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Hyperphosphatemia Treatment & Management

  • Author: Eleanor Lederer, MD, FASN; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
Updated: Dec 16, 2015

Approach Considerations

The major strategies for treating hyperphosphatemia are as follows:

  • Diagnosis of the cause in order to initiate specific therapy: Eg, patients with hyperphosphatemia due to administration of liposomal amphotericin B who continue to require antifungal therapy may be switched to the amphotericin B lipid complex formulation, which contains less inorganic phosphate [40]
  • Limitation of phosphate intake: Patients with chronic kidney disease are advised to avoid foods that are especially high in phosphate; high-phosphate foods include dairy products; meats, nuts, and other high-protein foods; processed foods; and dark colas
  • Enhancement of renal excretion of phosphate: Hyperphosphatemia due to tumor lysis responds to enhancement of urinary losses through forced saline diuresis

The clinical condition most often requiring curtailment of ingestion is renal failure. Because intestinal absorption of phosphate and phosphate content in a typical diet is high, maintenance of phosphate homeostasis is dependent on renal excretion of the ingested excess. Therefore, when renal failure develops and hyperphosphatemia ensues, the sole means of controlling it is limitation of intake.

Optimal phosphate control in dialysis patients is extremely challenging. Despite the remarkable improvements made in dialysis techniques over the years, phosphate control has not been substantially improved. An alternative approach for dialysis-dependent patients that is presently being investigated is daily nocturnal dialysis. Dialysis performed in this manner, as opposed to intermittent thrice-weekly dialysis, seems to markedly decrease or even abolish the necessity for phosphate binders.[41]

Dey et al reported achieving phosphate control with thrice-weekly sessions by using hemodiafiltration, which combines diffusion and convection, rather than hemodialysis. Their program consisted of nocturnal sessions lasting a median of 8 hours. In the 14 patients in their study, pre-dialysis phosphate levels fell from a mean of 1.52 ± 0.4 to 1.06 ± 0.1 mmol/L (P <0.05), and use of phosphate binders became unnecessary.[42]

Surgical care

Surgery may sometimes be required for removal of large calcium phosphate deposits occurring in patients with tumoral calcinosis or long-standing renal failure. Perform parathyroidectomy in patients with renal failure who have tertiary (autonomous) hyperparathyroidism complicated by hypercalcemia, hyperphosphatemia, and severe bone disease.


The following consultations may be required:

  • Endocrinologist: To determine if the patient has hypoparathyroidism or one of the various forms of pseudohypoparathyroidism
  • Nephrologist: To evaluate and treat hyperphosphatemia associated with renal failure


Calcium levels, phosphate levels, and renal function should be monitored at intervals consonant with the severity of the underlying disorder.


Phosphate Binders

Dietary restriction alone may suffice for control of hyperphosphatemia in persons with mild renal insufficiency, but it is inadequate for patients with advanced renal insufficiency or complete renal failure. Such individuals require the addition of phosphate binders to inhibit gastrointestinal absorption of phosphate. These medications, which are taken concomitantly with meals, directly interact with the phosphate in the food, preventing intestinal absorption. The following classes of phosphate binders are widely used[43] :

  • Aluminum-containing phosphate binders
  • Calcium-containing phosphate binders
  • Phosphate binders that contain no aluminum or calcium

Administration of phosphate binders is the only truly long-term therapy for chronic hyperphosphatemia due to renal failure. Monitor calcium and phosphate levels, especially when treating patients with calcium-containing phosphate binders, because of the possibility of severe, life-threatening hypercalcemia.[44]

Calcium citrate and aluminum-containing binders should probably not be used together, because the citrate may enhance aluminum absorption.

Aluminum-containing phosphate binders

The aluminum-containing binders were the first to be used to treat hyperphosphatemia, but they have largely been abandoned because of the toxic effects of absorbed aluminum. Initially, the amount of aluminum absorbed was thought to be trivial; with long-term use, however, many patients developed a constellation of clinical symptoms attributable to aluminum, including dementia, severe osteomalacia, and anemia.

Bone biopsies performed on patients with aluminum intoxication revealed deposition of aluminum along the mineralizing front of bone, preventing normal mineralization. Aluminum levels in the fasting state and after a challenge with desferrioxamine confirmed the increased total body aluminum load. Aluminum-containing phosphate binders should be used only when other agents have failed to adequately control phosphate levels.

