Clay Shirky on publishing

Saw this on Twitter (thanks Brian):

I retweeted it, but sometimes a retweet is not enough.

 

Publishing is not evolving. Publishing is going away. Because the word “publishing” means a cadre of professionals who are taking on the incredible difficulty and complexity and expense of making something public. That’s not a job anymore. That’s a button. There’s a button that says “publish,” and when you press it, it’s done.

–Clay Shirky

It’s so good I think I will publish it, and by that I mean press a button:

Two more NephTalk Podcasts

I was given the opportunity to work with Satellite Healthcare on their NephTalk podcast and hosted three episodes. The first one, on infection in dialysis units, was posted via RSS and picked up by iTunes. But the next two episodes I hosted were not posted to the RSS feed and so won’t show up in your podcast player of choice (by which I mean Overcast).

So you you’ll have to listen to them like your grand father did, as he walked to school bare foot, through the snow, uphill, both ways, via a web player. Sorry.

Joel Topf, M.D. interviews Steven D. Weisbord, M.D., lead researcher on a study recently published in the New England Journal of Medicine.

Joel Topf, M.D. interviews Linda F. Fried, M.D., lead researcher on a study recently completed for the U.S. Department of Veterans Affairs.

The “How I do a Presentation” Presentation

This morning I gave a lecture on how to do a presentation to the residents at St John Hospital and Medical Center.

Here is the presentation:

How to give a Lecture (375 MB)

I used some material from this older version

Meta lecture (148 MB)

Much of the lecture was just stepping through the SGLT2i presentation and demonstrating the different techniques I use to annotate my talks.

Resources you should use to make superior presentations:

Presentation Zen Blog by Garr Reynolds

Presentation Book by Garr Reynolds

The Noun Project for icons

Visual Abstract example and Primer by Andrew Ibrahim

New to Twitter? Here is a short course on counting Tweets

One of the things that is intoxicating about social media is watching  how many people see, interact and respond to your content. This is at the heart of the difference between the little red circle on Twitter (dopamine!) versus the the little red circle on Mail (dread!).

Tracking likes and Retweets

The simplest analytics are shown below the tweet and anyone can see them.

This tweet from new NSMC intern Dr. Dave has 5 retweets and 28 likes.

Impressions and Engagements

The next level of analytics can only done one’s own tweets. Select one of your tweets, preferably one with a picture or a link, or both, and press “View Tweet activity”

This opens up a panel that reveals two new analytics: Impressions and Total engagements.

Impressions are a bit confusing. Here Impressions represent the number of people the Tweet was actually displayed to. So someone that was scrolling through twitter and this tweet passed her eyes would add one to the impression. This is very different than how that same term is used by Symplur (see below).

Engagements are the total number of people who have interacted with the tweet in some way. Click View all engagements to see what that means.

Twitter does a nice job of tracking and breaking down the elements that make up engagements.

Analyzing Your Twitter account

The next level in analytics is looking at your twitter account. Make sure you are logged into your twitter account on the web and then type in https://analytics.twitter.com

The analytics page has an explosion data. The top gives you your 28 day trend for Twitter.

January is not looking like a good month for me.

There is a menu of additional pages of information. The only one that I find useful is Tweets. More on that later.

Scrolling down you see a summary of every month you have been on Twitter Actually I’m not sure how far it goes back, but pretty far. For each month it tells you:

  1. Your Top Tweet. The tweet from that month with the most impressions
  2. Your Top media Tweet. The tweet with an embedded picture, video, gif, or poll(?) with the most impressions (if your Top Tweet has attached media, the Top Media Tweet will be the tweet with the second most impressions)
  3. Top Follower. The Twitter account that followed you that month with the most followers. Some of my months don’t list a top follower. I wonder if that is because that person no longer follows me? (And no I don’t know why Follower is capitalized)
  4. Top mention. The Tweet that mentioned you that garnered the most impressions that month.
Nothing dispels the notion that number of followers translates to interesting person faster than scrolling through your history of Top Followers. They are rarely someone interesting. Not you Soledad, I think you are very interesting, I’m talking about other people.

Next to these four pieces of information is a summary of your use of Twitter that month. I find it interesting to scroll through and see how your Twitter activity climbs and falls month to month.

Now click on Tweets at the top of the page (between Home and Audiences)

At the top Twitter shows you a histogram with the number of tweets (grey) and impressions (blue). On the right rail there are a series of histograms with the daily count of some of the components that make up engagements.

The bulk of the page is a collection, in reverse chronologic order, of all of your Tweets for the month. If you want to look at another time period you can do that with the date picker in the top right corner of the page. For each tweet you can see impressions and engagements and the rate (engagements/impressions). For each tweet you can click to reveal the full breakdown of engagements.  You can sort and filter the list by pressing Top Tweets and get a short list of your top Tweets.

There are a few more tabs to explore in Analytics, but I have not found them useful.

Hashtag Analytics

At the end of every #NephJC and #AskASN, Matt and I race to see who can post the analytics for the chat first. To do this we are taking advantage of a service called Symplur. Symplur tracks all health hashtags. If you come up with a new health hashtag for a conference, you should go to Symplur and register that a hashtag. To use Symplur, go to their homepage and click on the magnifying glass and enter your medical hashtag.

