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)

Since the structural requirements for all known biological activities of parathyroid hormone (PTH(1-84)) are virtually satisfied by the amino-terminal 34 amino acid fragment, PTH(1-34), we investigated whether this fragment could elaborate the overall actions of the intact hormone in the whole animal by comparing the effects of equimolar infusions of each peptide to dogs and rats. Infusion of bovine PTH(1-84) (bPTH(1-84)) at 17 pmol/kg per h for 20 h to three dogs or at 100 and 200 pmol/kg per h to groups of six rats for 5 days produced greater hypercalcaemia (3.02 +/- 0.03, 2.52 +/- 0.07 and 3.24 +/- 0.11 mmol/l respectively) than equimolar infusions of human PTH(1-34) (hPTH(1-34)) (2.61 +/- 0.03, 2.46 +/- 0.05 and 2.71 +/- 0.09 mmol/l respectively). A significant calcium rise was not observed in dogs until after 4 h of PTH infusion. No rise in plasma calcium was apparent in rats, however, until the third day of PTH infusion. Only in parathyroidectomized rats was there a rise in plasma calcium within 24 h of starting an infusion of PTH. The hypercalciuria and plasma phosphate responses in dogs during equimolar infusions of hPTH(1-34) and bPTH(1-84) were not significantly different. However, by day 5 of infusion in rats greater hypercalciuria was produced by bPTH(1-84). Although infusion of hPTH(1-34) and bPTH(1-84) caused rises in urinary cyclic AMP excretion (measured only in the dog) of immediate onset and equal magnitude, bPTH(1-84) tended to produce greater phosphaturia than hPTH(1-34) in both species. If the assumption is correct that the half-lives of hPTH(1-34) and bPTH(1-84) in the circulation are similar and provided that hPTH does not inherently have less biological activity than bPTH, then during equimolar infusions of these peptides into dogs and rats, the greater responses observed with bPTH(1-84) suggest that intact PTH may have a direct action of its own in vivo before being metabolized into smaller biologically active fragments. In additional experiments using parathyroidectomized rats, the infusion rate of bPTH(1-84) required to restore normocalcaemia was 26 pmol/kg per h. Although near-normal calcaemia and intestinal calcium absorption could still be maintained when the infusion rate was increased to 39 pmol/kg per h, hypercalciuria and phosphaturia became apparent.
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PMID:Effects of parathyroid hormone and the synthetic 1-34 amino-terminal fragment in rats and dogs. 684 24

Hypercalciuria may be due to increased bone resorption, increased intestinal absorption, increased renal excretion or due to hypophosphatemia. Examination of the serum for calcium, phosphorus, parathyroid hormone and 1,25(OH)2D3, and of the urine for calcium, phosphorus and cyclic AMP will help arrive at the correct diagnosis. Therapies specific for each type of hypercalciuria are available and can be used. However, a more simplified diagnostic approach, and the use of thiazide diuretics for therapy, will usually suffice in the majority of patients.
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PMID:Hypercalciuria: diagnosis and management. 700 51

Outpatient renal stone formers belonging to the established urolithiasis subgroups and controls were examined with respect to urinary and serum citrate (Cit) and several associated variables. Only in the normocalciuric majority of calcium and in uric acid stone formers was Cit in 24-hour urine decreased, but was normal in 2-hour fasting morning, and in 3-hour postprandial urine following a Cit-free test meal. Serum Cit was elevated in normocalciuria, renal and resorptive hypercalciuria. This Cit constellation was associated with either normal (absorptive, renal hypercalciuria) or low (normocalciuria, uric acid stone formers) parathyroid gland function as assessed by serum parathyroid hormone and nephrogenous urinary cyclic AMP, except in patients with primary hyperparathyroidism. In 2-hour morning urine the magnesium/creatinine ratio (normocalciuria) and ammonia excretion (uric acid stone formers) were decreased, while ammonia in 24-hour urine was low in all stone formers. It is suggested that Cit metabolism is altered in renal stone disease in general, and that in normocalciuria, stone inhibitors (Cit; magnesium) may be deficient.
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PMID:Citrate in urine and serum and associated variables in subgroups of urolithiasis. Results from an outpatient stone clinic. 712 65