Calcium-containing phosphate binders

The next phosphate binders to be introduced were the calcium-containing binders, such as calcium carbonate and calcium citrate. These drugs, which are still used extensively, have the advantage of inhibiting phosphate absorption while providing the patient with a required mineral, calcium. The disadvantage of these drugs has been the relatively high incidence of hypercalcemia occurring in patients. There have also been concerns about the contribution of large exogenous calcium loads to the occurrence of soft tissue calcification in end-stage renal disease.

Several studies, including the Calcium Acetate Renagel Evaluation (CARE) study, have shown that calcium acetate is more cost-effective than sevelamer (discussed below) as a phosphate binder. Although concern has been raised about its purported link to cardiovascular calcification, calcium acetate can be used effectively with doses of elemental calcium that meet the Kidney Disease Outcome Quality Initiative (KDOQI) guidelines.

Phosphate binders with no aluminum or calcium

The above concerns about calcium-containing binders led to the development of a class of phosphate binders that contain neither aluminum nor calcium. At present, several drugs in this class, including the following, are in clinical use:

  • Sucroferric oxyhydroxide (Velphoro)
  • Sevelamer (Renagel)
  • Lanthanum carbonate (Fosrenol)
  • Ferric citrate (Auryxia)

For patients taking calcium-containing phosphate binders who have had demonstrable extraskeletal calcification or recurrent hypercalcemia, sevelamer and sucroferric oxyhydroxide are excellent alternatives and are well-tolerated in the control of serum phosphorus in dialysis patients.

Sucroferric oxyhydroxide

Sucroferric oxyhydroxide (Velphoro) is an iron-based phosphate binder that when taken with meals adsorbs dietary phosphate in the GI tract.

Approval for sucroferric oxyhydroxide (1-3 g/day) was based on the results of a phase 3 study that compared the drug’s dose titration and maintenance phases with those of sevelamer (2.4-14.4 g/day). Sucroferric oxyhydroxide and sevelamer efficacy were maintained during long-term use, with no notable difference in safety observed between the treatment groups. Moreover, sucroferric oxyhydroxide had a lower pill burden than did sevelamer.[45, 46]

In an open-label phase 3 extension study that compared sucroferric oxyhydroxide with sevelamer in 644 dialysis patients with hyperphosphatemia, sucroferric oxyhydroxide maintained its serum phosphorus-lowering effect over 1 year. Sucroferric oxyhydroxide was generally well tolerated over the long term, and patients showed no evidence of iron accumulation.[47]


Sevelamer and calcium-containing phosphate binders can be used in combination to minimize adverse effects; however, the major barrier to their use is patient noncompliance. The patient is required to ingest 3-6 large capsules with every meal, which is more than most human beings can comply with for extended periods. A study, however, demonstrated that once-daily sevelamer was as effective as thrice-daily sevelamer in the control of serum phosphorus, which may improve patient compliance.[48]

In addition to its effects as a phosphate binder, sevelamer has also been shown to improve the lipid profile in patients with hyperphosphatemia.

Lanthanum carbonate

Lanthanum has been shown to be a safe and equally efficacious agent in short-term studies, but concerns of long-term administration and toxicity exist. Furthermore, these agents are significantly more expensive than calcium salts, which may contribute to patient noncompliance. A 16-week, phase 4 study conducted by Vemuri et al found that patients who converted from other phosphate-binder medications to lanthanum carbonate maintained productive serum phosphorus levels with much satisfaction and lessened tablet burden.[49]

Ferric citrate

Oral ferric citrate was approved in September 2014 for the control of serum phosphorus levels in patients with chronic kidney disease on dialysis. Approval was based on a randomized trial in 441 adults with end-stage renal disease who were receiving hemodialysis or peritoneal dialysis 3 times per week for at least 3 months. Participants were treated either with ferric citrate or with active control (calcium acetate or sevelamer carbonate) for 52 weeks. Phosphorus levels were similar in the ferric citrate and active control groups, as were adverse events, which occurred in 39.1% of patients receiving ferric citrate and 49.0% of patients receiving active control. Patients receiving ferric citrate had significantly higher mean ferritin levels (899 ng/mL vs 628 ngmL; P < 0.001), transferrin saturation (39% vs 30%; P < 0.001), and less need for IV iron (12.95 mg/week vs 26.88 mg/week; P < 0.001) compared with active control.[50]

Cardiovascular considerations

Although long-term ingestion of aluminum-containing binders has known toxic effects, no definitive studies suggest that the chronic use of any of the other binders confers either a benefit or a disadvantage in terms of mortality.

