Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extensive experimental evidence has established a significant role of calciferol in the maintenance of normal calcium homeostasis. Present knowledge indicates that vitamin D(3) must first be converted to 25-OH-D(3) and then to 1,25(OH)(2)D(3), the most active known form of the steroid. Many of the factors regulating the rate of production of this last steroid from its precurser have been evaluated, and the concept that vitamin D functions as a steroid hormone seems to be well established. Deranged action of calciferol, caused by impaired metabolism of the steroid or through altered sensitivity of target tissues, may be involved in the pathophysiology of several disease states with abnormal calcium metabolism. It is noted that liver disease, osteomalacia due to anticonvulsant therapy, chronic renal failure, hypophosphatemic rickets, hypoparathyroidism, hyperparathyroidism, sarcoidosis and idiopathic hypercalciuria have possible relation to alterations in metabolism or action of vitamin D. The future clinical availability of 1,25(OH)(2)D(3) and other analogs of this steroid may offer potential therapeutic benefit in the treatment of certain of the disease entities discussed.
 ...
PMID:Metabolism and action of the hormone vitamin D. Its relation to diseases of calcium homeostasis. 436 34

An unusual metabolic bone disease which developed in 11 adults receiving total parenteral nutrition (TPN) for more than 3 months was characterised by the insidious onset of bone pain which became very severe and caused considerable disability. Serum levels of calcium, phosphorus, 25-hydroxy-vitamin D, and serum immunoreactive parathyroid hormone were normal. Patchy osteomalacia with impaired mineralisation and decreased bone turnover were seen on histomorphometric analysis of bone biopsy specimens. All patients receiving long-term TPN had hypercalciuria, but no biochemical features that distinguished patients with symptoms from those without. Skeletal symptoms generally resolved 1-2 months after stoppage of the TPN infusions, despite nutritional deterioration. The pathogenesis of this syndrome remains unknown.
 ...
PMID:Bone disease associated with total parenteral nutrition. 610 76

The objectives of this study were to evaluate the effects of vitamin D(3) (D(3)) and 1,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)) on uremic bone disease independent of their action on the intestine. The histomorphology of tibial metaphyses in uremic (5/6 nephrectomized [5/6 Nx]) rats fed a low-calcium-low-phosphorus (LCLP) diet was compared with sham-operated (SO) rats fed an LCLP diet and 5/6 Nx rats fed an LCLP diet and given 15,000 IU D(3) or 5 units (135 ng) 1,25-(OH)(2)D(3) daily for 7 days. A marked osteomalacia characterized by an increased percentage of active and inactive trabecular osteoid surface and thickened growth plates developed in proximal tibial metaphyses in 5/6 Nx rats given the placebo, compared with SO rats. These bone changes were associated with relative hypophosphatemia, hypophosphaturia, and hypercalciuria in 5/6 Nx rats. In 5/6 Nx rats treated with D(3) or 1,25-(OH)(2)D(3) the growth plates had undergone mineralization and vascular invasion and were markedly reduced in thickness. Other parameters of osteomalacia in trabecular bone were not different from 5/6 Nx rats given the placebo. There was a significant decrease in osteoclasts per millimeter of trabecular surface perimeter in D(3)- and 1,25-(OH)(2)D(3)-treated rats. These bone changes were associated with hypercalcemia, hyperphosphatemia, and hyperphosphaturia, compared with 5/6 Nx rats given the placebo. It was concluded that in uremic rats fed the LCLP diet, shortterm treatment with either pharmacologic levels of D(3) or 1,25-(OH)(2)D(3) corrected only lesions in the growth plate. Osteoid seams were not reduced in treated rats, although the serum calcium-phosphorus product was elevated. The 5/6 Nx rat fed the LCLP diet appears to be a useful model for the rapid induction of uremic osteomalacia in adult animals.
 ...
PMID:Short-term effects of vitamin D3 and 1,25-dihydroxyvitamin D3 on osteomalacia in uremic rats fed a low calcium-low-phosphorus diet. 626 57

24-h urinary cyclic adenosine 3', 5'-monophosphate/creatinine (cAMP/Cr) ratio was assessed in 10 patients with hypoparathyroidism, 6 with primary hyperparathyroidism, 7 with normocalcemic hypercalciuria and recurrent nephrolithiasis, 14 with osteomalacia, 25 with Paget's disease and 53 with symptomatic postmenopausal osteoporosis. In hypoparathyroid subjects the mean values of 24 h cAMP/Cr ratio were significantly lower than the control values, whereas in patients with parathyroid adenoma the mean values were higher and fell after parathyroid surgery. Patients with nephrolithiasis due to absorptive hypercalciuria showed low or normal cAMP/Cr ratio, whereas in those with osteomalacia and mean values of cAMP/Cr ratio were significantly higher than the control values and decreased after vitamin D treatment. The mean value of the 24 h urine cAMP/Cr ratio was normal in patients with Paget's disease or postmenopausal osteoporosis and increased significantly after long term treatment with calcitonin or diphosphonate. This increase paralleled a significant decrease of calcium plasma level. A significant improvement of fractional calcium absorption was observed in women with postmenopausal osteoporosis at the end of treatment with calcitonin or diphosphonate.
 ...
PMID:The 24-h urinary cyclic adenosine 3', 5' monophosphate/creatinine ratio: an useful approach to the diagnosis of parathyroid disorders and function. 627 46

