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)

Hypercalcemia occurred in a patient with leiomyosarcoma when multiple lung metastases developed. Despite normal plasma parathyroid hormone (PTH) levels and low 1,25-dihydroxyvitamin D, this hypercalcemic patient had a marked hypercalciuria and phosphaturia associated with an increased excretion of nephrogenous cyclic AMP (NcAMP). Administration of cisplatin ameliorated both the hypercalcemia and hypercalciuria without any reduction in tumor size of NcAMP excretion. Terminally, acute pancreatitis occurred producing a profound hypocalcemia. In the extract of tumor tissue obtained post mortem, bioactivity stimulating the generation of cyclic AMP in osteogenic cells was demonstrated along with the immunoreactive PTH-related protein (PTH-rP). the first report of a solid non-epithelial malignancy producing PTH-rP and associated with humoral hypercalcemia of malignancy. The hypercalcemia in this case caused acute pancreatitis, which led to a profound hypocalcemia.
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PMID:A case of leiomyosarcoma associated with humoral hypercalcemia of malignancy: demonstration of biological and immunological activities of parathyroid hormone-related protein in the tumor extract. 255 69

The effect of dietary protein load on the incidence of nephrolithiasis was studied in rats and men. Three groups of adult male Wister rats were fed with a standard protein diet, a high protein diet, or a low protein diet for 4 weeks. In the high protein group, calcium excretion was significantly increased and citrate excretion was remarkably decreased. This group also exhibited low grade metabolic acidosis due to catabolism of excess amino acids, and increases in urinary cyclic AMP excretion and bone resorption. These findings indicate that protein-induced hypercalciuria is due to low grade metabolic acidosis, which directly affects renal handling of calcium. Long-term calcium loss in the urine may lead to negative calcium balance and hyperfunction of the parathyroid gland may induce bone resorption. The influence of 40 g animal protein load on urinary risk factors of calcium stone formation was investigated in 23 healthy males and 26 patients with nephrolithiasis. All subjects were given control diets each day containing 60 g protein for a week and during the next week each received an additional 40 g animal protein. In the controls, added dietary protein resulted in decreased urinary citrate and increased urinary uric acid, with no change in urinary calcium or cyclic AMP excretion. In contrast, the patients showed increased urinary calcium and cyclic AMP as well as decreased urinary citrate. Further examination of the patients revealed that the significant increases of calcium and cyclic AMP excretion occurred only in hypercalciuric patients, who seemed to be classified into renal hypercalciuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Influence of dietary animal protein on renal stone disease]. 255 15

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

Vitamin D deficiency is associated with a generalized aminoaciduria which has been shown to be independent of parathyroid hormone (PTH) and urinary cyclic AMP excretion. To further characterize the mechanism underlying the tubulopathy, weanling rats were placed on one of the following diets for 5 weeks: (1) control [0.7% phosphorus (P), 5.5 micrograms % vitamin D]; (2) D-P- (0.1% P, 0 vitamin D); (3) D+P- (0.1% P, 5.5 micrograms % vitamin D); (4) D-P+ (0.3% P, 0 vitamin D); (5) D-P++ (0.7% P, 0 vitamin D). All diets contained 1.2% calcium (Ca). A group of rats raised on D-P++ for 4 weeks were fed D-P- for 7 days after which they received 500 pmol of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3; SUPP] or an equal volume of the vehicle (ETH). The above diets resulted in partial vitamin D depletion in that 1,25(OH)2D levels were 50.25-79 pg/ml in the presence of very low 25(OH)D concentrations. Augmentation in the urinary excretion of 6 out of 8 amino acids measured was observed in P depletion irrespective of vitamin D status. For the most part, acute supplementation with 1,25(OH)2D3 did not ameliorate the tubulopathy. Plasma PTH and Ca concentrations remained normal in all diets, except D+P-, where plasma Ca was 15.88 +/- 0.54 mg/dl. P depletion was associated with hypercalciuria, hypophosphatemia, avid reabsorption of P and growth retardation, irrespective of vitamin D status. Using taurine as a representative of the amino affected, there was a strong correlation between urinary taurine on the one hand and dietary P content (r = 0.613), plasma P (r = 0.399) and 1,25(OH)2D levels (r = -0.576) on the other. The present study suggests that the aminoaciduria of vitamin D deficiency is not related to elevated levels of PTH. A similar defect may be produced by P depletion, suggesting the possibility of a common pathway for the effect.
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PMID:Effect of vitamin D deficiency on amino acid excretion in the phosphate-depleted rat. 281 86

