Consequences and management of hyperphosphatemia in patients with renal insufficiency

Kidney Int Suppl. 2005 Jun;(95):S1-7. doi: 10.1111/j.1523-1755.2005.09500.x.

Abstract

Consequences and management of hyperphosphatemia in patients with renal insufficiency. Progressive renal insufficiency leads to hyperphosphatemia, hypocalcemia, and secondary hyperparathyroidism. Bone demineralization in secondary hyperparathyroidism may induce fractures, while joint and subcutaneous precipitations of calcium pyrophosphate limit mobility, and may cause crippling. Strategies to preempt bone and joint destruction in chronic kidney disease and end-stage renal disease have focused on limiting dietary phosphorus, intra-gut binding of ingested phosphorous, enhancing calcium absorption, and limiting parathyroid hormone secretion. Deciding which regimen is most effective to meet these treatment objectives challenges nephrologists; they often uncover conflicting evidence about which abnormal metabolite should be the prime treatment objective. Especially vexing is the question of whether hypercalcemia is a cardiotoxic consequence of calcium-based phosphate binders.

Publication types

  • Review

MeSH terms

  • Acetates / therapeutic use
  • Calcinosis
  • Calcium / blood
  • Calcium Compounds
  • Cardiovascular Diseases / diagnostic imaging
  • Cardiovascular Diseases / mortality
  • Diet
  • Humans
  • Hyperparathyroidism, Secondary / physiopathology
  • Phosphates / blood*
  • Renal Dialysis
  • Renal Insufficiency / complications*
  • Renal Insufficiency / epidemiology
  • Renal Insufficiency / physiopathology
  • Tomography, X-Ray Computed

Substances

  • Acetates
  • Calcium Compounds
  • Phosphates
  • Calcium
  • calcium acetate