Here is the video:
Here is the Keynote: Toluene explained
Some addenda to my Curbsiders podcast on NAGMA
In my discussion on The Curbsiders I talked about the urine anion gap as a way to estimate urine ammonium. Here are the figures I would have shown for the urine anion gap, if the Curbsiders was a television show rather than a podcast:
The urine anion gap is wildly inaccurate at estimating urine ammonium. In this study of 1,044 people with chronic kidney disease, the urine anion gap was 42, while the urine ammonium was only 21:
Would you trust a technique to measure serum sodium if it was twice the actual serum sodium?
There is a second way to estimate the urine ammonium, the urine osmolar gap. The urine osmolar gap was devised to escape a different weakness in the urine anion gap, the problem with large amounts of urine anions, like ketones or hippurate.
The osmolar gap assumes that the difference between the measured and calculated osmolality will largely be made up by ammonium salts.
Here is a tweetorial about this, if that is your thing:
Part One: Don’t trust equations:
One of the weird truths about nephrology is that you spend your fellowship learning all of the equations and then for the first few years after fellowship you learn that they are rubbish.
Don't believe me…
— Joel M. Topf, MD FACP (@kidney_boy) August 2, 2018
Part Two: But you need to understand the equations so you can use them properly, the urine anion and osmolar gap:
I spoke about the urine anion gap with the @curbsiders but I want to emphasize what is oing on here:
In metabolic acidosis the kidneys try to excrete excess acid as ammonium NH4+. This is essential because even at a pH of 4.4, the hydrogen concentration is
— Joel M. Topf, MD FACP (@kidney_boy) August 2, 2018
The other mistake I made was an over simplification on how NH4+ is made. I said NH3 was made in the proximal tubule but it is more complicated than that. A lot more complicated. From David Goldfarb:
The proximal tubule makes 2 molecules of NH4+ via Glutaminase which also produces a 1 alpha-ketaglutamate (AKG). The AKG generates 2 molecules of HCO3 which is added to the blood. The NH4 gets tossed into the tubular fluid. So for every NH4+ created in the proximal tubule, one bicarb gets added to the blood.
Curbsiders #104: Renal Tubular Acidosis
This is the back half of my Acid-Base talk, a detailed dive into non-anion gap metabolic acidosis with an examination of renal tubular acidosis. This one turned out pretty good.
Here is a link to the Curbsiders page for this episode.
This is the sequel to #88 Acid base, boy bands, and grandfather clocks with Joel Topf MD
Before that I did episode #67 and #69 on chronic kidney disease
Before that was #48 Hyponatremia Deconstructed
And I started my Curbsiders career with #31 Diuretics, leg cramps and resistant hypertension.
So non-anion gap metabolic acidosis is my fifth or sixth appearance on the Curbsiders. Thanks guys.
Resident lecture on NAGMA
One hour lecture on NAGMA. Just some small changes edits from the last time I gave it. It is one of the few lectures that is still in PowerPoint. It is due for a complete overhaul. It also needs a slide on the treatment of RTA that covers the amount of bicarbonate in a 650 mg tablet (8 mmol) and the fact that distal (type 1) RTA requires a limited amount of bicarbonate (at most 1 mmol/kg). This is appropriate for residents and medical students.
If you are interested in ward teaching and RTA, take a look at this post by Robert Centor.
Also this is a nice article on the issue of saline having a pH of 5.5, covering both the reason (its the PVC bag) and the implications (none).