To the Editor We read with interest the article by Lazarus et al in a recent issue of JAMA Internal Medicine.1 We believe this is a well-done study with a good design and sound methods, but we have some remarks and suggestions that may be of importance.
Proton pump inhibitors (PPIs) are weak bases with pKa level of 4 and are mainly activated in the acidic parietal cell canaliculi in the gastric mucosa where they bind covalently with the hydrogen potassium ATPase.2 Whether PPIs inhibit the hydrogen ATPase in the renal tubuli is questionable. The electrolytes and pH in urine do not seem to be affected,3 and the mechanism behind a possible deterioration of renal function by PPIs is not understood.