Skip to main content

Hyper- and Hypophosphataemia

  • Chapter
Book cover Calcium in Internal Medicine
  • 192 Accesses

Abstract

Abnormalities in serum concentrations of phosphate, whether hyperphosphataemia or hypophosphataemia, are caused by abnormalities in the following conditions: 1) abnormalities in oral intake and in intestinal absorption of phosphate, 2) abnormalities in renal excretion of phosphate, and 3) abnormal shift of phosphate from cells to extracellular fluid or abnormal shift of phosphate into cells. When considering the differential diagnosis of abnormalities in serum phosphate levels, these three mechanisms should be considered to enable correct treatment. In this chapter, homeostasis of phosphate metabolism in adults is described first, followed by hypophosphataemia and hyperphosphataemia.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 39.99
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 54.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Nordin BEC Nutritional considerations. In: Nordin BEC, editor. Calcium, phosphate, and magnesium metabolism. Edinburgh: Churchill Livingstone, 1976; 1–35.

    Google Scholar 

  2. Suki WN, Rouse D. Renal transport of calcium, magnesium, and phosphate. Philadelphia: W.B. Saunders; 1996;472–515.

    Google Scholar 

  3. Taketani Y, Miyamoto K, Chikamori M, Tanaka K, Yamamoto H, Tatsumi S, etal. Characterization of the 5′ flanking region of the human NPT-1 Na+/phosphate co-transporter gene. Biochim Biophys Acta 1998;1396:267–72.

    PubMed  CAS  Google Scholar 

  4. Tatsumi S, Miyamoto K, Kouda T, Motonaga K, Katai K, Ohkido I, et al. Identification of three isoforms for the Na+-dependent phosphate co-transporter (NaPi-2) in rat kidney. J Biol Chem 1998;273: 28568–75.

    Article  PubMed  CAS  Google Scholar 

  5. Yanagawa N, Nakhoul F, Kurokawa K. Physiology of phosphorus metabolism, in clinical disorders of fluids and electrolytes, 5th ed, Narins RG, editor. New York: McGraw-Hill, 1995;345–50.

    Google Scholar 

  6. Portale AA, Halloran BP, Morris Jr RC, Lonergan ET. Effect of aging on the metabolism of phosphorus and 1,25-dihydroxyvitamin D in healthy men. Am J Physiol 1996;270:E483–90.

    PubMed  CAS  Google Scholar 

  7. Sorribas V, Lotscher M, Loffing J, Biber J, Kaissling B, Murer H, et al. Cellular mechanisms of the age- related decrease in renal phosphate reabsorption. Kidney Int 1996;50:855–63.

    Article  PubMed  CAS  Google Scholar 

  8. Suda T, Takahashi N, Martin TJ. Modulation of osteoclast differentiation. Endocr Rev 1992;13:66–80.

    PubMed  CAS  Google Scholar 

  9. Yasuda H, Shima N, Nakagawa N, Yamaguchi K, Kinosaki M, Mochizuki S, etal. Osteoclast differentiation factor is a ligand for osteoprotegerin/osteoclastogenesis-inhibitory factor and is identical to TRANCE/RANKL. Proc Natl Acad Sci USA 1998;95:3597–602.

    Article  PubMed  CAS  Google Scholar 

  10. Anderson DM, Maraskovsky E, Billingsley WL, Dougall WC, Tometsko ME, Roux ER, etal. A homologue of the TNF receptor and its ligand enhance T-cell growth and dendritic cell function. Nature 1997;390:175–9.

    Article  PubMed  CAS  Google Scholar 

  11. Yasuda H, Shima N, Nakagawa N, Yamaguchi K, Kinosaki M, Goto M, etal. A novel molecular mechanism modulating osteoclast differentiation and function. Bone 1999;25:109–13.

    Article  PubMed  CAS  Google Scholar 

  12. Katai K, Segawa H, Haga H, Morita K, Arai H, Tatsumi S, etal. Acute regulation by dietary phosphate of the sodium-dependent phosphate transporter (NaP(i)-2) in rat kidney. J Biochem (Tokyo) 1997;121:50–5.

    CAS  Google Scholar 

  13. Travis SF, Sugerman HJ, Ruberg RL, Dudrick SJ, Delivoria-Papadopoulos M, Miller LD, etal. Alterations of red-cell glycolytic intermediates and oxygen transport as a consequence of hypophosphatemia in patients receiving intravenous hyperalimentation. N Engl J Med 1971;285:763–8.

