I was invited to speak at the Wayne State Alumni Day. It felt pretty special to come back to my old medical school and speak. They put together a great morning of lectures for their CME session.
I got a lot of push-back from the audience on these first two sections. One participant was was very frustrated with the message and felt it was irresponsible to present the data showing the apparent lack of toxicity from contrast and NSAIDs.
I lived through the great anemia debacle and after that I swore that I would no longer trust the experts. I wouldn’t swallow the guidelines whole. If the data didn’t back it, neither would I.
I love NephSAP. It is the greatest life long education product that I use. In my mind, it is the crown jewel of an ASN membership. Thank-you Bob Narins.
We have embedded it into our fellowship curriculum. When I do the questions I get blown away. They are really hard. I have to go searching hard to answer them. I figure I’d get aroound 50% without access to Dr. Google and the Preview Search box. The only exception is the fluid and electrolyte issues. I can handle those pretty well. This month’s NephSAP I nailed with only two misses. One of those misses annoys me. Here is the question:
So the TL;DR summary is you have a transplant patient with some graft dysfunction likely due to the concurrent volume depletion. His potassium is elevated and he has some worrying ECG changes (peaked Ts and a prolonged PR interval). Of note, he is on two medications that can provoke hyperkalemia: tacrolimus and trim/sulfa. This month’s NephSAP has a great section on why tacrolimus causes hyperkalemia. Tacro causes a drug induced Gordon’s syndrome:
Gordon Syndrome (pseudohypoaldosteronism type 2) is a gain-in-function mutation of the thiazide sensitive NaCl co-transporter in the distal convoluted tubule. The increased sodium resorption means there is no/little sodium available for the eNaC in the cortical collecting duct. No sodium resorption means no negative charge in the tubule driving potassium and hydrogen excretion.
The clinically relevant pearl is that calcineurin inhibitor induced hyperkalemia is particularly sensitive to thiazide diuretics. So I was hunting for some HCTZ or indapamide among the foils.
Nope.
Then I went looking for some saline to correct this patient’s hypovolemic acute kidney dysfunction and increase kaluresis.
Nope.
So I was left with the unenviable position of picking among choices that I would not actually do in this circumstance.
Fludrocortisone. I am a big fan of fludro in the treatment of hyperkalemia. But in this situation where there is both eNac antagonism by the trim/sulfa and tacro blocking distal sodium delivery, this did not seem like an effective treatment.
Patiromer. No data on patiromir for acute management of hyperkalemia, but not a bad option and this NephSAP did show some data on speed of treatment so I went with this.
Hemodialysis. This seems a bit extreme for an increase in creatinine from 1.2 to 1.4. But if the patient had a functional hemodialysis access, this is something I could be convinced to do.
But the right answer was our old friend bicarbonate. I thought we killed this one in the 90’s.
The answer key says:
A sodium bicarbonate infusion would not only correct the hypovolemia, but would enhance lumen electronegativity in the cortical collecting, thereby facilitating potassium secretion.
Reference 76 sounds intriguing. It is a KI article from 1977. It was an uncontrolled, but still somewhat convincing study. See the full open access manuscript here.
My beef comes from the NephSAP authors taking their eye off the ball. We don’t want to lower the potassium, we want to avoid arrhythmia. The consensus in nephrology is that IV calcium is the best way to avoid arrhythmia and the NephSAP authors specifically state that IV calcium is given. My concern is why should we then give a treatment that will counteract the antidote to hyperkalemic cardiotoxicity? Raising the pH decreasea the ionized calcium. Will that precipitate arrhythmia? I don’t know. I’m not sure anyone does. Without convincing prospective data I’m sticking with saline.
I love podcasts. I listen to them on my commute and when I walk my dog twice a day.
Bo the Dog
In the last year I have become addicted to The Curbsiders, what I consider the best internal medicine podcast. These three guys get interesting experts and interview them on topics with a primary care angle. They do a good job of digging deep to get good engagement from them and though they are respectful they do ask challenging questions (though honestly, I thought I got all softballs, listen to the podcast on coronary calcium scores for some probing questions).
Most importantly they are entertaining. I don’t need NephSAP audio digest. That stuff kills me. Never absorbed a sentence of it. The Curbsiders make listening to medical science fun.
Looks like they stopped doing these in 2013. Anyone miss them?
And this week they had me as a guest. I enjoyed the experience immensely, but in an hour of talking off the cuff I made some embarrassing mistakes:
In describing water reabsorption I said it occured in the cortical collecting duct rather than the medullary collecting duct.
In describing my cure for cramps I tell the story of Gitelman’s and say it is like congenital loop diuretics rather than congenital thiazide diuretics
I mucked up the story about MRFIT and how it allowed a head to head comparison of HCTZ and chlorthalidone. I really oversold what happened.
it was observed that in the 9 clinics that predominately used HCTZ, mortality was 44% higher in the special intervention (SI) group compared with the usual care (UC) group.10 The opposite was true in the 6 clinics that predominately used chlorthalidone. The MRFIT Data Safety Monitoring Board changed the protocol near the end of the trial to exclusively use chlorthalidone. In the initial clinics that used HCTZ that had a 44% higher mortality in the SI group, the trend was reversed after the protocol was changed to chlorthalidone, and they then had a 28% lower risk (P=0.04 for comparison of coronary heart disease mortality at the 2 time periods).
Like sending out newsletters, in Podcasts (especially when you are the guest) once it is recorded, you own your words with no chance to edit them.
Give The Curbsiders a listen, I think you’ll enjoy them.
The reason I knew that nephrology is Greek goes back to the early days of the The Fluid and Electrolyte Companion. We were planning the book and Sarah Faubel and I wanted to have a lot of little icons for little interesting factoids for the book. Here is the key for what made the cut:
But in earlier versions we had a lot of other icons. And one of the ideas was to have an icon for medical Latin but quickly we found that most words we wanted to define were actually Greek. We created a Medical Greek Icon, but it didn’t really work so we ended up using the light bulb. Here is an example of Medical Greek as found in the Book.
This is what the unused medical Latin icon looked like:
The other problem are the names on this picture, everyone of them has the spelling squiglies under the names. Here the problem is that the screen shot was taken in editing mode The two solutions are to export the document to images or put the document in Show Mode and take the screen shot. Demo time:
NephMadness launched today for the fifth consecutive year. The fourth sequal to an original is a precarious place to be. Exhibit A: Fast and the Furious resorted to bringing in Dwayne Johnson. We looked into it and sadly, he was not available.
So it was with this ominous precedent that we began the journey to NephMadness. In our fifth year we were able to get 31 completely fresh concepts, with the only repeat being antiPLA2r which showed up in the inaugural NephMadness in 2013.
The regions have a few more repeats as we revisited Dialysis, Nutrition, Genetics and Biomedical Research. The theme for the year is Old versus New. More on that in an upcoming editorial (just one of a number of posts that didn’t quite get finished for the launch).
If you are not familiar with NephMadness, these two videos maybe helpful.
