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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined parathyroid gland function in 47 patients with idiopathic hypercalciuria in an effort to determine whether serum levels of parathyroid hormone (PTH) and/or urinary excretion of cyclic adenosine monophosphate (cyclic AMP) can discriminate between the various forms of hypercalciuria. Although we could separate our 47 patients into two groups, 21 patients with renal hypercalciuria (RH) and 15 patients with absorptive hypercalciuria (AH), there remained a group of 11 patients who did not exactly correspond to either group. Basal serum PTH was normal in the two groups: for RH, 10.32 +/- 0.93; for AH, 11.43 +/- 1.10 microliter Eq/ml. Similarly, urinary cyclic AMP did not differ between the two groups: for RH, 4.88 +/- 0.5; for AH, 4.87 +/- 0.55 nmoles/dl/min GFR. Moreover, the response of the parathyroid glands to acute hypocalcemia produced by intravenous infusion of EDTA was not different among patients with AH, RH, and control subjects. Only one patient showed a marked increase of serum PTH in response to acute hypocalcemia, and the bone biopsy revealed increased osteoclastic resorption. In conclusion, our data show that serum levels of PTH and urinary cyclic AMP do not differentiate between the various forms of idiopathic hypercalciuria. The EDTA test demonstrated that secondary hyperparathyroidism is very uncommon in these patients.
Kidney Int Suppl 1983 Dec
PMID:Absence of secondary hyperparathyroidism in most patients with renal hypercalciuria. 633 Apr 24

Twenty-three calcium stone formers with idiopathic hypercalciuria were entered into an open study to examine the effects of flurbiprofen (Froben) on urinary calcium excretion. Five patients were withdrawn because of side effects. A statistically significant reduction in urinary calcium excretion was noted after 2 (P = 0.004) and 6 (P = 0.001) weeks' treatment. There was a significant increase in urinary calcium excretion after stopping the treatment (P = 0.0006). The results suggest that flurbiprofen reduces calcium excretion in the urine but the high incidence of side effects may limit its use in routine treatment of hypercalciuria.
Br J Urol 1983 Dec
PMID:A non-steroidal anti-inflammatory drug (flurbiprofen) to control idiopathic hypercalciuria resistant to dietary manipulation. 636 Feb 94

Squamous carcinomas are the most common cause of humoral hypercalcemia of malignancy (HHM) in humans. To develop an animal model of this syndrome, CD-1 female mice were painted with dimethylbenzanthracene, which produced cutaneous squamous carcinomas in the majority of those painted. Greater than 90% of tumor-bearing mice developed a syndrome of hypercalcemia, hypophosphatemia, hypercalciuria, elevated plasma 1,25-dihydroxyvitamin D, normal immunoreactive PTH, elevated urinary cAMP, and accelerated bone resorption compared to control mice. Tumor excision reversed the hypercalcemia and hypophosphatemia, and autopsies revealed no evidence of skeletal or other metastases. Dietary calcium restriction did not affect the hypercalcemia in tumor-bearing mice. Extracts of tumor tissue contained potent bioactivity paralleling that of bovine (b) PTH in a PTH-sensitive canine renal cortical adenylate cyclase assay. The activity was trypsin sensitive and partially inhibitable by Nle, Tyr bPTH amide. The activity coeluted with chymotrypsinogen (mol wt, 25,700) on Sephacryl S-200 chromatography, well ahead of bPTH. This is the first description of an animal squamous carcinoma that produces HHM. With the exception of elevated plasma 1,25-dihydroxyvitamin D levels, the syndrome precisely mimics that seen in human HHM. The presence of a biologically active protein larger than PTH in tumor extracts, similar to that extracted from human tumors, suggests a common mode of pathogenesis. This model should be useful in further studying the pathophysiology of HHM.
Endocrinology 1984 Dec
PMID:Squamous carcinoma model of humoral hypercalcemia of malignancy. 649 73

