Use of alkaline calcium salts as phosphate binder in uremic patients.
In order to prevent aluminum toxicity induced by the association of aluminum phosphate binder with 1 alpha(OH) vitamin D3 derivatives and the use of deferoxamine with its own hazards to diagnose and treat this toxicity, we have shown in 1982 that it was possible to replace the iatrogenic association of aluminum phosphate binder with 1 alpha OH vitamin D derivatives by oral calcium carbonate taken with the meals in order to bind phosphate and correct the negative calcium balance. This led to the disappearance of the crippling aluminic osteomalacia and adynamic bone diseases in our center. The effectiveness of CaCO3 without 1 alpha(OH)D3 derivatives in the control of hyperparathyroidism in dialysis patients has been proven by the appearance in four patients of our dialysis population of an histological idiopathic adynamic bone disease associated with relative hypoparathyroidism, and by the finding that more than 50% of our dialysis population treated by this sole treatment have plasma concentration of intact PTH below twice the upper limit of normal (that is, the threshold above which only significant histological osteitis fibrosa is observed). Besides the compliance problem, the limit of CaCO3 is the occurrence of hypercalcemia which occurs in about 8% of the measurements. Since calcium acetate binds twice as much phosphate for the same dose of elemental calcium as CaCO3, its use has been recommended. However, clinical experience has shown that in spite of the fact that half the dose of calcium element given as acetate does actually control predialysis plasma phosphate as well as CaCO3, the incidence of hypercalcemia is not decreased, probably because calcium availability at the alkaline pH of the intestine is much greater with Ca acetate. When hypercalcemia is frequent (and not explained by autonomized hyperparathyroidism, adynamic bone disease, overtreatment with vitamin D, granulomatosis or neoplasia) it is necessary either to decrease the dose of calcium and complete the necessary binding of phosphate by adding small doses of Mg(OH)2 or Mg carbonate, provided the dialysate Mg is decreased to 0.2 to 0.35 mmol/liter to prevent hypermagnesemia or to decrease the dialysate calcium (DCa) concentration. The decrease of DCa can be made either just when hypercalcemia occurs or on a systemic basis according to the amount of CaCO3 used and to the necessity of associating 1 alpha(OH) vitamin D3 derivatives.(ABSTRACT TRUNCATED AT 400 WORDS)
Fournier
A
A
Service de Néphrologie, Hôpital Sud, CHU Amiens, France.
Morinière
P
P
Ben Hamida
F
F
el Esjer
N
N
Shenovda
M
M
Ghazali
A
A
Bouzernidj
M
M
Achard
J M
JM
Westeel
P F
PF
D000535:Aluminum / Q000009:adverse effects / Q000378:metabolism; D002114:Calcinosis / Q000139:chemically induced; D002117:Calcitriol / Q000627:therapeutic use; D002118:Calcium / Q000009:adverse effects / Q000378:metabolism / Q000627:therapeutic use*; D003676:Deferoxamine / Q000627:therapeutic use; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000517:prevention & control; D010710:Phosphates / Q000378:metabolism*; D006435:Renal Dialysis; D014511:Uremia / Q000378:metabolism / Q000628:therapy*
D010710:Phosphates; D000535:Aluminum; D002117:Calcitriol; D003676:Deferoxamine; D002118:Calcium