Metabolic acidosis and abnormal calcium metabolism in patients on maintenance hemodialysis.
- Author:
Sung Woo HAN
1
;
Woo Jung PARK
;
Sang Hoon HYUN
;
Ja Ryoung KOO
;
Ro Won CHUN
;
Hyung Jik KIM
;
Dong Wan CHAE
;
Jung Woo NOH
;
Gheun Ho KIM
Author Information
1. Department of Internal Medicine, Hallym University College of Medicine, Chuncheon, Korea.
- Publication Type:Original Article
- Keywords:
Metabolic acidosis;
Hemodialysis;
End-stage renal disease;
Calcium
- MeSH:
Acid-Base Equilibrium;
Acidosis*;
Arteriovenous Fistula;
Biomarkers;
Calcium*;
Dialysis;
Humans;
Hydrogen-Ion Concentration;
Kidney Failure, Chronic;
Metabolism*;
Parathyroid Hormone;
Prescriptions;
Prevalence;
Renal Dialysis*
- From:Korean Journal of Medicine
2000;58(4):420-429
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Mild metabolic acidosis is frequently found among the stable patients treated with maintenance hemodialysis. However, its clinical effects have yet to be clarified. This study was undertaken to estimate the prevalence of metabolic acidosis in the patients undergoing chronic hemodialysis and to evaluate the clinical significance of metabolic acidosis, especially in relation to calcium metabolism. METHODS: In 124 patients undergoing maintenance hemodialysis, analysis of arterial blood gas and measurement of various biochemical markers and parathyroid hormone were carried out with predialysis blood obtained from arterial side of arteriovenous fistula. RESULTS: Ninety two patients(74.2%) had metabolic acidosis. Their arterial pH was 7.32+/-0.01, arterial bicarbonate concentration 17.1+/-0.3 mEq/L, and PaCO2 33.1+/-0.5 mmHg. The patients with metabolic acidosis showed a lower calcium(7.90+/-0.16 vs. 8.68+/-0.17 mg/dL, p< 0.05), and higher phosphorus(4.96+/-0.16 vs. 3.68+/-0.39 mg/dL, p< 0.05), alkaline phosphatase(233.6+/-22.7 vs. 145.9+/-13.7 U/L, p< 0.05) and parathyroid hormone(176.5+/-23.7 vs. 52.8+/-14.4 pg/mL, p< 0.05) levels compared to those with normal acid-base balance. In the patients with metabolic acidosis, PaCO2 level showed a positive correlation with arterial bicarbonate concentration(r=0.62, p< 0.001). The lower arterial bicarbonate was, the higher serum potassium(r=-0.24, p< 0.05), phosphorus(r=-0.42, p< 0.001) and anion gap(r=-0.28, p< 0.01) were. When the patients were divided into two groups according to the dialysate buffer used, the lower calcium-acetate group showed lower total calcium(7.28+/-0.25 vs. 7.96+/-0.17 mg/dL, p< 0.05) and ionized calcium(0.85+/-0.05 vs. 1.08+/-0.04 mmol/L, p< 0.05) levels and higher alkaline phosphatase(457.1+/-170.2 vs. 209.4+/-15.9, p< 0.05) and parathyroid hormone (364.4+/-83.7 vs. 155.4+/-23.6 pg/mL, p< 0.05) levels compared to the higher calcium-bicarbonate group. CONCLUSION: Current hemodialytic practice is less than ideal, as evidenced by a high prevalence of metabolic acidosis. The metabolic acidosis in maintenance hemodialysis is associated with abnormal calcium metabolism, suggesting that a more aggressive correction of metabolic acidosis may be required by individualizing dialysis prescription.
