title: Effect of oral glucose administration on serum potassium concentration in hemodialysis patients.
abstract: BACKGROUND
  Extrarenal potassium disposal is particularly critical in patients with end-stage renal disease. Exogenous insulin stimulates this disposal by enhancing potassium uptake into cells in hemodialysis (HD) patients and healthy subjects. However, the effect of physiological levels of endogenous insulin on this disposal in these patients or healthy subjects is unknown.
  
  
  METHODS
  Effects of an oral glucose tolerance test (37.5, 75, and 150 g) on serum potassium levels were determined in 13 HD patients and 7 healthy controls. Serum potassium and insulin levels and plasma aldosterone and epinephrine levels were measured before and after glucose loads.
  
  
  RESULTS
  In HD patients and controls, serum insulin levels increased to a similar magnitude in parallel with increased serum glucose levels, but serum potassium levels decreased significantly only in HD patients. In HD patients, plasma aldosterone or epinephrine levels were not changed significantly after a glucose load. In HD patients, the decrease in serum potassium levels was dependent on the increase in serum insulin levels and was more prominent when 150 g of glucose was administered. In HD patients, the decrease in serum potassium levels correlated negatively (r = -0.45; P < 0.001) with the increase in serum insulin levels, and maximal decrease in serum potassium levels correlated negatively (r = -0.54; P < 0.001) with maximal increase in serum insulin levels.
  
  
  CONCLUSIONS
  Endogenous production of physiological concentrations of insulin in response to exogenous glucose administration decreases serum potassium levels only in HD patients, independently of plasma aldosterone and epinephrine levels.
authors.affiliation: Department of Nephrology, Jichi Medical School, Minamikawachi, Japan. smuto@jichi.ac.jp
authors.forename: Shigeaki
authors.initials: S
authors.lastname: Muto
authors.forename: Kiyoko
authors.initials: K
authors.lastname: Sebata
authors.forename: Hitomi
authors.initials: H
authors.lastname: Watanabe
authors.forename: Fumie
authors.initials: F
authors.lastname: Shoji
authors.forename: Yoshie
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: Michie
authors.initials: M
authors.lastname: Ohashi
authors.forename: Takako
authors.initials: T
authors.lastname: Yamada
authors.forename: Hisako
authors.initials: H
authors.lastname: Matsumoto
authors.forename: Tomoko
authors.initials: T
authors.lastname: Mukouyama
authors.forename: Takekazu
authors.initials: T
authors.lastname: Yonekura
authors.forename: Sachiko
authors.initials: S
authors.lastname: Namiki
authors.forename: Eiji
authors.initials: E
authors.lastname: Kusano
mesh_terms: D000284:Administration, Oral; D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D004837:Epinephrine / Q000097:blood; D045604:Extracellular Fluid / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000008:administration & dosage / Q000493:pharmacokinetics / Q000494:pharmacology*; D005951:Glucose Tolerance Test; D006706:Homeostasis; D006801:Humans; D007328:Insulin / Q000097:blood / Q000378:metabolism; D000078790:Insulin Secretion; D007668:Kidney / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000097:blood / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D011188:Potassium / Q000097:blood*; D006435:Renal Dialysis
chemical_list: D001786:Blood Glucose; D007328:Insulin; D000450:Aldosterone; D005947:Glucose; D011188:Potassium; D004837:Epinephrine