Theoretically, the high calcium load of a calcium-containing phosphate binder could perpetuate or worsen vascular calcification, which does correlate with cardiovascular mortality in chronic kidney disease patients, when compared with non–calcium-containing phosphate binders. In fact, the use of non–calcium-containing binders does result in less vascular calcification; however, a beneficial effect on mortality has not been consistently demonstrated.[51, 52, 53, 54, 55, 56]


Increased Renal Excretion

The strategy for treatment of hyperphosphatemia in patients with normal renal function is to enhance renal excretion. This can be accomplished most effectively by volume repletion with saline coupled with forced diuresis with a loop diuretic such as furosemide or bumetanide.

The marked increase in intravascular volume with saline globally inhibits proximal renal tubule absorption of solutes, in this specific case, phosphate, thus promoting phosphaturia.

The increased distal tubule delivery of phosphate overwhelms the ability of that portion of the nephron to absorb phosphate, leading to a negative phosphate balance.


Management of Secondary Hyperparathyroidism

Just as better control of hyperphosphatemia in patients with renal failure helps to prevent the nearly universal development of secondary hyperparathyroidism, better control of hyperphosphatemia is achieved through control of secondary hyperparathyroidism. The agents commonly used to control secondary hyperparathyroidism are vitamin D metabolites and the calcium-sensing receptor agonists.

A study by Hansen et al found that alfacalcidol and paricalcitol were equally effective in the suppression of secondary hyperparathyroidism in patients on hemodialysis.[57]


Management of Hypoparathyroidism

For the rare cases of hypoparathyroidism, calcium and vitamin D are prescribed, predominantly for treatment of the hypocalcemia. Given with meals, the oral calcium can ameliorate the hyperphosphatemia of hypoparathyroidism, although this effect has to be carefully balanced against the phosphate absorption–promoting effects of the vitamin D. Over the long term, this therapy may result in nephrocalcinosis. Recombinant PTH injections can be considered but are not commonly used in clinical practice, because of the efficacy of calcium and vitamin D, as well as the cost and inconvenience of injected PTH.

Contributor Information and Disclosures

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, International Society of Nephrology, American Society for Biochemistry and Molecular Biology, American Federation for Medical Research, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa

Disclosure: Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.


Rosemary Ouseph, MD Professor of Medicine, Director of Kidney Transplant, University of Louisville School of Medicine

Rosemary Ouseph, MD is a member of the following medical societies: American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplant Surgeons

Disclosure: Nothing to disclose.

Vibha Nayak, MD Assistant Professor of Nephrology, Director of Home Dialysis, Kidney Disease Program, University of Louisville School of Medicine

Vibha Nayak, MD is a member of the following medical societies: American Society of Nephrology

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.


Jeffrey L Arnold, MD, FACEP Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center

Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physicians

Disclosure: Nothing to disclose. Andrew J Dailey, MD Fellow, Department of Medicine, Division of Nephrology, University of Louisville School of Medicine

Disclosure: Nothing to disclose.

Stephanie Dianne Hill Dailey, MD Fellow, Department of Medicine, Division of Nephrology, University of Louisville School of Medicine

Disclosure: Nothing to disclose.

Peter MC DeBlieux, MD Professor of Clinical Medicine and Pediatrics, Section of Pulmonary and Critical Care Medicine, Program Director, Department of Emergency Medicine, Louisiana State University School of Medicine in New Orleans

Peter MC DeBlieux, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Radiological Society of North America, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Robin R Hemphill, MD, MPH Associate Professor, Director, Quality and Safety, Department of Emergency Medicine, Emory University School of Medicine

Robin R Hemphill, MD, MPH is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Leigh A Patterson, MD Assistant Professor, Residency Director, Department of Emergency Medicine, Brody School of Medicine at East Carolina University

Leigh A Patterson, MD is a member of the following medical societies: American College of Emergency Physicians, American Institute of Ultrasound in Medicine, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Christie P Thomas, MBBS, FRCP, FASN, FAHA Professor, Department of Internal Medicine, Division of Nephrology, Departments of Pediatrics and Obstetrics and Gynecology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics

Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Royal College of Physicians

Disclosure: Nothing to disclose.