From 1957 through 1981, 550 cervical explorations for presumed primary hyperparathyroidism were performed in 536 patients at the North Carolina Baptist Hospital. Fifty-one of those patients who did not have persistent hypercalcemia are the basis of this report. Twenty-six patients with hypercalciuria and normal renal function had recurrent passage of calcium-containing renal stones, but never had documented hypercalcemia. Only five patients (19%) had positive findings at exploration: small, hyperplastic glands (n = 3); small adenomas (n = 2). Seventeen of the 23 patients for whom follow-up data were available continued to form and pass renal stones postoperatively, including three of the five patients with "pathologic" glands (follow-up range: 4 months to 21.3 years; mean--7 years, 9 months). Twenty-five patients (also with normal renal function) had chronic calcium nephrolithiasis, hypercalciuria, and isolated or occasional elevations of serum calcium ranging from 10.6 to 10.9 mg/dl. Thirteen of these patients had abnormal parathyroid glands: adenomas (n = 12); hyperplasia (n = 1). All but two of the 13 were cured of their nephrolithiasis, but all ten of the patients with no abnormal glands for whom follow-up data were available continued to pass renal stones (follow-up range--8 months to 18 years; mean--5 years, 7 months). Thus, our experience with treating "normocalcemic" hyperparathyroidism has been disappointing. Although a substantial number of patients with occasional mild hypercalcemia may benefit from cervical exploration, those patients are not, by definition, truly normocalcemic. Metabolic evaluation can separate hypercalciuric recurrent stone formers with autonomous secondary hyperparathyroidism from patients with suppressible secondary hyperparathyroidism, and can thus more accurately identify patients who may benefit from parathyroid exploration.
Am Surg 1983 Dec
PMID:Normocalcemic hyperparathyroidism revisited. 654 87

Four preterm infants receiving long-term furosemide therapy were examined for hypercalciuria, hyperparathyroidism, renal calcification, and bone demineralization. All four infants had increased urinary calcium excretion. Three infants had high serum concentrations of parathyroid hormone, and in these three infants, bone mineral content was below the mean of "osteopenic" preterm infants of comparable gestational and postnatal age. In two of these infants, there was ultrasound evidence of renal calcification. In one infant, autopsy disclosed bone changes of hyperparathyroidism, gallstones, and calcification in the heart and kidney.
Am J Dis Child 1983 Dec
PMID:Secondary hyperparathyroidism and bone disease in infants receiving long-term furosemide therapy. 663 31

The "stone clinic effect" refers to the effect of encouraging a high intake of fluid and avoiding dietary excesses on stone formation and growth in patients with urolithiasis. To determine the extent of this effect we reviewed the clinical courses of 108 patients with idiopathic calcium urolithiasis and indeterminant metabolic activity. There was no evidence of stone growth or new stone formation (metabolic inactivity) after a mean followup of 62.6 months in 63 of the 108 patients (58.3 per cent), including 12 of 17 (70.6 per cent) with hypercalciuria and 7 of 15 (46.7 per cent) with hyperuricosuria. Comparison of initial and followup 24-hour urine volumes demonstrated a significant increase in patients who were metabolically inactive at followup (p less than 0.0005), while no increase was detected in patients who were metabolically active at followup. We recommend that specific drug therapy should not be given to patients with idiopathic calcium urolithiasis until the stone clinic effect has been evaluated.
J Urol 1983 Dec
PMID:The stone clinic effect in patients with idiopathic calcium urolithiasis. 664 90

Kidney stones are common, and most of them are of the calcium oxalate type. Metabolic evaluation ranging from extensive to cursory has been recommended by different experts; however, some evaluation does seem warranted, even if only a single stone has occurred. Crystallographic analysis of the stone, if recovered, and measurement of urinary excretion of calcium and uric acid are indicated. Blood chemistries, measurement of urine pH, and measurement of urinary constituents besides calcium and uric acid are probably indicated as well, but controversy exists as to whether classification of hypercalciuria is necessary for management of most patients. Most, but not all, of the literature supports the use of thiazides to prevent calcium oxalate stones and the use of allopurinol in those calcium stone formers who have hyperuricosuria. In fact, allopurinol appears to be useful in patients with calcium stones even if no metabolic abnormality is discovered.
Postgrad Med 1982 Dec
PMID:Kidney stones: current issues in diagnosis and therapy. 675 15

