneformers.
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PMID:Bone resorption and hypercalciuria in calcium stoneformers. 301 44

To examine the effects of mineralocorticoidism on calcium (Ca) absorption and to define the mechanism, rats received a high-salt diet and injections of vehicle or deoxycorticosterone acetate (DOCA). Net (44.2 vs. 31.4 mg/day) and percent Ca absorption (28.1 vs. 20.1%) was increased after 5 days of DOCA. This was associated with increased duodenal 45Ca uptake. Thus despite the hypercalciuria, Ca balance was similar. Although the hypercalciuria persisted chronically, the gut effects were sustained, which maintained normal ionized Ca, bone Ca, and Ca balance. Urinary cyclic adenosine monophosphate was elevated by DOCA. Compared with appropriate controls, neither DOCA alone nor polydipsia (elicited by dextrose) produced similar magnitudes of hypercalciuria as DOCA plus high-salt diet. These maneuvers also failed to increase Ca absorption. Neutralization of the metabolic alkalosis neither attenuated the DOCA-induced hypercalciuria nor abolished the Ca hyperabsorption. In vitamin D-deprived rats, the hypercalciuria but not the intestinal effects of DOCA were reproduced. Serum 1,25-dihydroxyvitamin D3 levels were increased during chronic DOCA treatment (224 vs. 139 pg/ml). These data best fit the hypothesis that increased Ca absorption is secondary to the calciuric effects of DOCA and high-salt diet and is mediated via the increased parathyroid hormone and 1,25-dihydroxyvitamin D3 activities.
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PMID:Chronic DOCA treatment increases Ca absorption: role of hypercalciuria and vitamin D. 301 51

109 patients with calcium-containing nephrolithiasis and 10 normal controls underwent oral calcium load test. After thorough examination, 6 of the 109 patients were diagnosed as having primary hyperparathyroidism (PHPT) and the remainder as having normocalcemic nephrolithiasis without PHPT. Following the oral calcium load test, the latter were operationally divided into 3 groups - normocalciuric nephrolithiasis (NN), n = 78; absorptive hypercalciuria (AH), n = 10, and renal hypercalciuria (RH), n = 15 - according to the criteria reported by Pak et al. Before the oral calcium load test, nephrogenous adenosine 3',5'-monophosphate (NcAMP), urinary adenosine 3'-5'-monophosphate (urinary cAMP), and plasma immunoreactive parathyroid hormone (iPTH) were determined to evaluate parathyroid function. This function, as assessed by mean basal NcAMP in the NN, AH and RH groups as well as the PHPT group, was significantly increased as compared with that in the normal controls. Within the NcAMP-elevated 4 groups, the mean basal NcAMP was highest in the PHPT group followed by the RH, AH and NN groups. In view of the mean basal NcAMP, disregarding the PHPT group, the NN and AH groups seemed to be intermediate types between the normal controls and the RH groups. Similar, but less distinctive results were obtained in the determination of urinary cAMP and plasma iPTH. On the other hand, when leaving the PHPT group out, the mean basal urinary calcium creatinine ratio (Ca/Cr) was highest in the RH group followed by the AH and NN groups, and lowest in normal controls, suggesting that the NN and AH groups were intermediate between normal controls and the RH group. The mean basal urinary Ca/Cr ratio in the PHPT group was moderately elevated but not remarkable. Almost similar tendencies were observed in 24-hour urinary calcium excretions on a calcium-restricted diet. A weakly positive correlation (r = 0.232, p less than 0.05) between basal NcAMP and basal urinary Ca/Cr ratio was observed in accumulated cases of the NN, AH and RH groups, whereas a negative correlation (r = -0.664, p less than 0.05) was obtained in normal controls. It is concluded that a possible abnormal calcium metabolism is suggested in stone formers without PHPT. Additionally, it is speculated that 'relative hypercalciuria' in NN and hypercalciuria in AH and RH might be accounted for in a single line of a primary renal leak of calcium.
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PMID:Possibility of elevated parathyroid function in patients with calcium-containing nephrolithiasis as compared with normal controls. 303 19

