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XI. Conclusions

Pi is a key ion in the body, with important diverse functions. The maintenance of serum Pi levels is dependent on normal kidney function. As a result, patients with kidney disease are often hyperphosphatemic. Elevations in serum Pi are associated with increased morbidity and mortality in patients with CKD, may hasten loss of residual renal function, and can cause secondary hyperparathyroidism. Unfortunately, current removal of Pi with thrice weekly hemodialysis or daily peritoneal dialysis is not adequate for normal dietary intake. As a result, phosphate binders are a mainstay of therapy in patients with CKD.

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References

  1. Cupisti A, Morelli E, D’Alessandro C, et al. Phosphate control in chronic uremia: don’t forget diet. J Nephrol 2003;16(1):29–33.

    PubMed  CAS  Google Scholar 

  2. Kayne LH, D’Argenio DZ, Meyer JH, et al. Analysis of segmental phosphate absorption in intact rats. A compartmental analysis approach. J Clin Invest 1993;91(3):915–22.

    PubMed  CAS  Google Scholar 

  3. Tenenhouse HS. Regulation of phosphorus homeostasis by the type IIa na/phosphate cotransporter. Annu Rev Nutr 2005;25:197–214.

    Article  PubMed  CAS  Google Scholar 

  4. Favus MJ. Factors that influence absorption and secretion of calcium in the small intestine and colon. Am J Physiol 1985;248(2 Pt 1):G147–57.

    PubMed  CAS  Google Scholar 

  5. Lotscher M, Kaissling B, Biber J, et al. Role of microtubules in the rapid regulation of renal phosphate transport in response to acute alterations in dietary phosphate content. J Clin Invest 1997;99(6):1302–12.

    PubMed  CAS  Google Scholar 

  6. Parfitt AM. Targeted and nontargeted bone remodeling: relationship to basic multicellular unit origination and progression. Bone 2002;30(1):5–7.

    Article  PubMed  CAS  Google Scholar 

  7. Hofbauer LC, Khosla S, Dunstan CR, et al. The roles of osteoprotegerin and osteoprotegerin ligand in the paracrine regulation of bone resorption. J Bone Miner Res 2000;15(1):2–12.

    Article  PubMed  CAS  Google Scholar 

  8. Lories RJ, Luyten FP. Osteoprotegerin and osteoprotegerin-ligand balance: a new paradigm in bone metabolism providing new therapeutic targets. Clin Rheumatol 2001;20(1):3–9.

    Article  PubMed  CAS  Google Scholar 

  9. Sasaki N, Kusano E, Ando Y, et al. Glucocorticoid decreases circulating osteoprotegerin (OPG): possible mechanism for glucocorticoid induced osteoporosis. Nephrol Dial Transplant 2001;16(3):479–82.

    Article  PubMed  CAS  Google Scholar 

  10. Schiavi SC, Kumar R. The phosphatonin pathway: new insights in phosphate homeostasis. Kidney Int 2004;65(1):1–14.

    Article  PubMed  CAS  Google Scholar 

  11. Brame LA, White KE, Econs MJ. Renal phosphate wasting disorders: Clinical features and pathogenesis. Semin Nephrol 2004;24(1):39–47.

    Article  PubMed  CAS  Google Scholar 

  12. Larsson L, Rebel K, Sorbo B. Severe hypophosphatemia—a hospital survey. Acta Med Scand 1983;214(3):221–3.

    PubMed  CAS  Google Scholar 

  13. Cockcroft DW, Gault MH. Prediction of creatinine clearance from serum creatinine. Nephron 1976;16(1):31–41.

    PubMed  CAS  Google Scholar 

  14. Levey AS, Bosch JP, Lewis JB et al. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study Group. Ann Intern Med 1999;130(6):461–70.

    PubMed  CAS  Google Scholar 

  15. DiPalma JA, Buckley SE, Warner BA, et al. Biochemical effects of oral sodium phosphate. Dig Dis Sci 1996;41(4):749–53.

