For years one of the fronts that social media advocates battled was the freedom to tweet at meetings. A number of meetings (we are looking at you ATC) were less than welcoming. I suspect many conferences were used to selling access to the meeting to people who did not participate through video tape, audio recordings or other means and they saw the social media coverage as unnecessary competition.
Why let bloggers and social media gadfly provide for free what we can sell.
Conferences are also typically run by people not on social media and who are unfamiliar with the norms of those communities. Organizers paraded excuses of academic purity and protecting authors. The issues are well documented here.
This all bubbled over last week at the American Diabetes Association national meeting in San Diego (#2017ADA). The organizers tried to enforce a no pictures policy:
One take down notice, lead to another, lead to another and suddenly the @AmDiabetesAssn feed was nothing but take down notices:
I think Swapnil hit the crux of the issue with this Tweet:
Hey ADA, why even have a hashtag and twitter presence for #2017ADA ? Information wants to be free. Welcome thanks the modern age!
If a conference is going to wade into the world of Twitter and encourage people to participate and spread the knowledge and experience of the conference they must play by the rules of the social media platform they are using. MedTwitter is firmly in the camp of information wants to be free. Encouraging people to tweet while at the same time abandoning one of their core tenets is going to fail every time.
In the end the ADA was made to look like fools (for the second time in two years, check out this story from 2016, and note that the embargo was designed to keep the information secret for 30 minutes before the article was published). And towards the end of the week the ADA appeared to be backtracking:
One quote, one tweet:
Linda Cann, the association’s senior vice president, was quoted by Liz Neporent, ” The association will be reevaluating the policy after the meeting is over”
I’ve been chair of the sci sessions oversight comm- its the docs who decide policy – till now presenters wanted protection. It will change
I think this marks the end of photo bans at conferences. The ADA tweet stream was such a mess and the photo ban distracted from any scientific messaging the conference wanted to convey that no conference will again try to enforce a similar ban. You may still see signs and slides urging people not to tweet but you can say good bye to aggressive take down notices and heavies hired to patrol the conference rooms.
Matt Sparks and I have been working on ASN for a couple of years and with a final push from the ASN Communication Committee, the ASN Council has reversed their (unenforced) photo ban. This will be the rule going forward. The good guys won this one.
My practice has a number of nurse practitioners and physician assistants. The partners do quarterly teaching sessions for them. It is some of my favorite teaching. They come to each session with a lot of experience and the sessions are more like guided conversations rather than traditional lectures. I usually try to frame the session with a clinical practice guideline and we just go through it step by step. This time I did autosomal dominant polycystic kidney disease. I couldn’t find a clinical practice guideline, so I just went with the KDIGO Controversies paper and went from there.
Update from Twitter (where else?)
You mentioned in your post there is no CPG in ADPKD. There is a Canadian one recently published:https://t.co/TFBeI0Kw02
We use these to make sure we cover all aspects of the disease during the session. They really don’t stand alone. They serve primarily as an outline of the conversation.
Autosomal-dominant polycystic kidney disease (ADPKD): executive summary from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference (PDF)
Blood Pressure in Early Autosomal Dominant Polycystic Kidney Disease HALT-PKD (PubMed)
Extended Follow-Up of Unruptured Intracranial Aneurysms Detected by Presymptomatic Screening in Patients with Autosomal Dominant Polycystic Kidney Disease (PMC full text)
KHA-CARI Autosomal Dominant Polycystic Kidney Disease Guideline: Management of Renal Stone Disease (PDF)
The Natural Course of Unruptured Cerebral Aneurysms in a Japanese Cohort (NEJM)
Tolvaptan in Patients with Autosomal Dominant Polycystic Kidney Disease TEMPO 3:4 (NEJM)
The Tweets:
Look at this chart from KDIGO ADPKD conference. Looks like there are mistakes. pic.twitter.com/IYJE2vWbaU
I went through the PBFluids back catalog to find three posts on the dangers of running marathons. Two on hyponatremia and one on coronary calcium. Enjoy. Hope to see you on the Twitter with hashtag #NephJC on May 23, at 9pm EST, and May 24, at 8pm GMT.
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.
