USMLE Hypokalemia in RTA type 2

[SymB11]

Can anyone explain how renal tubular acidosis type 2 leads to hypokalemia?

From what I've read up so far, it seems like there are two opposing forces happening that affect potassium levels in the serum vs. urine. The defect in HCO3- reabsorption at PCT results in metabolic acidosis, which leads to hyperaldosteronism because patients tend to get dehydrated, and hypderaldosteronism results in hypokalemia.

But doesn't RTA type 2 also lead to urine acidification by alpha-intercalated cells as an attempt to distally correct the metabolic acidosis, which would lead to hyperkalemia? Is there something else I'm not factoring in here?

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[Transposony]

Type 2 RTA leads to urinary K+ wasting and hypokalemia due to persistent hyperaldosteronism (due to volume contraction).

The defect in proximal reabsorption of filtered HCO3- >>>>>> decreased proximal NaCl reabsorption >>>>>> salt wasting>>>>>>Hyperaldosteronism>>>>>>hypokalemia.


Just scroll down to "similar threads" for more discussion on the topic.

 

[Transposony]

But doesn't RTA type 2 also lead to urine acidification by alpha-intercalated cells as an attempt to distally correct the metabolic acidosis, which would lead to hyperkalemia? Is there something else I'm not factoring in here?

For every HCO3- you lose in urine, you gain one H+ in plasma.
Therefore, the urine is initially alkaline due to decreased proximal reabsorption of filtered HCO3- >>>>>increase HCO3- delivery to distal tubule.
This happens till the body total HCO3- pool is slowly drained out & when a steady state is reached at around 15-18 mEq/L of HCO3- plasma concentration where the filtered HCO3- is decreased to match the nephron's ability to reabsorb it. Now, there is not much HCO3- to neutralize the secreted H+ in the PCT leading to low urinary pH.
Hypokalemia occurs because K+ is secreted to maintain luminal electroneutrality and from increased distal tubular Na+ reuptake..

 

[SymB11]

That makes a lot more sense, thanks!