Potassium increase or decrease with metabolic acidosis, confused?

Join the discussion
Registration is free. Ask a follow-up in this thread, or start your own.
2 replies · 6K views
sameeralord
Messages
659
Reaction score
3
Ok in metabolic acidosis, renal compensation is increase in aldosertone, which cause hydrogen and potassium excretion leading to hypokalemia. But in metabolic acidosis transcellular movement occurs and there is hyperkalemia. What is the final result for potassium level. Hyper or hypo?
 
Biology news on Phys.org
sameeralord said:
Ok in metabolic acidosis, renal compensation is increase in aldosertone, which cause hydrogen and potassium excretion leading to hypokalemia. But in metabolic acidosis transcellular movement occurs and there is hyperkalemia. What is the final result for potassium level. Hyper or hypo?

Which one do you think? You just said "renal compensation" which is relatively slow. The final result, or at least the desired result, is physiologic acid-base neutrality (pH 7.35-7.45) and normal serum potassium levels.
 
Last edited:
Since you haven't responded, I can only assume you've posted a question, but are not interested in entering into a discussion of the issues involved in arriving at an answer. Others might be interested so I'll elaborate.

In primary metabolic acidosis, the initial response is the movement of H+ ions into cells in exchange for K+ ions, as you said. This can lead to hyperkalemia but it does not affect total body potassium. The main compensatory response for metabolic acidosis is usually respiratory; accomplished by a degree of hyperventilation to expel CO2. This shifts the reaction:CO2+H2O <-> H2CO3 to the left thus decreasing carbonic acid levels and producing a secondary respiratory alkalosis. This will usually compensate for the primary acidosis up to about pH 7.2. As the pH normalizes, K+ returns to the cells in exchange for H+ (actually hydronium ions). The kidneys accomplish the final adjustment of pH, but would not be expected to over-compensate.

This this is the "stop-gap" mechanism. The cause of the acidosis needs to be addressed.
 
Last edited: