In the proximal tubule, you have a Na/H exchanger on the luminal membrane thats gonna be pumping Na in to the cell and protons out into the lumen. The protons are being made inside the cell from the reaction of carbonic anhydrase, CO2, and water. So that H+ that is being pumped into the lumen reacts with NH3 to make NH4, which is then excretable and not damaging to your body. If you take a carbonic anhydrase inhibitor, you are going to be inhibiting that reaction (CO2 + H2O ---- HCO3 + H), which is providing you the protons that are being secreted into the lumen and combining with NH3. So, with CA inhibitors you get an increase in NH3, which is not excretable, and you get NH3 toxicity, which I think is what causes the neuropathy.