Of 100 consecutive patients with recurrent renal calculi, 43 had idiopathic hypercalciuria (IH) on outpatient evaluation. Hypercalciuria was classified as diet-dependent or fasting; all patients had normal serum iPTH and urinary cyclic AMP, and serum phosphate and TmPO4/GFR were reduced in IH compared to normocalciuric stone formers. In 16 patients with IH, clearance studies revealed an elevated urine flow are factored for GFR (V/GFR) as compared with normal controls (p less than 0.05). In 12 patients, serum PTH was normally suppressed by calcium infusion but TmPO4/GFR was persistently reduced. Acute and chronic phosphate administration significantly reduced urine calcium excretion but did not correct the abnormal V/GFR. We conclude that in IH of both the fasting and the diet-dependent type, there is a defect in the proximal tubular reabsorption of sodium and fluid as well as PTH-independent tubular phosphate wasting. The proximal tubular defect is not a consequence of hypercalciuria nor of phosphate depletion but may be a cause of these abnormalities.
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PMID:Proximal tubular defects in idiopathic hypercalciuria: resistance to phosphate administration. 716 88

The influence of experimental colitis, induced by trinitrobenzenesulphonic acid with ethanol, on bone mineralisation and mineral metabolism was investigated in male rats. Three days after colitis induction, there was a significant rise (p < 0.01) in urinary calcium excretion, which was still present 20 days later (p < 0.05). Three weeks after colitis induction, urinary hydroxyproline excretion was significantly increased (p < 0.01), while urinary cyclic AMP and phosphorus decreased. Colitis was associated with reduced bone density (p < 0.025), ash weight (p < 0.05) and calcium/volume ratio (p < 0.05), whereas no change was found for bone volume and the phosphorus/volume and magnesium/volume ratios. Serum minerals remained unchanged. We conclude that chronic experimental colitis in the rat leads to resorptive hypercalciuria, increased urinary hydroxyproline and osteopenia. Considering site of inflammation, diet, sex, and absence of therapy, inflammatory mediators, e.g. cytokines, with known catabolic effects on bone, might be involved in the pathogenesis of osteopenia.
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PMID:Effect of experimental colitis on bone metabolism in the rat. 806 26

We report a new kindred of hereditary hypophosphatemic rickets with hypercalciuria. The symptomatic child and several relatives had increased renal phosphate clearance leading to hypophosphatemia, hyperabsorptive hypercalciuria, low PTH and increased 1,25-(OH)2D serum level. However, association with vitamin D deficiency and normal urinary excretion of cyclic AMP might suggest another tubular defect in phosphate transport.
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PMID:Hereditary hypophosphatemic rickets with hypercalciuria: report of a new kindred. 1134 Mar 56

Adenine phosphoribosyltransferase (APRT) deficiency, cystinuria, Dent disease, familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC), and primary hyperoxaluria (PH) are rare but important causes of severe kidney stone disease and/or chronic kidney disease in children. Recurrent kidney stone disease and nephrocalcinosis, particularly in pre-pubertal children, should alert the physician to the possibility of an inborn error of metabolism as the underlying cause. Unfortunately, the lack of recognition and knowledge of the five disorders has frequently resulted in an unacceptable delay in diagnosis and treatment, sometimes with grave consequences. A high index of suspicion coupled with early diagnosis may reduce or even prevent the serious long-term complications of these diseases. In this paper, we review the epidemiology, clinical features, diagnosis, treatment, and outcome of patients with APRT deficiency, cystinuria, Dent disease, FHHNC, and PH, with an emphasis on childhood manifestations.
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PMID:Hereditary causes of kidney stones and chronic kidney disease. 2333 84


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