  1. Prie D, Huart V, Bakouh N, Planelles G, Dellis O, Gerard B, et al. Nephrolithiasis and osteoporosis associated with hypophosphatemia caused by mujtations in the type 2a sodium-phosphate cotransporter. N Engl J Med. 2002. 347:98991. [Medline].

  2. Segawa H, Onitsuka A, Kuwahata M, et al. Type IIc sodium-dependent phosphate transporter regulates calcium metabolism. J Am Soc Nephrol. 2009 Jan. 20(1):104-13. [Medline]. [Full Text].

  3. Collins JF, Bai L, Ghishan FK. The SLC20 family of proteins: dual functions as sodium-phosphate cotransporters and viral receptors. Pflugers Arch. 2004. 447:647-652. [Medline].

  4. Nowik M, Picard N, Stange G, et al. Renal phosphaturia during metabolic acidosis revisited: molecular mechanisms for decreased renal phosphate reabsorption. Pflugers Arch. 2008 Nov. 457(2):539-49. [Medline].

  5. Virkki LV, Biber J, Murer H, Forster IC. Phosphate transporters: a tale of two solute carrier families. Am J Physiol Renal Physiol. 2007. 293:F643-F654. [Medline].

  6. Shaikh A, Berndt T, Kumar R. Regulation of phospahte homeostasis by the phosphatonins and other novel mediators. Pediatr Nephrol. 2008. 23:1203-1210. [Medline]. [Full Text].

  7. Mirams M, Robinson BG, Mason RS, Nelson AE. Bone as a source of FGF23: regulation by phosphate?. Bone. 2004 Nov. 35(5):1192-9. [Medline].

  8. Liu S, Zhou J, Tang W, et al. Pathogenic role of Fgf23 in Hyp mice. Am J Physiol Endocrinol Metab. 2006 Jul. 291(1):E38-49. [Medline].

  9. Razzaque MS. FGF23-mediated regulation of systemic phosphate homeostasis: is Klotho an essential player. Am J Physiol Renal Physiol. 2009. 296:F470-F476. [Medline]. [Full Text].

  10. Pande S, Ritter CS, Rothstein M, et al. FGF-23 and sFRP-4 in chronic kidney disease and post-renal transplantation. Nephron Physiol. 2006. 104(1):p23-32. [Medline].

  11. Nishida Y, Taketani Y, Yamanaka-Okumura H, et al. Acute effect of oral phosphate loading on serum fibroblast growth factor 23 levels in healthy men. Kidney Int. 2006 Dec. 70(12):2141-7. [Medline].

  12. Sherman RA. Hyperphosphatemia in Dialysis Patients: Beyond Nonadherence to Diet and Binders. Am J Kidney Dis. 2015 Oct 21. [Medline].

  13. Prie D, Beck L, Urena P, Friedlander G. Recent findings in phosphate homeostasis. Curr Opin Nephrol Hypertens. 2005. 14:318-324. [Medline].

  14. Ichikawa S, Imel EA, Kreiter ML, et al. A homozygous missense mutation in human KLOTHO causes severe tumoral calcinosis. J Clin Invest. 2007 Sep. 117(9):2684-91. [Medline]. [Full Text].

  15. Ichikawa S, Sorenson AH, Austin AM, Mackenzie DS, Fritz TA, Moh A, et al. Ablation of the Galnt3 gene leads to low-circulating intact fibroblast growth factor 23 (Fgf23) concentrations and hyperphosphatemia despite increased Fgf23 expression. Endocrinology. 2009. 150:2543-2550. [Medline]. [Full Text].

  16. Lammoglia JJ, Mericq V. Familial tumoral calcinosis caused by a novel FGF23 mutation: response to induction of tubular renal acidosis with acetazolamide and the non-calcium phosphate binder sevelamer. Horm Res. 2009. 71:178-184. [Medline].