In a clinical study of 275 idiopathic stone formers the GFR was significantly raised in hypercalciuric patients compared with normal controls P less than 0.001). The possibility that the mechanism underlying hypercalciuria and raised GFR may be prostaglandin-mediated was considered because it is now well established that prostaglandins regulate intra-renal haemodynamics and influence tubular electrolyte excretion. Experiments were performed in conscious Sprague Dawley rats to determine the changes in calcium and sodium excretion following prostaglandin synthetase inhibition with indomethacin. Both calcium and sodium excretion together with urine flow were significantly reduced (P less than 0.002). Further experiments were performed in anaesthetised monkeys (Macacca fascicularis) to see if the inhibitory effect of indomethacin was reversible. Exogenous prostaglandin (PGE2) infusion resulted in a marked calciuretic response without producing changes in GFR or blood pressure. Selected hypercalciuric patients were treated with indomethacin, which resulted in a significant fall in urinary calcium excretion (P less than 0.001). This clinical and experimental study suggests that PGE2 is the hormone which determines the renal handling of calcium by controlling renal tubular function.
Br J Urol 1981 Dec
PMID:The influence of renal prostaglandins on glomerular filtration rate (GFR) and calcium excretion in urolithiasis. 679

Urinary excretion rate of oxalate was measured in 79 patients with idiopathic calcium (Ca) nephrolithiasis and the results were compared with those obtained in 28 healthy volunteers. The group of stone formers consisted of 20 patients with idiopathic hypercalciuria (IHC) of the absorptive type, 23 patients with IHC of the renal type, 11 patients with hypercalciuria secondary to dietary factors, 1 patient with hyperuricosuria (as an isolated finding) and 24 patients without hypercalciuria nor hyperuricosuria. Classification was based upon the urinary excretion rate of uric acid, as well as that of calcium measured under 3 different dietary conditions (i.e. free diet, free diet supplemented with 3 g Ca/day for 3 days, and diet free of dairy products for 5 days). On a free diet, normal values of oxaluria ranged from 125 to 435 mumol/24 h; an elevated value was observed in 11 (14%) patients, 5 of whom belonged to the subgroup without hypercalciuria nor hyperuricosuria. On a low Ca diet, mild hyperoxaluria occurred in 3 controls and in 19 patients, the tendency to develop hyperoxaluria being particularly marked in the subgroup with absorptive-IHC. Moreover, there was a positive correlation between oxaluria on a low Ca diet and the estimated degree of intestinal absorption of Ca. This study confirms the finding that on a free diet, the incidence of mild hyperoxaluria amongst idiopathic stone formers is rather low. It shows, however, that a significant percentage of patients classically referred to as "without metabolic disorder" have in fact slight hyperoxaluria, an observation with a potential therapeutic impact. Finally, it shows that on a low Ca diet, patients with absorptive-IHC are particularly prone to develop hyperoxaluria: the latter observation renders questionable the relevance of a low Ca diet for patients with absorptive IHC, unless their intake of oxalate is simultaneously reduced.
Schweiz Med Wochenschr 1982 Dec 04
PMID:[Incidence of hyperoxaluria in idiopathic calcium nephrolithiasis]. 717 77

The occurrence of calcareous renal stones in 12 members of a family was consistent with an autosomal dominant mode of inheritance. All 6 members with stones who were evaluated were shown to have absorptive hypercalciuria. The mother of 2 members with stones did not suffer stones but had biochemical evidence of absorptive hypercalciuria (increased intestinal calcium absorption, hypercalciuria and normal parathyroid function). Nephrolithiasis was encountered only in the progeny of members who had stones of biochemical absorptive hypercalciuria. The results suggest that physiological feature(s) of absorptive hypercalciuria may be an expression of the genetic trait.
J Urol 1981 Dec
PMID:Familial absorptive hypercalciuria in a large kindred. 732 Nov 8


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