To evaluate the cause of hypercalciuria, we carried out the oral calcium tolerance test before and after parathyroidectomy in a patient with primary hyperparathyroidism who had recurrent and multiple nephrolithiasis. Preoperative laboratory examination showed hypercalcemia, hypophosphetamia, hypercalciuria, decrease in % tubular reabsorption of phosphorus and strikingly elevated urinary cyclic AMP excretion. The oral calcium tolerance test indicated a significantly greater increase in serum calcium (delta serum calcium: 1.4 mg/dl vs 0.8 mg/dl) and a significantly greater suppression of urinary cyclic AMP excretion (delta U-cyclic AMP:-3.56 moles/gCre vs-1.17 moles/gCre) before parathyroidectomy than after. These results showed that hypercalciuria in this case was induced not only by the significant increase in the filtrated load of calcium but by the reduction in the resorption of calcium in the distal tubule caused by the significantly suppressed parathyroid hormone effect.
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PMID:[A case report: primary hyperparathyroidism--comparison before and after parathyroidectomy by oral calcium tolerance test]. 283 26

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

Urinary excretions of calcium and cyclic AMP were studied in male recurrent stone-formers after an overnight fast and following an oral calcium load. The results from eight patients with established hypercalciuria (greater than 7.5 mmol Ca/24 h) were compared with those from eight age matched normocalciuric stone-formers. The urinary calcium/creatinine ratio was higher in the hypercalciuric group both when fasting and calcium loaded whilst their urinary cyclic AMP was lower in both 24-h and calcium-loaded collections. Five of the eight hypercalciuric patients exhibited an increased urinary calcium/creatinine ratio whilst fasting. These findings support the view that renal calcium wasting, in association with suppression of parathyroid activity, is common among men with idiopathic hypercalciuria. Dietary calcium restriction may lead to bone loss in patients with obligatory renal calcium wasting and enteric adsorption is rarely applicable to the treatment of stone disease. Therefore, the demonstration of a high fasting urinary calcium/creatinine ratio is a strong indication for therapeutic agents which act to suppress renal calcium loss to treat hypercalciuria.
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PMID:Renal calcium conservation in recurrent stone-formers with idiopathic hypercalciuria. 298 70

We studied the effects of oral furosemide, 80 mg/day for 7 days, on the response of urinary excretion of phosphate and cyclic AMP to exogenous parathyroid extract (PTE) in 6 normal subjects. All 6 subjects had marked increases in urinary calcium and a significant increase in urinary cyclic AMP from the control to the furosemide periods: this suggests that furosemide-induced hypercalciuria produced elevated parathyroid activity. After treatment with furosemide, the response of urinary cyclic AMP and phosphate to PTE was blunted. During the subsequent calcium infusion (4 mg/kg), urinary cyclic AMP was suppressed to subnormal values, and the response to PTE returned to normal. The evidence suggests that furosemide may blunt the response to PTE, perhaps as a result of the elevated parathyroid activity produced by furosemide-induced hypercalciuria and lowering of plasma-ionized calcium. This blunting effect of furosemide on the response of urinary phosphate and cyclic AMP to PTE should be considered in the evaluation of parathyroid function in patients taking furosemide.
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PMID:The effects of oral furosemide on the response of urinary excretion of cyclic adenosine monophosphate and phosphate to parathyroid extract in normal subjects. 299 30

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


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