Phosphorus metabolism, disorders

Calcitonin is a 32-amino-acid polypeptide hormone that was hrst purihed in 1962 by Copp and Cheney (121). It was originally thought as a product from parathyroid glands, but later it was discovered to be made by the C cells of the thyroid gland. Calcitonin participates in calcium and phosphorus metabolism, lowers plasma calcium and phosphate levels, and it has been used as a drug for bone and mineral disorders for a long time. 

Knochel, J. P. (1994). Disorders of phosphorus metabolism. In "Harrison s Principles of Internal Medicine" (K. Isselbacher, ed.), Vol. 2. McGraw-Hill, New York. 

FIGURE 61-2 Adapted, widi permission, from Yanagawa N, Lee DBN Renal handling of calcium and phosphorus. In Disorders of Bone and Mineral Metabolism. FL Coe, MJ Favus (eds). Philadelphia, Lippincott Williams Wilkins, 1992. 

Disorders of the calcium-phosphate metabolism are additional risk factors for renal disease progression. Several factors related to disturbed calcium-phosphorus metabolism, such as hyperphosphatemia, hyperparathyroidism, lack of... 

Phosphorus MRS studies of depressed subjects strongly indicate that this disorder arises from altered brain energy metabolism 944 Hydrogen MRS has revealed unique and consistent metabolic characteristics in the brains of patients with probable AD 944 Hydrogen and phosphorus MRS have proven to be useful tools in the characterization of several epilepsies 944... 

T. Kato, S. Takahashi, T. Shioiri and T. Inubushi, Brain phosphorous metabolism in depressive disorders detected by phosphorus-31 magnetic resonance spectroscopy. /. Affect. Disord., 1992, 26,223-230. 

Knowledge of phosphorus and citrate metabolism in vitamin D poisoning and in idiopathic hypercalcemia of infancy is very incomplete and somewhat contradictory, but in certain respects the changes in these electrolytes in these two disorders may differ. 

Holick, M. F, (1996). Evaluation and treatment of disorders in calcium, phosphorus, and magnesium metabolism. In Textbook of Primary Care Medicine" (J. Noble, ed.). Mosby, 5t. Louis. 

Fluid and electrolyte disorders and metabolic acidosis are primarily the result of altered transport mechanisms within the kidney and decreased elimination of solutes (see Chaps. 49, 50, and 51). Malnutrition may also occur as dietary changes such as phosphorus restriction are implemented. Foods high in phosphorus are generally also high in protein therefore restriction of these protein sources contributes to malnutrition. Malnutrition may also develop due to decreased appetite in those with severe kidney disease. The likelihood of developing these secondary complications and comorbidities increases as GFR declines. 

Slatopolsky E, Hruska KA. Disorders of phosphorus, calcium and magnesium metabolism. In Schrier RW, ed. Diseases of the Kidney and Urinary Tract, Vol. 3, 7th ed. Philadelphia, Lippincott, Wilhams and Wilkins, 2001 2607-2660. 

Other chronic disorders cause osteomalacia. " " Phosphate depletion from low dietary intake, phosphate-binding antacids, and oncogenic osteomalacia (potentially phosphaturic effect) can cause osteomalacia. Hypophosphatasia is an inborn error of metabolism in which deficient activity of alkaline phosphatase causes impaired mineralization of bone matrix. Acidosis from renal dysfunction, distal renal tubular acidosis, hypergammaglobulinemic states (e.g., multiple myeloma), and drugs (e.g., chemotherapy) compromises bone mineralization. Renal tubular disorders secondary to Fanconi s syndrome, hereditary diseases (e.g., Wilson s disease, a defect in copper metabolism), acquired disease (e.g., myeloma), and toxins (e.g., lead) cause osteomalacia to varying degrees. Chronic wastage of phosphorus and/or calcium limits mineralization, which may be further compromised by acidosis and secondary hyperparathyroidism. 

Beoadus AE (1993) Physiological Junctions of calcium, magnesium and phosphorus and mineral ion balance. In Favus MJ, ed. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, pp. 41-46. Raven Press New York. 

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