musings of a salt whisperer
Last week I posted a tweetorial on pseudohyperkalemia due to CLL and a high white blood cell count.
This case peaked with a potassium of 9.5. Pretty frightening, but that was nothing compared to the potassium of 15.5 I saw in 2014. Details here.
I had another case of pseudohyperkalemia in 2011. That one was due to thrombocytosis.
In response to my Tweetorial, Yash Chivate shared a case of pseudohyperkalemia of his own.
Awesome, current resource on onconephrology from the ASN. Nineteen chapters with everything you need to be a superior consultant nephrologist
The more you learn the cheaper that ASN membership looks.
I received this DM today (my DMs are open. I was nervous about opening DMs but a year later I would rate the experiment as a delightful success. It has opened up Twitter to many new discussions that otherwise would not have occurred).
Hi Dr. Topf, I’m a final year medical student from the UK. I’ve been following you for a while due to my interest in renal medicine. Are there any books/online resources that you would recommend to learn renal physiology? I feel that I lack fundamental principles and concepts which I’d like to improve. Thanks!
Arnav
This is actually a relatively common question and I am going to attempt to write this post so I can link to it in the future.
The answer depends on the goals of the student
Slim, readable. Good choice.
This is designed to be part of a workshop but it can be read on its own.
This list is for the learner who is looking to know what to do.
Of course I’m one of the authors and I edited every single word in this book but a year later I still am amazed at how well this review book walks the tightrope of being concise without over simplifying complex topics. I may be biased, but I think this is an excellent book.
Before Secrets this was my go to recommendation, but this book is getting long. I’m beginning to think this may be too long for a student resident on a one month nephrology rotation. That said you can’t find better renal educators that editors than Gilbert and Weiner.
Fluid, Electrolyte and Acid Base Companion
It is strange that one of the things I am most proud of in my entire career is a book I wrote as a resident but it is no exaggeration to say this book for transformative for my life. I poured five years of work into this project and i think it stands up. However you should skip the tremendously outdated and overly complex section on the treatment hyponatremia and instead read the European Clinical Practice Guidelines.
Burton Rose’s Clinical Physiology of Acid Base and Electrolyte Disorders.
People look at the copyright on Rose’s electrolyte book and conclude the book is out of date.
It is.
It doesn’t matter.
Rose excels at providing the reader a cohesive mental model of how the kidneys work so that things make sense. Then if you need to learn more and get a more up to date and nuanced view of how the kidney works it is pretty simple to plug those updates into your mental model of the kidney.
Use the following:
Read the first three cover-to-cover and then cover-to-cover again. The KDIGO Guidelines will give you the state-of-the-art for many of the important issues in Nephrology and the full guidelines provide a solid scientific rational for why the guideline are the way they are. You should have more than a superficial familiarity with the guidelines. Use UpToDate and Nature Reviews to go deep on every weird, rare, or interesting patient. Use the last one to stay up to date with clinical research. That’ll do. That’ll do quite nicely.
What did I miss? What are your favorites. Hit me up on #MedTwitter or slide into my DMs.
Some good updates from Twitter
And Mir Tariq Ali reminded me of major omission to my list. I forgot Daugirdas’ Handbook of Dialysis. This is the third book that every nephrology fellow should read cover to cover and then read again.
My team was consulted for acute kidney injury (AKI) and hyperkalemia. Before we saw the patient they had already been given the standard, calcium, bicarb, and insulin/glucose cocktail. This had no effect. Potassium went from 6.4 to 6.4.
The patient was still making urine. The AKI was due to emergency surgery with an impressive estimated blood loss (translation: blood loss measured in liters). We gave a liter of NS, 80mg of IV furosemide and 0.2 mg of oral fludrocortisone. Potassium went from 6.4 to 3.4 despite a further increase in the serum creatinine.
Remember to use the kidney for treating hyperkalemia. Even in AKI you can get impressive results.
Renal clearance of potassium is entirely dependent on the cortical collecting duct, specifically the principal cells. It is a multi-step process:
That is how potassium is excreted but, how is potassium regulated? There are two primary components to regulation:
The medical management we provided takes care of both aspects of potassium regulation, the furosemide and saline makes sure there is a robust supply of sodium delivered distally and the fludrocortisone makes sure there is ample aldosterone activity to assist with potassium clearance.
Last week I wrote this tweetorial
I had been thinking about this for a long time.
When you hear #TWDFNR talks about AKI the two things that are usually hammered are:
I actually like both of those tests, despite the pundit class dumping on them.
The FENa is vilified because in trials that look at its ability to separate out purely hemodynamic decreases in GFR from acute tubular necrosis it does poorly. This is especially disappointing because all of the board exams and med student level lectures on FENa says this is just what the test is all about. I concede that FENa in isolation is a bad test to determine the etiology of AKI. But as part of the global assessment of the patient, getting a FENa can be incredibly powerful.
Saying the FENa is useless is like testing to see if a blinded physician given only an aucultory exam could diagnose community acquired pneumonia. I think there is a good chance auscultation would fail that hurdle. But that doesn’t mean we should abandon our stethoscopes. The auscultory exam is one of a number of studies we do when assessing a patient who may have pneumonia. It is a valuable part of the global patient assessment.
Similarly, the FENa is part of my global assessment of a patient.
For example, I have a patient with cirrhosis and acute kidney injury. I look at the urine and see a mixture of hyaline casts and granular casts. Now, you need to be careful about granular casts in cirrhosis. As the bilirubin climbs, it can stain innocent hyaline casts to look brown, and they can start to look somewhat like muddy-brown casts. I don’t think that is what is happening on this slide, because I can see simultaneous dirty brown and hyaline casts. Then we checked the urine sodium and it was 50. This is off diuretics. This is remarkably high for a patient with cirrhosis and ascites. But there it is. The urine sodium is high and in agreement with U/A findings. I make a diagnosis of acute tubular necrosis.
