This is a bit complex and not a dumb question at all.
Recall that every cell has a K/H exchange. In times of hyperkalemia, K enters cells and H leaves, and vice versa.
With type IV RTA there is hyperkalemia, since it is analogous to hypoaldosteronism.
The ubiquitous K/H exchange then kicks out the H from cells in exchange for K from the serum. This contributes to the acidotic blood pH.
This also causes intracellular H to be lower - an intracellular alkalosis - in all cells including those of the proximal tubule.
Here's how the proximal tubule contributes:
Now, in the proximal tubule, acid-base balance is partially managed by glutaminase, which breaks down glutamine into H and NH3. Glutaminase expression is reduced by high intracellular pH. Since in this case H left the cell in exchange for K, the intracellular pH is high and glutaminase is not as active. Thus less NH3 is made.
NH3 is supposed to diffuse out of the cell and go downstream and buffer some H ions in the urine, but since you made less NH3, what few H ions get loose into the urine reduce the pH. This kind of explains the acidification of the urine in type IV RTA. The urine acidification in this disorder is due to something that happens at the proximal tubule as a result of the hyperkalemia, not due to the intercalated cell K/H luminal exchange in the collecting tubule like I had originally thought.