    Article  PubMed  CAS  Google Scholar 

  16. Better OS, Kleeman CR, Gonick HC, et al. Renal handling of calcium, magnesium and inorganic phosphate in chronic renal failure. Isr J Med Sci 1967;3(1):60–79.

    PubMed  CAS  Google Scholar 

  17. Moe SM, Drueke TB. Management of secondary hyperparathyroidism: the importance and the challenge of controlling parathyroid hormone levels without elevating calcium, phosphorus, and calcium-phosphorus product. Am J Nephrol 2003;23(6):369–79.

    Article  PubMed  CAS  Google Scholar 

  18. Llach F. Secondary hyperparathyroidism in renal failure: the trade-off hypothesis revisited. Am J Kidney Dis 1995;25(5):663–79.

    PubMed  CAS  Google Scholar 

  19. Brown EM. Mechanisms underlying the regulation of parathyroid hormone secretion in vivo and in vitro. Curr Opin Nephrol Hyperten 1993;2(4):541–51.

    Article  CAS  Google Scholar 

  20. Hsu CY, Chertow GM. Elevations of serum phosphorus and potassium in mild to moderate chronic renal insufficiency. Nephrol Dial Transplant 2002;17(8):1419–25.

    Article  PubMed  CAS  Google Scholar 

  21. LaClair RE, Hellman RN, Karp SL, et al. Prevalence of calcidiol deficiency in CKD: a crosssectional study across latitudes in the United States. Am J Kidney Dis 2005;45(6):1026–33.

    Article  PubMed  CAS  Google Scholar 

  22. DeSoi CA, Umans JG. Phosphate kinetics during high-flux hemodialysis. J Am Soc Nephrol 1993;4(5):1214–8.

    PubMed  CAS  Google Scholar 

  23. Gutzwiller JP, Schneditz D, Huber AR, et al. Estimating phosphate removal in haemodialysis: an additional tool to quantify dialysis dose. Nephrol Dial Transplant 2002;17(6):1037–44.

    Article  PubMed  CAS  Google Scholar 

  24. Delmez JA. Removal of phosphorus by peritoneal dialysis. Perit Dial Int 1993;13(Suppl 2):S461–3.

    PubMed  Google Scholar 

  25. Tomasellow S, Dhupar S, Sherman RA. Phosphate binders, K/DOQI guidelines, and compliance: the unfortunate reality. Dialysis Transplant 2004;33(5):236–40.

    Google Scholar 

  26. Mucsi I, Hercz G, Uldall R, Ouwendyk M, et al. Control of serum phosphate without any phosphate binders in patients treated with nocturnal hemodialysis. Kidney Int 1998;53(5):1399–404.

    Article  PubMed  CAS  Google Scholar 

  27. Acharya AS, Manning JM. Reaction of glycolaldehyde with proteins: latent crosslinking potential of alpha-hydroxyaldehydes. Proc Natl Acad Sci USA 1983;80(12):3590–4.

    Article  PubMed  CAS  Google Scholar 

  28. Sigrist MK, Devlin L, Taal MW, et al. Length of interdialytic interval influences serum calcium and phosphorus concentrations. Nephrol Dial Transplant 2005;20(8):1643–6.

    Article  PubMed  CAS  Google Scholar 

  29. Kestenbaum B, Sampson JN, Rudser KD, et al. Serum phosphate levels and mortality risk among people with chronic kidney disease. J Am Soc Nephrol 2005;16(2):520–8.

    Article  PubMed  CAS  Google Scholar 

  30. Lowrie EG, Lew NL. Death risk in hemodialysis patients: the predictive value of commonly measured variables and an evaluation of death rate differences between facilities. Am J Kidney Dis 1990;15(5):458–82.

    PubMed  CAS  Google Scholar 

  31. Block GA, Klassen PS, Lazarus JM, et al. Mineral metabolism, mortality, and morbidity in maintenance hemodialysis. J Am Soc Nephrol 2004;15(8):2208–18.

    Article  PubMed  CAS  Google Scholar 

  32. Block GA, Hulbert-Shearon TE, Levin NW, et al. Association of serum phosphorus and calcium × phosphate product with mortality risk in chronic hemodialysis patients: a national study. Am J Kidney Dis 1998;31(4):607–17.