Hypophosphateamia in patients with Ca lithiasis leads to the activation of the vitamin D endocrine system: the plasma 1.25(OH)2-D3 concentration is raised. The raised 1,25(OH)2-D3 biosynthesis causes an increase in intestinal Ca absorption, which in its turn explains the hypercalciuria. The syndrome originally presented by Albright and his pupils as "idiopathic hypercalciuria" in fact corresponds to a secondary, reactive D hypervitaminosis. According to the present findings the often wrongly used term "so-called idiopathic calciuria" should be replaced by the pathogenetically correcter term "hypophosphataemic calciuria". Efficient treatment of this syndrome consists in sufficient oral orthophosphate substitution. In the interests of a better understanding as a requirement for suitable treatment of this metabolic disorder, the vitamin D metabolites and their renal key enzymes, 25-OH-Vitamin-D3-1-Hydroxylase and 25-OH-Vitamin -D3-24-Hydroxylase, are described. The hormonal control add the activation and inactivation of the vitamin D endocrine system are explained independently of the individual Ca and phosphate requirement of the organism. The dependence of renal Ca excretion on the rate of glomerular filtration is pointed out once again. The clinical-diagnostic term hypercalciuria must not be applied globally but individually. Indications, counter-indications, dosage, duration and side-effects of the orthophosphate therapy are discussed.
 ...
PMID:[Calcium lithiasis II. Idiopathic or hypophosphatemic hypercalciuria? Vitamin D - metabolism and othophosphate therapy]. 627 97

Although the nutritional aspects related to bone development and subsequent bone loss have been appreciated for many years, they are now being reemphasized in view of current information concerning the vitamin D endocrine system, the development of new assay procedures and more sensitive radiologic techniques to assess changes in bone mass, and the realization that clinical problems related to bone loss will increase as individuals live longer. The vitamin D endocrine system is complex, involving the skin, liver, and kidney for synthesis of the vitamin D metabolites and, primarily, the intestine and bone for biologic expression. Numerous factors and disorders affecting the skin, gastrointestinal tract, and kidney will adversely affect vitamin D metabolism. Vitamin D deficiency is common in elderly individuals, especially those who are chronically ill, house-bound, and poorly nourished. Subclinical vitamin D deficiency and osteomalacia may also be complicating problems in elderly patients with osteoporosis and hip fractures. At present the role of the vitamin D endocrine system in the pathogenesis and treatment of osteoporosis is unclear. There is little evidence that vitamin D or its metabolites are helpful in osteoporosis, except perhaps to heal osteomalacia which may be present. It is hoped that encouraging results will follow the use of more potent vitamin D metabolites, either alone or in combination with other agents. Calcium homeostasis is affected by numerous dietary factors (including protein, phosphorus, fiber, and lactose) and drugs (including alcohol, diuretics, and antacids), and calcium absorption in the intestine and the ability to adapt to low-calcium diets will decrease with advancing age. There are conflicting reports concerning the relation between low-calcium intake and osteoporosis, and about the role of calcium intake in the development and then maintenance of bone mass. There is little doubt that many older individuals ingest less calcium than is recommended, especially at a time when even more may be required to maintain bone mass. Several studies show that calcium supplementation producing a total calcium intake of 1,200-1,500 mg/day can slow the rate of bone loss. When the high doses of calcium are given along with vitamin D, periodic monitoring of blood and urine calcium is necessary to avoid hypercalcemia and hypercalciuria.
 ...
PMID:The vitamin D endocrine system, calcium metabolism, and osteoporosis. 636 21

Calcium and phosphorus metabolism and balance were studied in 151 patients receiving total parenteral nutrition (TPN). Hypercalciuria was common, with mean (+/- SD) urinary calcium excretion 17.5 +/- 3.9 meq/24 hours (n = 2610). There was a significant positive correlation between urinary calcium excretion and parenteral calcium intake (r = 0.34, p less than 0.001). There was also a positive correlation between calcium balance and parenteral calcium intake (r = 0.61, p less than 0.001) in patients without extra-renal losses. Positive calcium balance was achieved with parenteral calcium intake greater than 15 meq/24 hours. Urinary phosphorus excretion correlated positively with parenteral phosphorus intake (r = 0.50, p less than 0.001). Phosphorous balance also correlated positively with parenteral phosphorus intake (r = 0.78, p less than 0.001). Positive phosphorus balance was achieved with parenteral phosphorus intake above 15 mmol/24 hours. Fifty-three patients received 1,000 IU vitamin D once weekly and showed no significant change in serum calcium. Ninety-eight patients received 1,000 IU vitamin D twice weekly and showed a gradual but significant mean increase over time in serum calcium.
 ...
PMID:Calcium and phosphorus metabolism during total parenteral nutrition. 640 Dec 3

