The plasma potassium concentration in metabolic acidosis: a re-evaluation.
The purpose of these investigations was to describe the mechanisms responsible for the change in the plasma [K] during the development and maintenance of hyperchloremic metabolic acidosis. Acute metabolic acidosis produced by HCI infusion resulted in a prompt rise in the plasma [K], whereas no change was observed during acute respiratory acidosis in the dog. After 3 to 5 days of acidosis due to NH4Cl feeding, dogs became hypokalemic; this fall in the plasma [K] was due largely to increased urine K excretion. Despite hypokalemia, aldosterone levels were not low, and the calculated transtubular [K] gradient was relatively high, suggesting renal aldosterone action. Thus, rather than anticipating hyperkalemia in patients with chronic metabolic acidosis due to a HCl load, the finding of hyperkalemia should suggest that the rate of urinary K excretion is lower than expected (ie, there are low aldosterone levels or failure of the kidney to respond to this hormone).
Magner
P O
PO
Renal Division, St. Michael's Hospital, Toronto, Ontario, Canada.
Robinson
L
L
Halperin
R M
RM
Zettle
R
R
Halperin
M L
ML
D000138:Acidosis / Q000097:blood* / Q000209:etiology; D000142:Acidosis, Respiratory / Q000097:blood; D000643:Ammonium Chloride; D000818:Animals; D004285:Dogs; D006851:Hydrochloric Acid; D006863:Hydrogen-Ion Concentration; D011188:Potassium / Q000097:blood*
D000643:Ammonium Chloride; D006851:Hydrochloric Acid; D011188:Potassium