title: Calcium acetate versus calcium carbonate as phosphate-binding agents in chronic haemodialysis.
abstract: Hyperphosphataemia plays a key role in the pathogenesis of renal osteodystrophy, and phosphate-binding agents are required in many chronic dialysis patients. Aluminium hydroxide and calcium carbonate are well-established phosphate binders, but their use is associated with toxicity or poor efficacy. Calcium acetate is known to be a potent phosphate binder, and has recently been used successfully in chronic dialysis patients. In this randomized cross-over trial in 31 chronic haemodialysis patients, equimolar doses of calcium acetate and calcium carbonate were administered for 6 weeks each. Compliance was estimated from tablet counts, and biochemical parameters were measured at the end of each treatment period. Of the 31 patients 23 completed both treatment arms; of the remainder, three withdrew due to adverse symptoms, hypercalcaemia necessitated treatment withdrawal in two, and three died. Non-compliance was significantly higher with acetate (18.3% tablets not taken) than with carbonate (8.7%). Serum phosphate was significantly lower after treatment with acetate (1.51 mmol/l) than with carbonate (1.80), as was the Ca x PO4 product (3.59 vs 4.18 respectively) and PTH (17.8 vs 25.4 pmol/l respectively). Serum calcium was significantly higher after acetate therapy (2.40 vs 2.32 mmol/l). No significant difference was found for sodium, potassium, bicarbonate, urea, creatinine, and haemoglobin. This study confirms that the treatment of hyperphosphataemia is more effective with calcium acetate than with calcium carbonate. For the first time an associated beneficial effect on secondary hyperparathyroidism has also been demonstrated. Patient tolerability of calcium acetate was considerably poorer, probably due in part to tablet formulation and bulkiness, as well as possible direct gastrointestinal effects of the acetate salt.
authors.affiliation: Ninewells Hospital and Medical School, Dundee, Scotland, UK.
authors.forename: S
authors.initials: S
authors.lastname: Pflanz
authors.forename: I S
authors.initials: IS
authors.lastname: Henderson
authors.forename: N
authors.initials: N
authors.lastname: McElduff
authors.forename: M C
authors.initials: MC
authors.lastname: Jones
mesh_terms: D000085:Acetates / Q000009:adverse effects / Q000627:therapeutic use*; D019342:Acetic Acid; D000328:Adult; D000368:Aged; D002118:Calcium / Q000097:blood; D002119:Calcium Carbonate / Q000009:adverse effects / Q000627:therapeutic use*; D018592:Cross-Over Studies; D004361:Drug Tolerance; D005260:Female; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000209:etiology / Q000517:prevention & control; D007676:Kidney Failure, Chronic / Q000097:blood / Q000150:complications / Q000628:therapy; D008297:Male; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000097:blood; D010349:Patient Compliance; D010710:Phosphates / Q000097:blood*; D006435:Renal Dialysis / Q000009:adverse effects / Q000379:methods*
chemical_list: D000085:Acetates; D010281:Parathyroid Hormone; D010710:Phosphates; D002119:Calcium Carbonate; D019342:Acetic Acid; D002118:Calcium