Characterization of acid-base status in maintenance hemodialysis: physicochemical approach.
Acidosis is a common and deleterious aspect of maintenance dialysis. Traditionally, it is considered to be an elevated anion gap acidosis caused by the inability to excrete nonvolatile anions. Stewart's approach made it possible to identify real determinants of the acid-base status and allowed quantification of the components of these disturbances, especially the unmeasured anions. We performed a cross-sectional study to identify and quantify each component of acidosis in hemodialysis maintenance patients. Sixty-four maintenance hemodialysis patients and 14 controls were enrolled in this study. Gasometrical and biochemical analysis were performed before the midweek dialysis session. Quantitative physicochemical analysis was carried out using the Stewart methodology. Hemodialysis patients were found to have mild acidemia (mean pH: 7.33 +/- 0.06 versus 7.41 +/- 0.05) secondary to metabolic acidosis (serum bicarbonate: 18.8 +/- 0.26 versus 25.2 +/- 0.48 mEq/l). The metabolic acidosis was due to retention of unmeasured anions (6.5 +/- 0.29 versus 3.1 +/- 0.62 mEq/l), hyperchloremia (105.1 +/- 0.5 versus 101.8 +/- 0.7 mEq/l), and hyperphosphatemia (5.90 +/- 0.19 versus 3.66 +/- 0.14 mg/dl). Compared with control values, the unmeasured anions and hyperchloremia had a similar acidifying effect (3.4 and 3.3 mEq/l), corresponding to almost 90% of the metabolic acidosis. Unmeasured anions and hyperchloremia are important components of acidosis in maintenance hemodialysis, in addition to phosphorus. Future studies to determine the etiology and consequences of hyperchloremic acidosis are warranted.
Libório
Alexandre Braga
AB
Nephrology Division, University of São Paulo School of Medicine, Hospital das Clínicas, FMUSP, Av. Doutor Enéas de Carvalho, 250-70, andar, sala-711F, 01246-903, São Paulo, Brazil. alexandreliborio@yahoo.com
Daher
Elizabeth F
EF
de Castro
Manuel Carlos Martins
MC
D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000209:etiology / Q000378:metabolism*; D000328:Adult; D000838:Anions / Q000378:metabolism; D001639:Bicarbonates / Q000097:blood; D002712:Chlorides / Q000097:blood; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism / Q000628:therapy; D008297:Male; D010758:Phosphorus / Q000097:blood; D006435:Renal Dialysis
D000838:Anions; D001639:Bicarbonates; D002712:Chlorides; D010758:Phosphorus