title: Substitution of calcium carbonate for aluminum hydroxide in patients on hemodialysis. Effects on acidosis, on parathyroid function, and on calcemia.
abstract: Substitution of calcium carbonate for aluminum hydroxide in patients on dialysis: effects on acidosis, parathyroid function, and calcemia. We studied the effects of substituting CaCO3 for aluminum-containing gels on metabolic acidosis and on the response of the parathyroid glands in 11 patients treated with chronic hemodialysis. The 8 men and 3 women were clinically stable, were known to be compliant, and had no clinical evidence of aluminum overload; they were not receiving vitamin D supplements; and they had been on dialysis for an average of 65.6 months (range: 13-188 months). After 3 weeks of CaCO3 administration plasma phosphate concentration remained well controlled, and plasma calcium concentration increased from 9.2 +/- 0.2 (2.3 +/- 0.1 mmol/l) to 10.1 +/- 0.2 mg/dl (2.5 +/- 0.1 mmol/l). Predialysis plasma bicarbonate concentration increased from 19.7 +/- 0.6 to 21.9 +/- 0.6 mmol/l. Plasma aluminum concentration decreased from 78.7 +/- 12.5 to 48.5 +/- 3.9 micrograms/l. Plasma PTH level increased from 2.0 +/- 0.7 to 3.3 +/- 0.8 ng/ml despite the concurrent increase in plasma calcium levels. All values returned to control levels following discontinuation of CaCO3 and resumption of aluminum gels. We conclude: (1) In addition to controlling hyperphosphatemia and increasing plasma calcium concentration, CaCO3 ameliorates metabolic acidosis. (2) Avoidance of oral aluminum intake is followed by prompt lowering of plasma aluminum levels. (3) PTH levels paradoxically increase despite the increment in plasma calcium concentration. The hypercalcemia seen with CaCO3 administration may be due, in part, to transient parathyroid hypersecretion that develops when aluminum administration is discontinued.
authors.affiliation: Servizio di Nefrologia ed Emodialisi, Ospedale San Paolo, Milano, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Anelli
authors.forename: D
authors.initials: D
authors.lastname: Brancaccio
authors.forename: R
authors.initials: R
authors.lastname: Damasso
authors.forename: P
authors.initials: P
authors.lastname: Padovese
authors.forename: M
authors.initials: M
authors.lastname: Gallieni
authors.forename: S
authors.initials: S
authors.lastname: Garella
mesh_terms: D000138:Acidosis / Q000209:etiology / Q000517:prevention & control*; D000536:Aluminum Hydroxide / Q000009:adverse effects / Q000627:therapeutic use*; D001639:Bicarbonates / Q000097:blood; D002118:Calcium / Q000097:blood*; D002119:Calcium Carbonate / Q000009:adverse effects / Q000627:therapeutic use*; D002245:Carbon Dioxide / Q000097:blood; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D008875:Middle Aged; D010280:Parathyroid Glands / Q000503:physiopathology*; D010281:Parathyroid Hormone / Q000097:blood*; D010313:Partial Pressure; D010710:Phosphates / Q000097:blood; D006435:Renal Dialysis / Q000009:adverse effects*
chemical_list: D001639:Bicarbonates; D010281:Parathyroid Hormone; D010710:Phosphates; D002245:Carbon Dioxide; D000536:Aluminum Hydroxide; D002119:Calcium Carbonate; D002118:Calcium