It’s an N of 1, but that’s all we have in clinical medicine, one N of 1 study after another.
The kidney ultrasound story is a much simpler than the FENa story. The argument that kidney ultrasound is of low yield and low cost effectiveness is due to the exrtemely low yield of U/S to find obstruction. In almost every case that you find obstruction, you suspected obstruction, and using it in cases without a clinical suspicion is like Acestes aiming at a non-existent target.
But the thing is, the treatment of obstruction is not dialysis, and if you fail to identify and correct the obstruction, no mixture of IV fluids, avoiding nephrotoxins, and regulating blood pressure will fix the obstruction. That obstruction will lead to renal failure and dialysis. In a world of $60,000 a month maintenance therapies, I refuse to miss even one easily correctable (but otherwise irreversible) cause of kidney failure.
The real #TWDFNR in AKI are:
The fallacy of the Protein Creatinine ratio was the subject of the afore mentioned tweetorial.
Some great comments and discussion from the tweetorial:
The problem with PTH in AKI is that it is useless. I see fellows and attendings ordering this and I have no idea what to do with it. Some people try to use the KDIGO PTH guidelines for ESKD. This seems to be totally evidence-less. PTH is an acute phase reactant in AKI. Part of the AKI syndrome is a drop in calcium, and after that PTH rises, just like it is supposed to. I don’t see any reason to suppose this secondary hyperparathyroidism is pathologic. I have seen some people order it to try to distinguish acute from chronic CKD. The reasoning being, that chronic kidney disease would have a high PTH and acute would not. This is not the case both acute and chronic kidney disease can have secondary hyperparathyroidism.
Stop ordering PTH in AKI. Stop checking urinary protein to creatinine ratio and start doing urinalysis and microscopy.
I wrote the following tweetorial last week and the response was amazing. Seems like everyone had an opinion.
The poll at the end of the tweetorial had over 1,500 votes with 90% split between “Definitive source” and “Equivalent to other textbooks”
A recurring thought among commenters was that textbooks are great for providing overviews and UpToDate is a more practical reference that will be both up-to-date and provide specific recommendations for your clinical question. I remember talking to Burton “call me Bud” Rose when he was hawking a still incomplete UpToDate in the halls of ASN Renal Week in the 90s. One thing he drilled in on was that his cards (a card is a single entry in UptoDate) always finish with a specific recommendation. He viewed this as a critical differentiator for UpToDate. He made his writers not just provide the data but pick a side.
One great comment was by Poonam Sharma
I think this might be the source of some physicians distaste for UpToDate. When we have a resident give a presentation to teach the rest of the team or residency, or fellowship program we want people to dig deeper than summarizing UpToDate.
Additionally people kept commenting on the importance of going to the primary literature. This is great in principal, but in practice the volume of primary literature is overwhelming. The KDIGO 2012 blood pressure recommendations have 453 references on blood pressure alone. If you seek to be an expert, going down the rabbit hole of primary literature is essential, but if you want to put all of that training to use taking care of patients, it is best to stick with guidelines, review articles, and, yes, UpToDate.
One final note, the villain of the initial tweet, Dustyn Williams, contributed to the conversation.
This is a model with how to deal with this type of hullabaloo. He avoided any ad-hominem defensiveness. He stated that this was a long time ago and he is no longer the same person. His thoughts on the topic have evolved. Nicely done. God knows what inappropriate and emotional things I have typed out in the past. And I am sure most of us will, in the future, need to deal with years-old statements returning zombie-like to chase us down. Dr. Williams provides an admirable model to follow.
COI: I am the author of a medical textbook.
I was invited back to The Curbsiders for a discussion about hypernatremia. I had a great time and through the magic of Hannah Abram’s production and Matt Watto’s edits it turned out pretty good. I listened Toit and I didn’t come up with any major gaffs. Take a listen. What do you think? As usual all comments should come through Twitter.
I posted this tweetorial to Twitter last month and I want to bookmark it here.
Earlier this year I got the opportunity to speak at Brigham and Women’s Nephrology division. I had spent a lot of time and thought in updating my Social Media and Medical Education talk. For the first time I added Podcasts and Tweetorials, two of the most exciting developments in social media medical education.
Then on the day of my presentation I had “technical problems” connecting my MacBook Air to BWH’s projector (what is this 2003?). So I logged into iCloud and ran an older version of the presentation from iCloud using the online version of Keynote on the PC connected to the projector. The idea that I can run my presentation, with fonts, images, animations on a browser version of Keynote on a PC is truly amazing. Hats off to the Apple engineers.
But that meant the newest version of the talk was still “unpublished.” So I was delighted to get a generous invitation from Vanderbilt to speak at medicine grand rounds.
So this past Thursday I traveled to Nashville and I was able to present this presentation. And now that it is “published”, I am offering the presentation for you to present, edit and repurpose in any way you desire (no permission required, go at it):
And what an amazing nephrology department. Holy moly what a deep bench. Loved getting a chance to talk with Ray Harris, Anna Burgner, Tom Golper, Jay Bhave, Kerri Cavanaugh, Alp Ikizler, Julie Lewis, Be a Concepcion, Davika Nair, Leslie Gewin. and Edward Gould.
If you are applying to nephrology fellowship and don’t have Vanderbilt on your list, you are doing it wrong.
Matt and I had the honor of putting together a session on social media for the NKF. We did not want to do intro to social media. The beginning of social media in medicine is over. We are in the beginning of the middle, and we wanted to deeper look than intro lectures can provide.
We had three talks.