In contrast to corn, wheat and triticale exhibit high phytase activities. This enzyme enhances phytic phosphorus availability, as demonstrated in pigs given wheat diets. To study the utilization of triticale phosphorus in pigs, the importance of dietary phytase content and the mineral and bone disorders related to high phytate feeding, a nutritional experiment was carried out in 12 growing pigs fed either a corn- or a triticale-based diet for 6 wk. The diets were almost identical except for the cereal component; their phosphorus contents were low (0.4%) and mainly phytic. The following parameters were measured: calcium and phosphorus balances, bone and plasma contents of calcium and phosphorus, plasma vitamin D metabolites and parathyroid hormone (PTH), bone bending moments and intestinal phosphatase activities. Both diets provoked a phosphorus deficiency, but hypophosphatemia occurred less rapidly, hypercalciuria and hypophosphaturia were less marked and phosphorus availability was greater when the triticale diet was fed. This was attributed to the high phytase content of triticale because intestinal phytase and alkaline phosphatase activities were similar in pigs fed either diet. Calcium absorption was not modified by calcium retention was greater for pigs fed triticale and led to higher bone scores. In conclusion, the higher the phytase activity of the diet, the greater the phytate P availability and the lower the bone-mineral disorders.
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PMID:Importance of cereal phytase activity for phytate phosphorus utilization by growing pigs fed diets containing triticale or corn. 303 49

1,25-Dihydroxyvitamin D (1,25-(OH)2D) plays a crucial role in the maintenance of blood calcium and phosphorus levels and in normal skeletal mineralization. The concentration of this metabolite in the blood is, by necessity, tightly regulated. The most important stimuli for renal 1,25-(OH)2D synthesis include parathyroid hormone (PTH), its second messenger cyclic adenosine monophosphate (cAMP) and phosphate deprivation. Hypocalcemia and calcitonin, initially thought to act via stimulation of PTH release, have now been shown to directly stimulate 1-hydroxylation. Estrogens also increase 1,25-(OH)2D production, probably by upregulating renal PTH receptors. Inhibitors of the renal 25-(OH)D 1 alpha-hydroxylase include 1,25-(OH)2D itself, hypercalcemia, and phosphate loading. The PTH-vitamin D axis as modulated by the serum ionized calcium level controls adaptation to alterations in dietary calcium and sodium intake and to changes in skeletal turnover based on the level of physical activity. Although normally the renal production of 1,25-(OH)2D is tightly regulated and changes little in response to vitamin D challenge, there are certain conditions in which 1,25-(OH)2D appears to be substrate-dependent. These include hypoparathyroidism, hyperparathyroidism, vitamin D deficiency, sarcoidosis and the anephric state, conditions in which PTH is not well-modulated by alterations in serum ionized calcium or in which extrarenal synthesis of 1,25-(OH)2D occurs. In several disorders, including absorptive hypercalciuria, pseudohypoparathyroidism, hypophosphatemic rickets, and tumoral calcinosis, the regulation of the renal 1 alpha-hydroxylase appears to be altered.
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PMID:Normal and abnormal regulation of 1,25-(OH)2D synthesis. 306 16

Hypercalciuria and negative calcium balance are complications of total parenteral nutrition (TPN). Because metabolism of the TPN formula generates an acid load that can induce hypercalciuria, we evaluated the effect of supplementing the formula with acetate. In a randomized crossover study six patients on continuous and six on cyclic TPN received no added acetate or 160 mmol acetate/d replacing 160 mmol chloride/d for 3 d each. Blood and urine measurements were obtained on day 3 of each formula. Acetate, which is metabolized to bicarbonate, increased blood pH and decreased renal acid excretion. Urinary Ca decreased in every patient from 422 +/- 63 to 240 +/- 46 mg/d (10.5 +/- 1.6 to 6.0 +/- 1.4 mmol/d) and from 468 +/- 68 to 285 +/- 54 mg/d (11.7 +/- 1.7 to 7.1 +/- 1.3 mmol/d) during continuous and cyclic TPN, respectively. Filtered Ca load decreased slightly whereas renal tubular Ca reabsorption increased significantly with acetate. Serum parathyroid hormone, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and urinary cyclic AMP were not different.
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PMID:Acetate and hypercalciuria during total parenteral nutrition. 314 73

A 14-year-old boy presented with the clinical and radiological features of rickets. Serum inorganic phosphate levels were constantly low, whereas serum calcium and parathyroid hormone levels were within the normal range. Laboratory investigation did not show any evidence for vitamin-D deficiency, chronic renal insufficiency, Fanconi syndrome, tubular acidosis, hepatic disease or intestinal malabsorption. A family study comprising 34 members over four generations revealed 10 other individuals to be affected and the mode of inheritance to be autosomal dominant. In addition to hypophosphataemia and normocalcaemia, the disease is characterized by elevated serum 1,25 dihydroxyvitamin D levels and hypercalciuria. This hereditary syndrome of renal hypophosphataemia differs from the common familial X-linked hypophosphataemia and the recently described autosomal recessive hypophosphataemic rickets with hypercalciuria by its dominant mode of inheritance; it differs from hypophosphataemic non-rachitic bone disease by the elevated serum 1,25 dihydroxyvitamin D levels and hypercalciuria.
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PMID:Autosomal dominant hypophosphataemia with elevated serum 1,25 dihydroxyvitamin D and hypercalciuria. 315 20


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