Then click on #NephJC in the search result page. This take you to the #NephJC page in Symplur.

Ignore the schedule in Symplur, NephJC moves around inside the month enough that they never have it right. To get the Symplur analytics for an event you need to scroll to the bottom of that page, use the date picker to select the time you are interested in and press Get Analytics.

This will give you the analytics for that time period. Here is the analytics for the ACC/AHA Hypertension chat on January 16th.Mentions is the number of times a person on Twitter was mentioned along side the hashtag in question (#NephJC in this case). Tweets is the number of tweets composed by the individual which contains the hashtag. And then there is Impressions. These impressions are not the same as the impressions that Twitter tracks. Twitter impressions are real. Symplur impressions are a lie. Symplur impressions are the number of tweets multiplied by the number of followers the author has. Since I have 11k followers, each of my tweets increases my impression count by 11k. Impressions rack up gaudy numbers fast and often a larger conference will have impression counts in the 100s of millions. This is absurd. Do not believe impressions. Matt and I, when we tweet the analytics for the chat, edit out impressions. However in one of our publications we did publish impression counts for NephJC. Matt swears it wasn’t him and I swear it wasn’t me but it’s in there. Sorry.

That’s the basics on Twitter analytics. A number of people have developed more advanced analytics that you might want to explore but I have not found that they add much witter experience. This is enough for me. Your mileage may vary.

Lecture on CKD-MBD

The St John Nephrology Fellowship is excellent. One of the reasons it is good is  we continually use feedback to fix holes. In last year’s in-service exam we found some weakness in calcium so I was asked to buff the fellows calcium knowledge.

Today I started that with a lesson on CKD-MBD where we focused on the KDIGO 2017 update. I pulled what I feel are the the most important articles in this area published recently. Here is what I pulled:

PRIMO. Paricalcitol in pre-dialysis CKD does not magically heal the heart.
Phosphate binder network meta analysis. Concluded that calcium-free based binders are better. All binders have lots of side effects.
The guideline
Executive summary of the guideline with a useful side-by-side comparison of the 2009 and 2017 guidelines.
Phosphorus binders in pre-CKD patients don’t do a lot of good and increase coronary calcification.
Evolve. Prospective data in CKD MBD that produced a nice separation in PTH and not much else.
FGF-23 still has not made it into the guidelines but it is the phantom menace soon to be unveiled.

What did articles did I miss? What are your favorite CKD-MBD articles

P.S. My favorite part of the guidelines, the part that tell you everything you need to know about KDIGO is 4.2.2:

Here it is in 2009:

And here it is in 2017

And the best part is how the level of evidence has not changed. 2C for both. It’s like they just woke one morning on a different side of the bed.

Great update from Swapnil

I will be doing Show and Tell on Social Media and Medicine Jan 31 at the University of Michigan

The University of Michigan invited me to speak on social media to the division of nephrology on January 31st. They asked me how I wanted to handle it and I told them that I would love to get an opportunity to show them rather than just tell them about  social media and they responded “How about both?”

Show: At 3pm I will guide the fellows and anyone else who shows up through the European NephJC Twitter journal club chat. We will be talking about metformin in advanced CKD.

Tell: Then after NephJC, I will roll into a traditional lecture on The History and Future of Medical Education.

Please join me in University Hospital 2nd floor, room 2C-224 UH at 3pm (for NephJC)or 4pm (for a lecture). I have been told the room can hold up to 80 people. It would be fun if we could fill it.

High-altitude renal syndrome

Everyone knows the famous George Mallory answer to the question about why he was climbing Mount Everest , “because it’s there.” But I just learned that he continued after that mic drop and spoke about doing science on these mountain climbing missions:

Sometimes science is the excuse for exploration. I think it is rarely the reason.

The three primary causes of high altitude sickness:

  1. Acute mountain sickness (AMS): headache, gastrointestinal symptoms (anorexia, nausea, vomiting), sleep disturbances, dizziness, fatigue
  2. High altitude pulmonary edema (HAPE)
  3. High altitude cerebral edema (HACE)

Lake Louise Acute Mountain Sickness severity score for acute mountain score:

Preventing AMS is usually dependent on limiting altitude gain, avoiding alcohol and drinking a lot of water.  Acetazolamide 125-250 bid is also effective.

The headache of acute mountain sickness can be decreased or avoided with medications:

Aspirin 320 mg po q4-hours x 3 doses, starting 1 to 2 hours prior to arrival

Ibuprofen 600 mg po q8-hours for at least 3 doses, starting 6 to 24 hours before ascent.

Ginko Biloba has been used with variable success as prophylaxis. 160-240 mg in divided doses

Dexamethasone 8 mg daily in divided doses can also be used for prophylaxis.

Nice review of AMS treatments and prophylaxis can be found here.

In studies looking at the etiology of AMS and HAPE, Vascular Endothelial Growth Factor and its soluble receptor sFlt-1 were thought to play a role. However in a study of 51 Denali mountaineers, blood levels were not associated with AMS.

The body has a number of strategies to adapt to high altitude trekking. Among the changes is the observation that the density of capillaries per unit of muscle rises. This sounds cool until you read that some scientists believe this is primarly due to a loss of muscle mass rather than growth in new capillaries.

Other strategies for adaptation include

  • Hyperpnea and tachypnea leading to hypocapnia
  • Hypoxia may trigger several receptors, including airway chemoreceptors
  • Tissue hypoxia also induces the production of hypoxia-inducible factor (HIF) transcription factors
  • Changes in metabolic pathways including oxidative metabolism, cell cycle and diminished myogenesis
  • Changes in hemoglobin oxygen affinity that alter arterial oxygen saturation and release to tissues
  • Increase in mitochondria and cytochrome oxidase occur but only after 7-9 days at altitude

Renal changes.

High-altitude renal syndrome is an asymptomatic chronic condition of high-altitude dwellers defined as:

  • High-altitude polycythemia
  • Systemic hypertension
  • Microalbuminuria
  • Hyperuricemia
  • Relatively preserved glomerular filtration rate

High altitude renal syndrome is part of the complex adaptive response to altitude.

Creatinine based GFR is unaffected by increases in altitude, however a study that used cystatin c based GFR assessment found a 3ml/min drop in GFR for every 1,000 meters the mountaineers ascended.

Interestingly, AMS was associated with higher eGFR.

Most electrolytes fall:

The decrease in serum bicarbonate comes from hypoxia induced respiratory alkalosis. Arterial pH at the top of Everest is estimated to be 7.7 to 7.8. PaO2 was 35 mmHg!

Trekkers in the mountains have hypovolemia due to increased insensible losses, increased anorexia, and decreased thirst. Additionally there is altitude induced diuresis. This diuresis seems to be an obligatory early phase of adaptation to altitude. The diuresis can cause a 1-3 liter loss of body water resulting in a 38% increase in blood viscosity at 5,800 meters.

The diuresis has variably been explained by suppression of ADH, increases in ANP and increases in BNP. Increases in BNP are associated with increased risk of AMS.

This paragraph is very interesting:

It remains unknown whether the altitude-induced decrease in plasma volume is adaptive or potentially harmful. If adaptive, then less effort should be made to correct ‘dehydration’, and fluid intake should be limited to simply following the thirst mechanism and to offsetting insensible losses (admittedly difficult to estimate, much less measure, on the mountain). Indeed, as discussed above, fluid retention rather than dehydration is associated with AMS. Perhaps diminished plasma volume is part of the body’s effort to supply oxygen to the most vital organs, overriding the not insubstantial risks of hyperviscosity and thrombosis associated with hemoconcentration.
There could be two beneficial effects of high-altitude diuresis:
  1. Early hemoconcentration elevates the blood concentration of hemoglobin prior to the slower onset of EPO-stimulated erythropoiesis
  2. Volume depletion reduces intravascular pressure and volume load on the lungs and brain, and may decrease renal oxygen consumption (90% of which reflects renal sodium reabsorption) due to diminished filtration

This article is excellent.

Spooky Sodium 👻: The Grand Rounds

At Lankenau Medical Center in Philadelphia at 8:00 AM, January 12. I will be talking about Spooky Sodium 👻.

Here is the title slide

If you can’t make it, first of all, what’s wrong with you? But second of all don’t worry, you can get the high points from the man who discovered them in this 13 minute TedX Talk from Vanderbilt.

And from this article in the NYT

And don’t forget about the excellent NephJC coverage, including an editorial from Rodby.

I will eventually post a slidecast of my presentation.

Hypercalcemia from 1,25 vitamin D toxicity

I received an outpatient consult for acute kidney injury. One of the things that makes Saint Clair Nephrology a remarkable nephrology group is our ability to get patients in quickly. While competing practices in the area have a 3-month wait list to see new patients we get patients in within a week. This patient was seen two days after his doctor called.

The patient was frightened. He had previously been healthy and his doctor told him his kidneys were failing and that he needed to see a nephrologist. He arrived with a creatinine in the high 2s from a base line of 1.2 mg/dL. Along with the AKI his blood pressure was touching 180 systolic, out of character for him. Of note on the initial labs his calcium was 13.6 mg/dL.

The initial work-up showed suppressed PTH. SPEP and UPEP were normal.

On the next visit I checked the 1,25 vitamin D and it was 117 IU. I suspected lymphoma or sarcoidosis but the chest x-ray was unremarkable and the patient did not have any palpable lymph nodes or abnormalities on the CBC. No weight loss, night sweats, or fevers. ACE levels were unremarkable.

On further questioning on his third visit, the patient mentioned he was taking a generic knock off of Mega Red Fish Oil. Fish oils can have significant amounts of vitamin D and the supplement is famously lax with quality control. He stopped the fish oil, we started him on oral prednisone and the 1,25 vitamin D level quickly responded within a couple of weeks. The patient had a full recovery from the hypercalcemia, hypertension, and acute kidney injury.

 

 

Update

Some great comments from Twitter