title: Extrarenal potassium homeostasis with maximal exercise in end-stage renal disease.
abstract: Serum potassium levels rise substantially during vigorous exercise as a result of the release of potassium from contracting muscle cells. Widespread use of erythropoietin has allowed for increased exercise capacity in patients with ESRD, raising the concern for severe exertional hyperkalemia. The aim of this study was to determine whether ESRD is associated with alterations in potassium and the neurohumoral mediators of extrarenal potassium disposal with maximal exercise. Eight stable hemodialysis patients (aged 37 +/- 16 yr, mean +/- SE) and eight healthy control subjects (aged 44 +/- 13 yr) exercised to exhaustion, using a graded cycle ergometer. There were no significant differences in exercise performance between groups as assessed by peak work rate, maximal oxygen consumption, and rate pressure product. Although the baseline potassium level was higher in the dialysis group (5.0 +/- 0.2 mEq/L) than in control subjects (4.5 +/- 0.1 mEq/L), both groups had a similar pattern of increase during exercise (with an increment of approximately 1 mEq/L) and a similar return to baseline after exercise. However, the dialysis patients had higher basal norepinephrine levels (820 +/- 104 versus 441 +/- 56 pg/mL, P < 0.01) and a greater response to exercise (3122 +/- 429 versus 1696 +/- 424 pg/mL, P < 0.01), higher basal insulin levels (11 +/- 1 versus 7 +/- 1 microU/mL, P < 0.05), higher insulin post-exercise levels (19 +/- 3 versus 11 +/- 1 microU/mL, P < 0.05), and higher basal aldosterone levels (621 +/- 250 versus 109 +/- 13 pg/mL, P < 0.05) with an increase response to exercise (1100 +/- 350 versus 350 +/- 17 pg/mL, P < 0.05). In summary, despite higher basal potassium, dialysis patients have normal potassium responses to maximal exercise. More vigorous insulin, catecholamine, and aldosterone levels may contribute to the maintenance of extrarenal potassium homeostasis in ESRD.
authors.affiliation: Department of Medicine, Beth Israel Hospital, Harvard Medical School, Boston, MA 02215, USA.
authors.forename: B A
authors.initials: BA
authors.lastname: Clark
authors.forename: C
authors.initials: C
authors.lastname: Shannon
authors.forename: R S
authors.initials: RS
authors.lastname: Brown
authors.forename: E V
authors.initials: EV
authors.lastname: Gervino
mesh_terms: D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood; D005260:Female; D006439:Hemodynamics; D006706:Homeostasis; D006801:Humans; D006947:Hyperkalemia / Q000209:etiology; D007328:Insulin / Q000097:blood; D007676:Kidney Failure, Chronic / Q000097:blood / Q000503:physiopathology* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D009119:Muscle Contraction / Q000502:physiology; D009638:Norepinephrine / Q000097:blood; D005082:Physical Exertion / Q000502:physiology*; D011188:Potassium / Q000097:blood*; D006435:Renal Dialysis
chemical_list: D007328:Insulin; D000450:Aldosterone; D011188:Potassium; D009638:Norepinephrine