Calcium concentration, urinary

A negative correlation was found between PbB and systolic pressure in Belgian men in the Cadmibel study (a cross-sectional population study of the health effects of environmental exposure to cadmium) (Staessen et al. 1991). In this study, blood pressure and urinary cation (positive ions found in the urine, such as sodium, potassium, and calcium) concentration data were obtained from 963 men and 1,019 women multiple stepwise regression analyses were conducted adjusting for age, body mass index, pulse... 

Prentice, A., Jaqou, L. M., Cole, T. J., Stirling, D. M., Dibba, B., and Fairweather-Tait, S. (1995). Calcium requirements of lactating Gambian mothers Effects of a calcium supplement on breast-milk calcium concentration, maternal bone mineral content, and urinary calcium excretion. Am. J. Clin. Nutr. 62, 58-67. 

A patient with psoriasis developed hypercalcemia and hypercalciuria after 28 days of treatment with tacalcitol (1208). He had been taking long-term thiazide therapy for his hypertension. When he used topical tacalcitol ointment his serum calcium concentration and urinary calcium excretion gradually increased to 3.55 mmol/1 and 0.475 g/day respectively. Within 7 days of withdrawal of tacalcitol, the serum calcium concentration had normalized. 

The major location of calcium in the body is in the skeleton, which contains more than 90% of the body calcium as phosphate and carbonate. Bone resorption and formation keeps this calcium in dynamic equilibrium with ionized and complexed calcium in blood, cellular fluids and membranes. Homeostasis is mainly regulated by the parathyroid hormone and vitamin D which lead to increased blood calcium levels, and by a thyroid hormone, calcitonin, which controls the plasma calcium concentration J5 Increasing the concentration of calcitonin decreases the blood calcium level, hence injections of calcitonin are used to treat severe hyperalcaemia arising from hyperparathyroidism, vitamin D intoxication or the injection of too high a level of parathyroid extract. High levels of calcitonin also decrease resorption of calcium from bone. Hypocalcaemia stimulates parathyroid activity, leading to increased release of calcium from bone, reduction in urinary excretion of calcium and increased absorption of calcium from the intestine. Urinary excretion of phosphate is enhanced. 

Approximately two thirds of all renal stones contain calcium phosphate or calcium oxalate. Many patients with such stones exhibit a renal defect in calcium reabsorption that causes hypercalciuria. This can be treated with thiazide diuretics, which enhance calcium reabsorption in the distal convoluted tubule and thus reduce the urinary calcium concentration. Salt intake must be reduced in this setting, as excess dietary NaCl will overwhelm the hypocalciuric effect of thiazides. Calcium stones may also be caused by increased intestinal absorption of calcium, or they may be idiopathic. In these situations, thiazides are also effective, but should be used as adjunctive therapy with decreased calcium intake and other measures. 

A 6-year-old girl with Hirschsprung s disease had jeju-nostomy at 1 month followed by parenteral nutrition (47). Her calcium intake was 1-1.5 mmol/kg/day. Her urinary calcium rose from 3 months of age her serum calcium concentrations remained within the reference range but started to rise when she was 3-4 years old. At 5-6 years of age she showed growth retardation and deteriorating renal tubular function with bilateral... 

The high prevalence of oxalate containing renal (tubular) and urinary tract calcifications is related to the low solubility of the oxalate-calcium salt. High urine oxalate excretion increases urine calcium oxalate supersaturation and, therefore the risk of crystal formation in tubular fluid and urine. In human urine, calcium concentration is about ten fold higher than oxalate on molar base. Relatively modest increases in urine oxalate excretion will have significant effects on urine supersaturation [49], especially in patients with hypercalciuria where calcium is even in greater excess of oxalate. Nevertheless, most people do not suffer from renal calcifications [50-54], suggesting that renal protection mechanisms exist. 

A first defence mechanism is fhaf a high urinary calcium concentration is able to reduce ADH-stimu-lated water permeability of the collecting duct via the calcium sensing receptor at the luminal site of the thick ascending loop of Henle, leading to an increased urinary volume and a reduced risk of supersaturation. 

Calcium salts, such as calcium oxalate, precipitate in urine specimens during and after collection. Specimens may be collected in a container containing acid to prevent calcium salt precipitation. A commonly used acid is HCl, 6 mol/L, with 20 to 30 mL added to the container for a 24-hour collection (1 to 2 mL for a random specimen). The safety of the patient and the patient s family in handling such a container may be a concern. The measured urinary calcium concentration must be corrected for the dilution by the acid solution when the urinary volume is low. The specimen should be kept well mixed during collection. Specimens collected without acid should be acidified and allowed to stand for 1 hour before thorough remixing and aliquot-ing. Some have questioned the ability of postcollection acidification to redissolve all of the calcium salts with or without heating. ... 

Adverse effects of oral calcium and vitamin D supplementation include hypercalcemia and hypercalciuria, especially in the hy-poparathyroid patient, in whom the renal calcium-sparing effect of parathyroid hormone is absent. Hypercalciuria may increase the risk of calcium stone formation and nephrolithiasis in susceptible patients. One maneuver to help prevent calcium stones is to maintain the calcinm at a low normal concentration. Monitoring 24-hour urine collections for total calcium concentrations (goal <300 mg/24 h) may also minimize the occurrence of hypercalciuria. The addition of thiazide dinretics for patients at risk for stone formation may result in a reduc-tionof both urinary calcium excretion and vitamin D requirements." ... 

The most common cause of hyperphosphatemia is a decrease in urinary phosphorus excretion secondary to decreased glomerular filtration rate. ° Retention of phosphorus decreases vitamin D synthesis and induces hypocalcemia, which leads to an increase in PTH. This physiologic response inhibits further tubular reabsorption of phosphorus to correct hyperphosphatemia and normalize serum calcium concentrations. Patients with excessive exogenous phosphorus administration or endogenous intracellular phosphorus release in the setting of acute renal failure may develop profound hyperphosphatemia. Severe hyperphosphatemia is commonly encountered in patients with chronic kidney disease, especially those with GFRs less than 15 mL/ min per 1.73 m (see Chap. 44). 

The relationship of the inorganic phosphate concentration to bone mineral is more complex. The normal range of plasma phosphate concentration is much larger than that of calcium, presumably because the phosphate concentration (unlike that of calcium) is influenced by dietary intake of phosphorus and by urinary excretion and because the parathyroids intervene to correct major changes in calcium concentration. The skeleton thus controls plasma calcium at a constant level but permits relatively large variations in plasma phosphate there is therefore no constant [calcium] [phosphate] product in plasma or tissue fluid... 

A wide range of plasma phosphorus concentration has been observed by other workers in primary hyperparathyroidism (C7) and explained in terms of diet and renal excretion. Unlike the calcium concentration, which is normally very constant regardless of dietary intake and urinary excretion, the concentration of inorganic phosphate in plasma is the resultant of the rate of phosphorus absorption from the gut and protein catabolism, on the one hand, and of renal excretion, on the other. Although the parathyroid hormone promotes phosphorus excretion, this is only one of the factors governing plasma phosphate concentration. Plasma phosphate in cases of hyperparathyroidism on a relatively high phosphorus intake may therefore not be distinguishable from that in normal subjects on a lower intake. 

The thiazides decrease the urinary calcium concentration by diminishing glomerular filtration and also enhance the urinary magnesium level. 

Mineral balance Calcium and bone metabolism have been assessed in 144 Indian subjects before and after 6 months of treatment with antiepileptic drugs [78. At the start of foUow-up, daily dietary calcium intake was lower than the dietary aUowance recommended by the Indian Council of Medical Research, and two-thirds of the recruited subjects were vitamin D deficient. Subjects with normal 25-hydroxycholecalciferol concentrations at baseline had significant falk in 25-hydroxycolecalciferol concentrations, urinary calcium concentrations, and tartrate-resistant acid phosphatase activity at the end of 6 months, irrespective of the antiepileptic drug used. 

Urinary tract Administration of furosemide to preterm infants may increase the risk of nephrocalcinosis. In 55 neonates bom before 32 weeks of gestation a multivariate analysis showed that the strongest independent susceptibility factor for nephrocalcinosis was furosemide therapy in a cumulative dose of over lOmg/kg (OR=48 95% Cl = 4, 585) [13 ]. The risk of nephrocalcinosis increased in proportion to the urinary calcium concentration (OR=4.5 for each 1 mmol/1 increase 95% Cl = 1.1,18). 

Exaggerated osteoclast activation leads to another bone disease — osteoporosis. In an ovariectomized rat model, the estrogen deficiency induces osteoporosis, which was reversed by continuous administration of NF-kB decoy using an osmotic pump. The reversal was indicated by attenuation of TRAP activity, significant increase in calcium concentrations in the femur and tibia, and a decrease in urinary deoxypyridinoline. In agreement, NF-kB decoy ODN infusion in an osteoporosis model of vitamin C-deficient rat dramatically improved the bone length, weight, and mineral density, as assessed by DEXA [24]. 

Bames, D.W.H., Bishop, M., Harrison, G.E. and Sutton, A. 1961 Comparison of the plasma concentration and urinary excretion of strontium and calcium in man. InternationalJournal of Radiation Biology 3 637-646. 

In mammals, phenobarbital and phenytoin increase serum ceruloplasmin concentrations (Aaseth and Norseth 1986). Chronic copper poisoning in sheep is exacerbated when diets contain heliotrope plants (Heliotropium sp., Echium spp., Senecio sp.). Aggravated effects of the heliotrope plants include reduced survival and a twofold to threefold increase in liver and kidney copper concentrations when compared to control animals fed copper without heliotropes (Howell et al. 1991). Rats given acutely toxic doses of 2,3,7,8-tetrachlorodibenzo-para-dioxin had elevated concentrations of copper in liver and kidney because of impaired biliary excretion of copper (Elsenhans et al. 1991). Morphine increases copper concentrations in the central nervous system of rats, and dithiocarbam-ates inhibit biliary excretion (Aaseth and Norseth 1986). In human patients, urinary excretion of copper is increased after treatment with D-penicillamine, calcium disodium EDTA, or calcium trisodium diethylenetriamine penta acetic acid (Flora 1991). 

While our data using this technique are still preliminary, we have observed that 25 yU/ml insulin inhibits the rate of calcium efflux from renal slices (28). This effect of insulin was gradually reduced at the higher concentrations of insulin. The effects of insulin on calcium exchange appear to be localized in the mitochondrial compartment. Further work is needed to determine whether insulin affects specific enzyme systems which are known to play a role in renal calcium transport, and which cellular or subcellular compartments are involved. This would substantially increase our understanding of the regulation of urinary calcium excretion, and of ways in which excessive loss of calcium by this route might be avoided. 

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