Metabolic acidosis aggravation and hyperkaliemia in hemodialysis patients treated by sevelamer hydrochloride.
Reports on acid-base side effects of sevelamer hydrochloride (SH), a new aluminum (Al)- and calcium (Ca)-free phosphate binder are rare and conflicting. In a retrospective analysis, we evaluated SH impact on metabolic acidosis and serum potassium (K) in hemodialysis (HD) patients. Two groups of stable HD patients were studied. Group A included 17 patients, M/F=15/2, 64 (42-80) years old, dialyzed since 130 (34-253) months, under SH for 24 months. Group B serving as controls was made of 7 patients, M/F=4/3, 67 (48-91) years old, dialyzed since 67 (27-174) months, under CaCO3 and/or Al(OH)3 as phosphate binders also for 24 months. Bicarbonate (BIC), K, Ca, phosphorus (P), Ca x P, alkaline phosphatase (ALP), and intact parathyroid hormone (iPTH) were recorded before (MO) and at the end (M24) of 24-month SH or CaCO3-Al(OH)3 treatment in group A and B patients. In group A, BIC fell from 20.02 +/- 1.43 to 17.89 +/- 2.30 mEq/ L, P=.002; and K rose from 5.45 +/- 0.51 to 5.75 +/- 0.49 mEq/L, P=0.02. In group B, BIC (19.8 +/- 3.03 to 19.0 +/- 3.3 mEq/L) and K (5.01 +/- 0.8 to 4.9 +/- 1.1 mEq/L) had nonsignificant changes. In group A, iPTH rose from 132.82 +/- 124.08 to 326.89 +/- 283.91 pg/mL, P=.0008; P fell from 5.92 +/- 1.48 to 4.9 +/- 1.01, P=.02; and Ca x P decreased from 52.04 +/- 9.7 to 45.58 +/- 10.42 mg2/dL2, P=.04. In group B, changes in iPTH from 240.71 +/- 174.7 to 318.57 +/- 260.2 pg/mL, P from 4.9 +/- 0.5 to 4.8 +/- 1.3 mg/dL, and CaxP product from 44.3 +/- 6.6 to 44 +/- 11.2 mg2/dL2 were nonsignificant. The changes observed in Ca and ALP in both groups were nonsignificant. Correlations in group A between metabolic acidosis (BIC) and SH doses, or iPTH and BIC, Ca, or P changes, were also found to be nonsignificant. Long-term use of SH, effectively controlling serum P levels and Ca x P values, is associated with acidosis aggravation and hyperkaliemia. Worsening of secondary hyperparathyroidism, also noted, needs to be confirmed and could be related to Ca/Al salt discontinuation and to metabolic acidosis aggravation itself.
Sonikian
Macroui A
MA
Nephrology Department, A. Fleming Hospital, Athens, Greece.
Pani
Ioanna T
IT
Iliopoulos
Anastasios N
AN
Koutala
Kaliopi G
KG
Marioli
Stamatia I
SI
Vlassopoulos
Dimosthenis A
DA
D000138:Acidosis / Q000139:chemically induced*; D000368:Aged; D002118:Calcium / Q000097:blood; D016022:Case-Control Studies; D004852:Epoxy Compounds / Q000009:adverse effects* / Q000627:therapeutic use; D005260:Female; D006801:Humans; D006947:Hyperkalemia / Q000139:chemically induced*; D008297:Male; D008875:Middle Aged; D028044:Phosphate-Binding Proteins / Q000009:adverse effects* / Q000627:therapeutic use; D010758:Phosphorus / Q000097:blood; D011073:Polyamines; D011095:Polyethylenes / Q000009:adverse effects* / Q000627:therapeutic use; D011188:Potassium / Q000097:blood; D006435:Renal Dialysis; D012189:Retrospective Studies; D000069603:Sevelamer; D013997:Time Factors
D004852:Epoxy Compounds; D028044:Phosphate-Binding Proteins; D011073:Polyamines; D011095:Polyethylenes; D010758:Phosphorus; D000069603:Sevelamer; D011188:Potassium; D002118:Calcium