    PubMed  CAS  Google Scholar 

  33. Marco MP, Craver L, Betriu A, et al. Higher impact of mineral metabolism on cardiovascular mortality in a European hemodialysis population. Kidney Int Suppl 2003(85):S111–4.

    Article  PubMed  Google Scholar 

  34. Young EW, Albert JM, Satayathum S, et al. Predictors and consequences of altered mineral metabolism: the Dialysis Outcomes and Practice Patterns Study. Kidney Int 2005;67(3):1179–87.

    Article  PubMed  CAS  Google Scholar 

  35. Stevens LA, Djurdjev O, Cardew S, et al. Calcium, phosphate, and parathyroid hormone levels in combination and as a function of dialysis duration predict mortality: evidence for the complexity of the association between mineral metabolism and outcomes. J Am Soc Nephrol 2004;15(3):770–9.

    Article  PubMed  CAS  Google Scholar 

  36. Okechukwu CN, Lopes AA, Stack AG, et al. Impact of years of dialysis therapy on mortality risk and the characteristics of longer term dialysis survivors. Am J Kidney Dis 2002;39(3):533–8.

    PubMed  Google Scholar 

  37. Cozzolino M, Dusso AS, Liapis H, et al. The effects of sevelamer hydrochloride and calcium carbonate on kidney calcification in uremic rats. J Am Soc Nephrol 2002;13(9):2299–308.

    Article  PubMed  CAS  Google Scholar 

  38. Jono S, McKee MD, Murry CE, et al. Phosphate regulation of vascular smooth muscle cell calcification. Circ Res 2000;87(7):E10–7.

    PubMed  CAS  Google Scholar 

  39. Moe SM, Chen NX. Pathophysiology of vascular calcification in chronic kidney disease. Circ Res 2004;95(6):560–7.

    Article  PubMed  CAS  Google Scholar 

  40. Reynolds JL, Joannides AJ, Skepper JN, et al. Human vascular smooth muscle cells undergo vesicle-mediated calcification in response to changes in extracellular calcium and phosphate concentrations: a potential mechanism for accelerated vascular calcification in ESRD. J Am Soc Nephrol 2004;15(11):2857–67.

    Article  PubMed  CAS  Google Scholar 

  41. Yang H, Curinga G, Giachelli CM. Elevated extracellular calcium levels induce smooth muscle cell matrix mineralization in vitro. Kidney Int 2004;66(6):2293–9.

    Article  PubMed  CAS  Google Scholar 

  42. Moe SM, Duan D, Doehle BP, et al. Uremia induces the osteoblast differentiation factor Cbfa1 in human blood vessels. Kidney Int 2003;63(3):1003–11.

    Article  PubMed  CAS  Google Scholar 

  43. London GM, Guerin AP, Marchais SJ, et al. Arterial media calcification in end-stage renal disease: impact on all-cause and cardiovascular mortality. Nephrol Dial Transplant 2003;18(9):1731–40.

    Article  PubMed  Google Scholar 

  44. Coco M, Rush H. Increased incidence of hip fractures in dialysis patients with low serum parathyroid hormone. Am J Kidney Dis 2000;36(6):1115–21.

    PubMed  CAS  Google Scholar 

  45. Blacher J, Guerin AP, Pannier B, et al. Arterial calcifications, arterial stiffness, and cardiovascular risk in end-stage renal disease. Hypertension 2001;38(4):938–42.

    PubMed  CAS  Google Scholar 

  46. Massry SG, Smogorzewski M. Mechanisms through which parathyroid hormone mediates its deleterious effects on organ function in uremia. Semin Nephrol 1994;14(3):219–31.

    PubMed  CAS  Google Scholar 

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Moe, S.M. (2006). Disorders of Phosphorous Homeostasis in CKD. In: Hsu, C.H. (eds) Calcium and Phosphate Metabolism Management in Chronic Renal Disease. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-33370-0_2

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  • DOI: https://doi.org/10.1007/978-0-387-33370-0_2

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