Ingestion of protein is known to increase urinary calcium excretion. By studying the effect of intravenous amino acid infusion on calcium excretion, the variables of diets and intestinal absorption are avoided. Five patients on total parenteral nutrition with otherwise constant nutrient infusions containing 240 mg of calcium were randomized to two different levels of amino acid infusion. On 1 g/kg ideal body weight amino acid infusion, two patients excreted more than 240 mg of calcium in the urine, while on 2 g/kg ideal body weight amino acid infusion all five patients lost more calcium in urine than was infused. Mean urinary calcium excretion was increased from 287 to 455 mg/day. On the higher amino acid dose, mean glomerular filtration rate increased from 102 to 143 ml/min. There was no effect of amino acid dose on serum calcium, ionized calcium, parathyroid hormone, and 25 (OH) vitamin D. Calcium excretion corrected for the glomerular filtration rate was increased at the higher amino acid dose, indicating a decrease in renal calcium reabsorption. Daily urinary excretion of sulfate, ammonia, and titratable acidity were increased during the high amino acid infusion. Hypercalciuria induced by high levels of amino acid infusion during total parenteral nutrition may contribute to the development of metabolic bone disease.
 ...
PMID:Amino acid-induced hypercalciuria in patients on total parenteral nutrition. 641 Aug 98

In hypoparathyroidism the absence of parathyroid hormone leads to a reduction in the absorption of calcium by renal tubular cells. In spite of treatment with vitamin D, hypercalciuria persists and normocalcaemia can only be maintained by providing the kidney with a large load of calcium. Thiazide diuretics enhance tubular calcium reabsorption and it has been suggested that they can be used as an alternative to vitamin D. Bendrofluazide in a dose of 10 mg daily was given to 9 patients with severe hypoparathyroidism in addition to their usual treatment with calcium and vitamin D. Following the introduction of Bendrofluazide the calculated renal threshold for calcium reabsorption (TmCa/GFR) increased by a mean value of 0.14 mmol/l, and the mean rise in serum calcium was 0.13 mmol/l. This increase was due to a direct effect of the drug and was not caused by salt restriction or changes in glomerular filtration rate. The rise in serum calcium is modest compared to the rise following the introduction of vitamin D and except for patients with mild hypoparathyroidism, thiazides are not an alternative to vitamin D. They may however reduce the oral calcium load required to maintain normocalcaemia.
 ...
PMID:Effect of bendrofluazide on calcium reabsorption in hypoparathyroidism. 648 26

The state of vitamin D nutrition depends on synthesis in the skin under the influence of sunlight as well as on dietary intake. In European countries that do not fortify milk with vitamin D, reduced sun exposure is the major factor leading to a fall in body stores of vitamin D with age and to a high frequency of hypovitaminosis D in the elderly sick. In the US, because vitamin D is added to milk and the use of vitamin D supplements is more common, the dietary intake of vitamin D is relatively more important than in Europe, and the total vitamin D intake and body stores of vitamin D are generally higher. Nevertheless, body stores of vitamin D probably fall with age in the US as they do in Europe, and it is likely that some sick elderly persons in the US, especially among those confined to institutions, become vitamin D deficient. For several reasons, the vitamin D requirement increases with age, and a total supply of 15 to 20 micrograms/day (600 to 800 IU) from all sources is recommended. Special attention should be paid to persons most likely to need supplementation, such as the housebound, persons with malabsorption, and persons with interruption of the enterohepatic circulation. Osteomalacia, the bone disease produced by severe vitamin D deficiency, is less common in the US than in Europe, but subclinical vitamin D deficiency may contribute to the pathogenesis of hip fractures, both through increased liability to fall and through PTH-mediated bone loss. The extent to which vitamin D deficiency contributes to hip fractures in the US is unknown, and is an important area for future research. Excess intake of vitamin D or of its metabolites may result in hypercalcemia and extra-osseous calcification, particularly in arterial walls and in the kidney, leading to chronic renal failure. The dose of vitamin D that causes significant hypercalcemia is highly variable between individuals but is rarely less than 1000 micrograms/day. Smaller doses can cause hypercalciuria and nephrolithiasis and possibly impaired renal function. Vitamin D administration may raise plasma cholesterol but there is no convincing evidence that the risk of myocardial infarction is increased. The recommended total supply for the elderly of 20 micrograms/day is most unlikely to be harmful, except in patients with sarcoidosis or renal calculi.
 ...
PMID:Vitamin D and bone health in the elderly. 676 68


<< Previous 1 2 3 4 5 6 7 8 9 10