  17. Barbieri AM, Filopanti M, Bua G, Beck-Peccoz P. Two novel nonsense mutations in GALNT3 gene are responsible for familial tumoral calcinosis. J Hum Genet. 2007. 52:464-468. [Medline].

  18. Verdonck J, Geuens G, Delaere P, Vander Poorten V, Evenepoel P, Debruyne E. Surgical findings and post-operative parathormone levels in patients with secondary hyperparathyroidism. B-ENT. 2009. 5(3):143-8. [Medline].

  19. Tonelli M, Sacks F, Pfeffer M, Gao Z, Curhan G, Cholesterol and Recurrent Events Trial Investigators. Relation between serum phosphate level and cardiovascular event rate in people with coronary disease. Circulation. 2005. 112:2627-2633. [Medline].

  20. Shuto E, Taketani Y, Tanaka R, Harada N, Isshiki M, Sato M, et al. Dietary phosphorus acutely impairs endothelial function. J Am Soc Nephrol. 2009. 20:1504-1512. [Medline]. [Full Text].

  21. Sabbagh Y, Carpenter TO, Demay MB. Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes. Proc Natl Acad Sci U S A. 2005 Jul 5. 102(27):9637-42. [Medline]. [Full Text].

  22. Ball CL, Tobler K, Ross BC, Connors MR, Lyon ME. Spurious hyperphosphatemia due to sample contamination with heparinized saline from an indwelling catheter. Clin Chem Lab Med. 2004 Jan. 42(1):107-8. [Medline].

  23. Cachat F, Bardy D, Durussel C, Di Paolo E. Spurious hyperphosphatemia in a patient with alteplase-locked central venous catheter. Pediatr Nephrol. 2006 Feb. 21(2):301-2. [Medline].

  24. Marcu CB, Hotchkiss M. Pseudohyperphosphatemia in a patient with multiple myeloma. Conn Med. 2004 Feb. 68(2):71-2. [Medline].

  25. Larner AJ. Pseudohyperphosphatemia. Clin Biochem. 1995 Aug. 28(4):391-3. [Medline].

  26. Leehey DJ, Daugirdas JT, Ing TS, Reid RW. Spurious hyperphosphatemia due to hyperlipidemia. Arch Intern Med. 1985 Apr. 145(4):743-4. [Medline].

  27. Beloosesky Y, Grinblat J, Weiss A, et al. Electrolyte disorders following oral sodium phosphate administration for bowel cleansing in elderly patients. Arch Intern Med. 2003 Apr 14. 163(7):803-8. [Medline].

  28. Gumurdulu Y, Serin E, Ozer B, Gokcel A, Boyacioglu S. Age as a predictor of hyperphosphatemia after oral phosphosoda administration for colon preparation. J Gastroenterol Hepatol. 2004. 19:68-72. [Medline].

  29. Markowitz GS, Stokes MB, Radhakrishnan J, D'Agati VD. Acute phosphate nephropathy following oral sodium phosphate bowel purgative: an underrecognized cause of chronic renal failure. J Am Soc Nephrol. 2005. 16:3389-3396. [Medline].

  30. Markowitz GS, Nasr SH, Klein P, Anderson H, Stack JI, Alterman L, et al. Renal failure due to acute nephrocalcinosis following oral sodium phosphate bowel cleansing. Hum Pathol. 2004. 35:675-684. [Medline].

  31. Yoo KD, Kang S, Choi Y, Yang SH, Heo NJ, Chin HJ, et al. Sex, Age, and the Association of Serum Phosphorus With All-Cause Mortality in Adults With Normal Kidney Function. Am J Kidney Dis. 2015 Sep 2. [Medline].

  32. Connolly GM, Cunningham R, McNamee PT, Young IS, Maxwell AP. Elevated serum phosphate predicts mortality in renal transplant recipients. Transplantation. 2009. 87:1041-1044. [Medline].

  33. Tentori F, Blayney MJ, Albert JM, Gillespie BW, Kerr PG, Bommer J, et al. Mortality risk for dialysis patients with different levels of serum calcium, phosphorus, and PTH: the Dialysis Outcomes and Practice Patterns Study (DOPPS). Am J Kidney Dis. 2008. 52:519-530. [Medline].

