Lin Y F, Shieh S D, Diang L K, Lin S H, Chyr S H, Li B L, Lu K C
Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Republic of China.
ASAIO J. 1994 Jul-Sep;40(3):M440-4. doi: 10.1097/00002480-199407000-00038.
Metabolic acidosis induces a combination of inhibited osteoblastic and stimulated osteoclastic activity. To determine the role of alkali therapy in osteoblast function in chronic renal failure, serum bone isoenzyme of alkaline phosphatase (BAP) and osteocalcin were assessed before and after bicarbonate infusion. Eighteen patients with mild to moderate metabolic acidosis, none of whom had received dialysis therapy, were enrolled in this study. Metabolic acidosis was corrected by continuous bicarbonate infusion while plasma ionized calcium was monitored at 5 min intervals and held at the preinfusion level by calcium solution infusion during the entire procedure. The end-point of the study was reached when the plasma bicarbonate was approximately 24 mmol/l or pH was approximately 7.4 and plasma ionized calcium was clamped at the preinfusion level with only a 0.01 mmol/l fluctuation. The plasma pH (7.31 +/- 0.04 vs. 7.40 +/- 0.03, P < 0.001), bicarbonate (18.46 +/- 2.49 vs. 23.66 +/- 2.72 mmol/l, P < 0.001), serum total calcium, and osteocalcin (15.61 +/- 6.45 vs. 18.79 +/- 6.71 mg/l, P < 0.05) levels were significantly increased, whereas serum concentrations of alkaline phosphatase and albumin levels were significantly decreased after bicarbonate infusion. The serum BAP (1.85 +/- 1.29 vs. 1.79 +/- 1.18 mukat/l, P = 0.252), and inorganic phosphorus levels showed no significant differences before and after bicarbonate infusion. These results demonstrate that rapid correction of metabolic acidosis improves osteoblast function and may underline the importance of maintaining normal acid-base homeostasis in chronic renal failure.
