Intensive hemodialysis has reduced serum phosphorus and phosphate binder use

Mineral and bone disease is a common complication of kidney failure.1 There is a significant gap between phosphorus absorption and clearance in conventional hemodialysis.2,3 In 2015, over 36% of hemodialysis patients had serum phosphorus persistently above the target range.4 Hyperphosphatemia is associated with higher risk of cardiovascular mortality and morbidity, but treating hyperphosphatemia with phosphate binders is burdensome to both patients and payers.1,5,6,7

Trials show intensive hemodialysis reduced serum phosphorus and the need for phosphate binders

Multiple randomized clinical trials show that intensive hemodialysis reduced serum phosphorus:

  • In the Frequent Hemodialysis Network trials, short daily and nocturnal schedules, each for six sessions per week, reduced serum phosphorus by 0.6 and 1.6 mg/dL, respectively, relative to three sessions per week.8
  • A similar effect of nocturnal hemodialysis was observed in an earlier Canadian trial.9
  • In the Frequent Hemodialysis Network daily trial, intensive hemodialysis significantly lowered estimated phosphate binder dose (EPBD) per day.8
  • In the Canadian nocturnal trial, intensive hemodialysis led to phosphate binder discontinuation in 73% of patients.9


Intensive hemodialysis effectively lowers serum phosphorus and markedly reduces the use of phosphate binders. Frequent nocturnal hemodialysis may positively address hyperphosphatemia to the extent that supplementation with dialysate phosphorus may be necessary to avoid development of hypophosphatemia. The effect of intensive hemodialysis on phosphorus concentration suggests that the progression of vascular calcification may be slowed, thereby leading to cardiovascular risk reduction.

Reduction in the use of phosphate binders not only decreases pill burden, but also contains a rapidly growing source of health care costs in the dialysis patient population, an especially important consideration in the setting of capitated reimbursement.


  1. Moe SM, Drüeke T, Lameire N, Eknoyan G. Chronic kidney disease-mineral-bone disorder: a new paradigm. Adv Chronic Kidney Dis. 2007;14(1):3-12. doi:10.1053/j.ackd.2006.10.005.
  2. Noori N, Kalantar-Zadeh K, Kovesdy CP, et al. Dietary potassium intake and mortality in long-term hemodialysis patients. Am J Kidney Dis. 2010;56(2):338-347.
  3. Hou SH, Zhao J, Ellman CF, et al. Calcium and phosphorus fluxes during hemodialysis with low calcium dialysate. Am J Kidney Dis. 1991;18(2):217-224.
  4. The DOPPS Practice Monitor. Accessed November 8, 2016.
  5. Tentori F, Blayney MJ, Albert JM, 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(3):519-530. doi:10.1053/j.ajkd.2008.03.020.
  6. Navaneethan SD, Palmer SC, Craig JC, Elder GJ, Strippoli GFM. Benefits and harms of phosphate binders in CKD: a systematic review of randomized controlled trials. Am J Kidney Dis.2009;54(4):619-637. doi:10.1053/j.ajkd.2009.06.004.
  7. Sekercioglu N, Busse JW, Mustafa RA, Guyatt GH, Thabane L. Cinacalcet versus standard treatment for chronic kidney disease: a protocol for a systematic review and meta-analysis. Syst Rev. 2016;5:2.doi:10.1186/s13643-015-0177-1.
  8. Daugirdas JT, Chertow GM, Larive B, et al. Effects of frequent hemodialysis on measures of CKD mineral and bone disorder. JASN. 2012;23(4):727-738. doi:10.1681/ASN.2011070688.
  9. Culleton BF, Walsh M, Klarenbach SW, et al. Effect of frequent nocturnal hemodialysis vs conventional hemodialysis on left ventricular mass and quality of life: a randomized controlled trial. JAMA. 2007;298(11):1291-1299. doi:10.1001/jama.298.11.1291.