  34. Hruska KA, Mathew S, Lund R, Qiu P, Pratt R. Hyperphosphatemia of chronic kidney disease. Kidney International. 2008. 74:148-157. [Medline]. [Full Text].

  35. Isakova T, Gutiérrez OM, Chang Y, et al. Phosphorus binders and survival on hemodialysis. J Am Soc Nephrol. 2009 Feb. 20(2):388-96. [Medline]. [Full Text].

  36. Block GA, Wheeler DC, Persky MS, et al. Effects of phosphate binders in moderate CKD. J Am Soc Nephrol. 2012 Aug. 23(8):1407-15. [Medline]. [Full Text].

  37. Shutto Y, Shimada M, Kitajima M, Yamabe H, Saitoh Y, Saitoh H, et al. Inadequate Awareness among Chronic Kidney Disease Patients Regarding Food and Drinks Containing Artificially Added Phosphate. PLoS One. 2013 Nov 13. 8(11):e78660. [Medline]. [Full Text].

  38. Marraffa JM, Hui A, Stork CM. Severe hyperphosphatemia and hypocalcemia following the rectal administration of a phosphate-containing Fleet pediatric enema. Pediatr Emerg Care. 2004 Jul. 20(7):453-6. [Medline].

  39. [Guideline] Hawley C. Serum phosphate. Nephrology. Apr 2006. 11(S1):S201-5.

  40. Sutherland SM, Hong DK, Balagtas J, Gutierrez K, Dvorak CC, Sarwal M. Liposomal amphotericin B associated with severe hyperphosphatemia. Pediatr Infect Dis J. 2008 Jan. 27(1):77-9. [Medline].

  41. Graham-Brown MP, Churchward DR, Smith AC, Baines RJ, Burton JO. A 4-month programme of in-centre nocturnal haemodialysis was associated with improvements in patient outcomes. Clin Kidney J. 2015 Dec. 8 (6):789-795. [Medline]. [Full Text].

  42. Dey V, Hair M, So B, Spalding EM. Thrice-Weekly Nocturnal In-Centre Haemodiafiltration: A 2-Year Experience. Nephron Extra. 2015 May-Aug. 5 (2):50-7. [Medline]. [Full Text].

  43. Ketteler M. Phosphate Metabolism in CKD Stages 3-5: Dietary and Pharmacological Control. Int J Nephrol. 2011. 2011:970245. [Medline]. [Full Text].

  44. Akizawa T, Kameoka C, Kaneko Y, Kawasaki S. Long-term treatment of hyperphosphatemia with bixalomer in Japanese hemodialysis patients. Ther Apher Dial. 2013 Dec. 17(6):612-9. [Medline].

  45. Kling J. New Phosphate Binder for Renal Failure Lowers Pill Burden. Medscape Medical News. Jun 4 2013. Available at Accessed: Dec 26 2013.

  46. Brooks M. FDA Clears New Phosphate Binder Velphoro. Medscape Medical News. Dec 3 2013. Available at Accessed: Jan 3 2014.

  47. Floege J, Covic AC, Ketteler M, Mann JF, Rastogi A, Spinowitz B, et al. Long-term effects of the iron-based phosphate binder, sucroferric oxyhydroxide, in dialysis patients. Nephrol Dial Transplant. 2015 Jun. 30 (6):1037-46. [Medline].

  48. Spaia S. Phosphate binders: Sevelamer in the prevention and treatment of hyperphosphataemia in chronic renal failure. Hippokratia. 2011 Jan. 15:22-6. [Medline]. [Full Text].

  49. Vemuri N, Michelis MF, Matalon A. Conversion to lanthanum carbonate monotherapy effectively controls serum phosphorus with a reduced tablet burden: a multicenter open-label study. BMC Nephrol. 2011 Sep 30. 12:49. [Medline]. [Full Text].

  50. Lewis JB, Sika M, Koury MJ, Chuang P, Schulman G, Smith MT, et al. Ferric Citrate Controls Phosphorus and Delivers Iron in Patients on Dialysis. J Am Soc Nephrol. 2014 Jul 24. [Medline].

