title: The mechanism of hypoglycemia caused by hemodialysis.
abstract: BACKGROUND
  Although it is well-known that plasma glucose concentration ((G)p) decreases during hemodialysis, the precise mechanism underlying this decrease has not yet been fully elucidated. The aim of the present study was to investigate the mechanism underlying hemodialysis-induced decrease (HID) in (G)p during the dialysis in vivo or in vitro.
  
  
  METHODS
  Using high CO2/ HCO3- dialysate, we measured (G)p by a hexose kinase method ((G)pHK) and concentrations of electrolytes, as well as pH, PCO2 and PO2 for both plasma and dialysate samples at pre- and postdialyzer sites obtained from hemodialysis patients with nondiabetic chronic renal failure (CRF). Furthermore, we studied the effect of PCO2 and acetazolamide (ACZ) on the changes in (G)pHK during the dialysis in vitro.
  
  
  RESULTS
  After the first dialysis of CRF patients, the (G)pHK decreased from 118.3 +/- 18.0 to 98.6 +/- 5.7 mg/dl (p < 0.05), the latter value being significantly lower than glucose concentration in dialysate samples (approximately 105 mg/dl) at predialyzer sites. In the experiments of blood samples from healthy volunteers, (G)pHK decreased significantly after elevating or lowering CO2 level in the dialysates. In contrast, when the difference in PCO2 between the blood and dialysate was reduced, the HID in (G)pHK was abolished during hemodialysis. The addition of 10(-4) M ACZ to the blood samples completely prevented the development of HID in (G)pHK caused by the perfusion of high or low CO2/HCO3- dialysates.
  
  
  CONCLUSIONS
  During hemodialysis using high CO2/HCO3- dialysate, the HID in (G)p results from the diffusion of glucose from plasma into erythrocytes, probably due to the consumption of glucose resulting from the accelerated anaerobic metabolism induced by the changes in the cytoplasmic pH of erythrocytes.
authors.affiliation: Department of Urology, Osaka Medical College, Osaka, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Takahashi
authors.forename: T
authors.initials: T
authors.lastname: Kubota
authors.forename: N
authors.initials: N
authors.lastname: Shibahara
authors.forename: J
authors.initials: J
authors.lastname: Terasaki
authors.forename: M
authors.initials: M
authors.lastname: Kagitani
authors.forename: H
authors.initials: H
authors.lastname: Ueda
authors.forename: T
authors.initials: T
authors.lastname: Inoue
authors.forename: Y
authors.initials: Y
authors.lastname: Katsuoka
mesh_terms: D000086:Acetazolamide / Q000494:pharmacology; D000368:Aged; D000369:Aged, 80 and over; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism*; D002245:Carbon Dioxide / Q000032:analysis / Q000097:blood; D002257:Carbonic Anhydrase Inhibitors / Q000494:pharmacology; D004573:Electrolytes / Q000032:analysis / Q000097:blood; D005260:Female; D015312:Hemodialysis Solutions / Q000737:chemistry*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007003:Hypoglycemia / Q000209:etiology*; D066298:In Vitro Techniques; D007676:Kidney Failure, Chronic / Q000097:blood / Q000503:physiopathology / Q000628:therapy; D008297:Male; D006435:Renal Dialysis / Q000009:adverse effects*
chemical_list: D001786:Blood Glucose; D002257:Carbonic Anhydrase Inhibitors; D004573:Electrolytes; D015312:Hemodialysis Solutions; D002245:Carbon Dioxide; D000086:Acetazolamide