    Article  PubMed  CAS  Google Scholar 

  14. Knochel JP, Barcenas C, Cotton JR, Fuller TJ, Haller R, Carter NW. Hypophosphatemia and rhabdomyolysis. J Clin Invest 1978;62:1240–6.

    Article  PubMed  CAS  Google Scholar 

  15. O’Connor LR, Wheeler WS, Bethune JE. Effect of hypophosphatemia on myocardial performance in man. N Engl J Med 1977;297:901–3.

    Article  PubMed  Google Scholar 

  16. Ishimura E, Miki T, Koyama H, Harada K, Nakatsuka K, Inaba M, etal. Effect of aminohydroxypropylidene diphosphonate on the bone metabolism of patients with parathyroid adenoma. Horm Metab Res 1993;25:493–7.

    Article  PubMed  CAS  Google Scholar 

  17. Fukumoto S, Takeuchi Y, Nagano A, Fujita T. Diagnostic utility of magnetic resonance imaging skeletal survey in a patient with oncogenic osteomalacia. Bone 1999;25:375–7.

    Article  PubMed  CAS  Google Scholar 

  18. Huang QL, Feig DS, Blackstein ME. Development of tertiary hyperparathyroidism after phosphate supplementation in oncogenic osteomalacia. J Endocrinol Invest 2000;23:263–7.

    PubMed  CAS  Google Scholar 

  19. Ohashi K, Ohnishi T, Ishikawa T, Tani H, Uesugi K, Takagi M. Oncogenic osteomalacia presenting as bilateral stress fractures of the tibia. Skeletal Radiol 1999;28:46–8.

    Article  PubMed  CAS  Google Scholar 

  20. Li Y, Song YH, Rais N, Connor E, Schatz D, Muir A, etal. Autoantibodies to the extracellular domain of the calcium-sensing receptor in patients with acquired hypoparathyroidism. J Clin Invest 1996; 97:910–14.

    Article  PubMed  CAS  Google Scholar 

  21. Pearce SH, Williamson C, Kifor O, Bai M, Coulthard MG, Davies M, etal. A familial syndrome of hypocalcemia with hypercalciuria due to mutations in the calcium-sensing receptor. N Engl J Med 1996;335:1115–22.

    Article  PubMed  CAS  Google Scholar 

  22. Nakamura Y, Matsumoto T, Tamakoshi A, Kawamura T, Seino Y, Kasuga M, etal. Prevalence of idio-pathic hypoparathyroidism and pseudohypoparathyroidism in Japan. J Epidemiol 2000;10:29–33.

    PubMed  CAS  Google Scholar 

  23. Schipani E, Weinstein LS, Bergwitz C, Iida-Klein A, Kong XF, Stuhrmann M, etal. Pseudohypoparathyroidism type lb is not caused by mutations in the coding exons of the human parathyroid hormone (PTH)/PTH-related peptide receptor gene. J Clin Endocrinol Metab 1995;80:1611–21.

    Article  PubMed  CAS  Google Scholar 

  24. Fukumoto S, Suzawa M, Takeuchi Y, Kodama Y, Nakayama K, Ogata E, et al. Absence of mutations in parathyroid hormone (PTH)ZPTH-related protein receptor complementary deoxyribonucleic acid in patients with pseudohypoparathyroidism type lb. J Clin Endocrinol Metab 1996;81:2554–8.

    Article  PubMed  CAS  Google Scholar 

  25. Barrett D, Breslau NA, Wax MB, Molinoff PB, Downs Jr RW. New form of pseudohypoparathyroidism with abnormal catalytic adenylate cyclase. Am J Physiol 1989;257:E277–83.

    PubMed  CAS  Google Scholar 

  26. Bastepe M, Juppner H. Pseudohypoparathyroidism. New insights into an old disease. Endocrinol Metab Clin North Am 2000;29:569–89.

    CAS  Google Scholar 

  27. Mantovani G, Romoli R, Weber G, Brunelli V, De Menis E, Beccio S, etal. Mutational analysis of GNAS1 in patients with pseudohypoparathyroidism: identification of two novel mutations [In Process Citation]. J Clin Endocrinol Metab 2000;85:4243–8.

    Article  PubMed  CAS  Google Scholar 

  28. Liu J, Litman D, Rosenberg MJ, Yu S, Biesecker LG, Weinstein LS. A GNAS1 imprinting defect in pseudohypoparathyroidism type IB [In Process Citation]. J Clin Invest 2000;106:1167–74.