  51. Frazao JM, Adragao T. Treatment of hyperphosphatemia with sevelamer hydrochloride in dialoysis patients: effects on vascular calcification, bone and a close look into the survival data. Kidney Int Suppl. 2008. 111:S38-S43. [Medline].

  52. Sprague SM. A comparative review of the efficacy and safety of established phosphate binders: calcium, sevelamer, and lanthanum carbonate. Curr Med Res Opin. 2007 Dec. 23(12):3167-75. [Medline].

  53. Marangon N, Lindholm B, Stenvinkel P. Nonphosphate-binding effects of sevelamer--are they of clinical relevance?. Semin Dial. 2008. 21:385-389. [Medline].

  54. Takei T, Otsubo S, Uchida K, et al. Effects of sevelamer on the progression of vascular calcification in patients on chronic haemodialysis. Nephron Clin Pract. 2008. 108(4):c278-83. [Medline].

  55. Connor A. Novel therapeutic agents and strategies for the management of chronic kidney disease mineral and bone disorder. Postgrad Med J. 2009. 85:274-279.

  56. Barreto DV, Barreto FdeC, de Carvalho AB, Cuppari L, Draibe SA, Dalboni MA, et al. Phosphate binder impact on bone remodeling and coronary calcification -- results from the BRIC study. Nephron Clin Pract. 2008. 110:c278-c283. [Medline].

  57. Hansen D, Rasmussen K, Danielsen H, Meyer-Hofmann H, Bacevicius E, Lauridsen TG, et al. No difference between alfacalcidol and paricalcitol in the treatment of secondary hyperparathyroidism in hemodialysis patients: a randomized crossover trial. Kidney Int. 2011 Oct. 80(8):841-50. [Medline].

Approximately 60-70% of dietary phosphate, 1000-1500 mg/day, is absorbed in the small intestine. Although vitamin D can enhance the absorption, especially under conditions of dietary phosphate depletion, intestinal phosphate absorption does not require the presence of active vitamin D. Specifically, high serum phosphate and high dietary phosphate intake do not significantly impair intestinal uptake. The movement of phosphate in and out of bone, the reservoir containing most of the total body phosphate, is generally balanced. Renal excretion of excess dietary phosphate intake ensures maintenance of phosphate homeostasis, maintaining serum phosphate at a level of approximately 3-4 mg/dL in the serum.
The vast majority of filtered phosphate is reabsorbed by type 2a sodium phosphate cotransporters located on the apical membrane of the renal proximal tubule. The expression of these cotransporters is increased by low dietary phosphate intake and several growth factors to enhance phosphate absorption. The expression is decreased by high dietary phosphate intake, parathyroid hormone (PTH), FGF23, and dopamine. Phosphate absorption in the remainder of the nephron is generally mediated by type 3 sodium phosphate cotransporters. No direct evidence has been found related to the regulation of these transporters in renal cells under physiologic conditions. The absorption in the proximal tubule is regulated such that the final excretion matches the dietary excess in order to maintain homeostasis.
Hyperphosphatemia inhibits 1-alpha hydroxylase in the proximal tubule directly and indirectly through stimulation of FGF23, thus inhibiting the conversion of 25-hydroxy vitamin D3 to the active metabolite, 1,25 dihydroxyvitamin D3. FGF23 additionally increases the expression of 24-hydroxylase, leading to inactivation of active 1,25 dihydroxyvitamin D3. The decrease in active vitamin D production with high phosphate is somewhat offset by the ability of hyperphosphatemia to stimulate the secretion of parathyroid hormone (PTH), which will increase the activity of 1-alpha hydroxylase. The result is generally a neutral effect on intestinal phosphate absorption. Hyperphosphatemia-stimulated PTH secretion is mediated through an as yet unidentified pathway. With normal renal function, the transient increase in PTH and decrease in vitamin D serve to inhibit renal and intestinal absorption of phosphate, resulting in resolution of the hyperphosphatemia. In contrast, under conditions of renal failure, sustained hyperphosphatemia results in sustained hyperparathyroidism. The hyperparathyroidism enhances renal phosphate excretion but also enhances bone resorption, releasing more phosphate into the serum. As renal failure progresses and the ability of the kidney to excrete phosphate continues to diminish, the action of PTH on the bone can exacerbate the already present hyperphosphatemia.
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