Calcium and Phosphorus Homeostasis

Several disorders have already been discussed the following are additional disorders of calcium and phosphorus homeostasis. In rickets in children and osteomalacia in adults, there is failure of mineralization of osteoid, with consequent softening of bones. In rickets, there is defective mineralization of bone and of the cartilaginous matrix 

An estimated 75 million people are affected by osteoporosis to some degree in the United States, Europe, and Japan. Osteoporosis is a systematic skeletal disease characterized by bone mass and microarchitectural deterioration with a consequent increase in bone fragility and susceptibility to fracture. Operationally, osteoporosis can be defined as a certain level of bone mineral density. The definition of osteoporosis is somewhat arbitrary and is based on epidemiological data relating fracture incidence to bone mass. Uncertainty also is introduced due to variability in bone densitometry measurements. Other clinical measures to assess the skeleton include collagen cross-links (measure of bone resorption) and levels of bone-specific alkaline phosphatase and osteocalcin (bone formation). A list of biochemical markers of bone remodeling is provided in Table 37-3. Measurement of total serum alkaline phosphatase level and urinary hydroxyproline or calcium levels is of limited value. 

Osteoporosis requires both increased resorption and one or more defects in bone formation. During adolescence, the rate of bone formation is higher than the rate of bone resorption in older persons the rate of bone resorption 

Biochemical Markers of Bone Formation and Bone Resorption 

Bone-specific alkaline phosphatase Rich in osteoblasts 

---

As renal function declines in patients with CKD, decreased phosphorus excretion disrupts the balance of calcium and phosphorus homeostasis. 0 The parathyroid glands release PTH in response to decreased serum calcium and increased serum phosphorus levels. The actions of PTH include ... 

However, results obtained by Koo et al. (1991) indicate that low to moderate lead exposure (average lifetime PbB level range of 4.9-23.6 pg/dL, geometric mean of 9.8 pg/dL, n=105) in young children with adequate nutritional status, particularly with respect to calcium, phosphorus, and vitamin D, has no effect on vitamin D metabolism, calcium and phosphorus homeostasis, or bone mineral content. The authors attribute the difference in results from those other studies to the fact that the children in their study had lower PbB levels (only 5 children had PbB levels >60 pg/dL and all 105 children had average lifetime PbB levels <45 pg/dL at the time of assessment) and had adequate dietary intakes of calcium, phosphorus, and vitamin D. They concluded that the effects of lead on vitamin D metabolism observed in previous studies may, therefore, only be apparent in children with chronic nutritional deficiency and chronically elevated PbB levels. Similar conclusions were reached by IPCS (1995) after review of the epidemiological data. 

See Chap. 52, Disorders of Sodium and Water Homeostasis, authored by James D. Coyle and Melanie S. Joy Chap. 53, Disorders of Calcium and Phosphorus Homeostasis, authored by Amy Barton Pai, Mark Rohrscheib, and Melanie S. Joy and Chap. 54, Disorders of Potassium and Magnesium Homeostasis, authored by Donald F. Brophy and Todd W. B. Gehr, for a more detailed discussion of this topic... 

Anderson, S.A., Ed. "Effects of Certain Vitamins and Minerals on Calcium and Phosphorus Homeostasis" Life Sciences Research Office, Federation of American Societies for Experimental Biology Bethesda, Maryland, 1982 pp. 1-93. 

Lukert BP, Adams JS. Calcium and phosphorus homeostasis in man. Effect Corticosteroids. Arch Intern Med 1976 136(ll) 1249-53. 

Rhodopsin, visual cycle, night vision Blood clotting factors II, VII, IX, and X Calcium and phosphorus homeostasis Antioxidant, glutathione oxidase... 

Vitamin D, along with parathyroid hormone and calcitonin, plays a primary role in calcium and phosphorus homeostasis in the body. Intensive research efforts over the past several years have elucidated a role for vitamin D in many other physiological processes as well. The biological actions of this seco-steroid are mediated primarily through the action of its polar metabolite, 1,25-dihydroxy vitamin D3 (l,25(OH)2D3). There is emerging evidence that l,25(OH)2D3 has many more target tissues than those involved in its classical role in the control of mineral metabolism. In addition, some of the actions of l,25(OH)2D3 may be mediated by mechanisms other than the classical steroid-receptor interaction. In this chapter we will provide a brief overview of the multiple actions of vitamin D3 and the pleiotropic mechanisms by which these actions are accomplished. 

Sanderson, P. H., Marshall, F., and Wilson, R. E., Calcium and phosphorus homeostasis in the parathyroidectomized dog evaluation by means of ethylene-diamine tetraacetate and calcium tolerance tests. J. Clin. Invest. 39, 662-670 (1960). 

Disorders of Sodium, Water, Calcium, AND Phosphorus Homeostasis... 

CHAPTER 49 DISORDERS OF SODIUM, WATER, CALCIUM, AND PHOSPHORUS HOMEOSTASIS... 

Fio. 12. Scheme of calcium and phosphorus homeostasis in progressive renal disease — , increases decreases GFR, glomerular filtration rate P, serum phosphorus Ca2+, serum ionized calcium Ca, calcium 1,25-DHCC, 1,25-dihydroxy cholecalciferol PTH, serum parathyroid hormone Cp, phosphate clearance. 

H)2D3 (calcitriol) is approximately 100 times more potent than 25-(0H)D3 in its actions, yet 25-(0H)D3 is present in the blood in a concentration that may be 100 times greater, which suggests that it may play some role in calcium and phosphorus homeostasis. 

Vitamin D is required for efficient absorption of calcium and phosphorus in the intestinal trad, and it is also necessary for calcium and phosphorus homeostasis within the body. Deficiency of vitamin D will, therefore, lead to calcium deficiency and will affect processes such as bone formation and egg-shell production. Bone mineralisation is dependent on the maintenance of Gi and phosphate levels. The effect of vitamin D on these processes is mediated by calbindin and is discussed in Section 10.6. Aluminium toxicity is, at least in part, accounted for by disturbance of calcium homeostasis. Aluminium compounds reduce vitamin D-dependent Gi absorption in chicks. They act by reducing the intestinal calbindin concentration (Dunn et al, 1993). 

Analytical and clinical validation of an RIA for the measurement of 1,25-dihydroxyvitamin D was performed by Clive and co-workers. Vitamin D is a critical regulator of calcium and phosphorus homeostasis. This assay was specific for both 1,25-dihydroxyvitamin D2 and D3. The data collected during this study demonstrated that the RIA validated was a robust, accurate, and precise tool for the assessment of vitamin D. 

---