    Article  PubMed  CAS  Google Scholar 

  29. Ishimura E, Nishizawa Y, Inaba M, Matsumoto N, Emoto M, Kawagishi T, etal. Serum levels of 1,25- dihydroxyvitamin D, 24,25-dihydroxyvitamin D, and 25-hydroxyvitamin D in nondialysed patients with chronic renal failure. Kidney Int 1999;55:1019–27.

    Article  PubMed  CAS  Google Scholar 

  30. Slatopolsky EA, Burke SK, Dillon MA. RenaGel, a non-absorbed calcium- and aluminium-free phosphate binder, lowers serum phosphorus and parathyroid hormone. The RenaGel Study Group. Kidney Int 1999;55:299–307.

    Article  CAS  Google Scholar 

  31. Slatopolsky E, Finch J, Denda M, Ritter C, Zhong M, Dusso A, etal. Phosphorus restriction prevents parathyroid gland growth. High phosphorus directly stimulates PTH secretion in vitro. J Clin Invest 1996;97:2534–40.

    CAS  Google Scholar 

  32. Block GA, Port FK. Re-evaluation of risks associated with hyperphosphataemia and hyperparathyroidism in dialysis patients: recommendations for a change in management. Am J Kidney Dis 2000;35:1226–37.

    Article  PubMed  CAS  Google Scholar 

  33. Alfrey AC, LeGendre GR, Kaehny WD. The dialysis encephalopathy syndrome. Possible aluminum intoxication. N Engl J Med 1976;294:184–8.

    Article  PubMed  CAS  Google Scholar 

  34. Parkinson IS, Ward MK, Feest TG, Fawcett RW, Kerr DN. Fracturing dialysis osteodystrophy and dial¬ysis encephalopathy. An epidemiological survey. Lancet 1979;1:406–9.

    CAS  Google Scholar 

  35. Pei Y, Hercz G, Greenwood C, Sherrard D, Segre G, Manuel A, etal. Non-invasive prediction of aluminium bone disease in haemo- and peritoneal dialysis patients. Kidney Int 1992;41:1374–82.

    Article  PubMed  CAS  Google Scholar 

  36. Fournier A, Oprisiu R, Albu AT, Dungaciu M, El Esper N, Morniere P. The crossover comparative trial of calcium acetate versus sevelamer hydrochloride (Renagel) as phosphate binders in dialysis patients. Am J Kidney Dis 2000;35:1248–50.

    Article  PubMed  CAS  Google Scholar 

  37. Collins AJ, St. Peter WL, Dalleska FW, Ebben JP, Ma JZ. Hospitalization risks between Renagel phosphate binder treated and non-Renagel treated patients. Clin Nephrol 2000;54:334–41.

    PubMed  CAS  Google Scholar 

  38. Chertow GM, Burke SK, Dillon MA, Slatopolsky E. Long-term effects of sevelamer hydrochloride on the calcium Х phosphate product and lipid profile of haemodialysis patients. Nephrol Dial Transplant 1999;14:2907–14.

    Article  PubMed  CAS  Google Scholar 

  39. Gonzalez-Compta X, Manos-Pujol M, Foglia-Fernandez M, Peral E, Condom E, Claveguera T, etal. Oncogenic osteomalacia: case report and review of head and neck associated tumours. J Laryngol Otol 1998;112:389–92.

    Article  PubMed  CAS  Google Scholar 

  40. Drezner MK. PHEX gene and hypophosphatemia. Kidney Int 2000;57:9–18.

    Article  PubMed  CAS  Google Scholar 

  41. Rowe PS, de Zoysa PA, Dong R, Wang HR, White KE, Econs MJ, etal. MEPE, a new gene expressed in bone marrow and tumors causing osteomalacia. Genomics 2000;67:54–68.

    Article  PubMed  CAS  Google Scholar 

  42. Shimada T, Mizutani S, Muto T, Yoneya T, Hino R, Takeda S, Takeuchi Y, Fujita T, Fukumoto S, Yamashita T. Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia. Proc Natl Acad Sci USA 2001;98:6500–5.

    Article  PubMed  CAS  Google Scholar 

Download references

Authors

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 2002 Springer-Verlag London Limited

About this chapter

Cite this chapter

Ishimura, E., Imanishi, Y., Inaba, M. (2002). Hyper- and Hypophosphataemia. In: Morii, H., Nishizawa, Y., Massry, S.G. (eds) Calcium in Internal Medicine. Springer, London. https://doi.org/10.1007/978-1-4471-0667-8_9

Download citation

  • DOI: https://doi.org/10.1007/978-1-4471-0667-8_9

  • Publisher Name: Springer, London

  • Print ISBN: 978-1-4471-1173-3

  • Online ISBN: 978-1-4471-0667-8

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics