Chronic kidney disease has the potential to induce sequelae that can have severe and mortal outcomes. In particular, impaired glomerular filtration can cause a hyperphosphatemic state, which, if left unchecked, can lead to
secondary hyperparathyroidism,
vascular calcification, and
renal osteodystrophy. Therapeutic management of
hyperphosphatemia must maintain both
phosphorus and
calcium serum concentrations within the recommended guidelines. The balance of both minerals is regulated by
parathyroid hormone; thus, an imbalance of one affects the other. In
end-stage renal disease, patients often present with hypocalcemic levels due to the kidneys' inability to generate active
vitamin D to promote
calcium absorption in the intestine. Absorption of
calcium can be increased by the administration of active
vitamin D analogues. Minimizing
phosphorus intake through a strict dietary regimen, combined with the use of
phosphate binders to absorb excess ingested
phosphate, can help to maintain serum
phosphate levels near the recommended concentration of 5.5 mg/dL.
Phosphate-binding compounds have evolved from the original
aluminum-based binders pioneered in the 1970s to
calcium-based binders such as
calcium acetate, and more recently, to the following additions to the nephrologist's armamentarium:
sevelamer--a polyhydrochloride
polymer, and
lanthanum carbonate. One of the top 2 common clinical treatments for
hyperphosphatemia,
calcium acetate, has an established history of efficacy since the 1980s, and has been shown to be cost effective and well tolerated, as well.