Only a 1st (almost 2nd) year here but it would seem that the patient has an acute metabolic acidosis caused by his use of Naproxen. My hypothesis is that he has chronic renal impairment (that was possibly subclincal prior to this?) secondary to his HTTN and DMII. The addition of naproxen, a renally excreted drug, was enough to disturb kidney function enough to cause the metabolic disturbances seen here.

A few questions
-His co2, o2, bicarb levels all look about normal. Wouldn’t there be an automatic respiratory attempt at correcting the pH by increasing respiration that would cause decreased bicarb and co2?
-Was there a arrhythmia when he presented?
-Was he on any diuretics for his HTTN? If so, assuming they were not K sparing and he was compliant, would that have somewhat alleviated his hyperkalemia? Or did it, and it just kept him from getting a legendarily high K?

Love these cases, please keep them coming.

I am a practicing nephrologist and have always enjoyed your many acid-base and electrolyte posts, but have only recently decided to stop lurking and start commenting. I agree with several of the points made by the above commenters, but would like to highlight some differences and additions.

So-called “Type 4 RTA” is a common feature of various disorders that impair collecting duct function; it is virtually never seen in the absence of structural renal disease. I would be willing to bet that the patient had pre-existing renal impairment, not just “ARF from Aleve”. Some patients with Type 4 RTA have impaired renin secretion, and that renin secretion depends in part on renal prostaglandins, the synthesis of which may have been impaired by the naproxen. I should also point out that hyperkalemia impairs ammoniagenesis in the kidney, as well as the entry of ammonium ions into the tubule – even so, the metabolic acidosis seems quite severe here for hyperkalemic distal RTA alone. Was there any other history to suggest another source of bicarbonate loss? Don’t forget that DKA can actually produce a non-gap acidosis, although you said that this was Type II DM. Finally, the poor respiratory compensation for the acidosis suggests underlying pulmonary disease, respiratory muscle paralysis from hyperkalemia, or both. This is clearly an ICU case…

On another note, would it be possible for you to not use so many medical abbreviations, or better yet explain your abbreviations?

In an earlier post about antibiotics, you used ARF for what I believe meant Acute Rheumatic Fever. Here though a commenter used ARF to mean either Acute Respiratory Failure, or Acute Renal Failure. I believe he meant the former. Either way, this is very confusing especially for students outside the United States. It’s not something I’m looking forward to dealing with when I get back, and believe I’ll have to print out a cheat sheet.