Everyone talks about the importance of mentors in career development, but there is another type of Fairy God Mother that doesn’t get as much press but can be just as important, this is the Sponsor. A sponsor doesn’t give advice and guide you like a mentor does, but when opportunities come up they think of you and put your name forward.
The most important sponsor in my career has been Chief of Medicine at Ascension St John, Lou Saravolatz. As a fellow, Dr. Saravolatz discovered a bug now known as Methicillin Resistant Staph Aureus (remind me, what world changing research are you doing in your fellowship?). But as Chief of Medicine he has been my (and a host of other docs) sponsor. Dr Saravolatz invited me to give my first grand rounds presentation in 2003. A talk on contrast nephropathy.
Today, I gave another talk on contrast nephropathy. Here are the files. I will try to get a video with my narration up in the next few days.
Powerpoint (I just export the Keynote presentation to Powerpoint so I suspect many of the animations are crap. It is here just to preempt the chorus of Twitter requests for it)
I also am posting the talk bit-by-bit as #Tweetorials.
The first:
I am going to do a few tweetorials based on my Contrast Nephropathy Grand Rounds. The first one goes through the evidence that CIN is rare; in fact way rarer than the commonly quoted 10-25% incidence. For more information on my whole presentation see: https://t.co/yGmo9pb5Yh
This is not an uncommon finding at medical schools around the country. I have been to lectures by Dr. Heung at Kidney Week and he is a gifted teacher. There is nothing wrong with him. The knee-jerk response is to do what Oakland University William Beaumont School of Medicine did and make lectures mandatory. I get a full auditorium for every one of my lectures. It strokes my (already formidible) ego, but I don’t think it is the right response.
The empty lecture hall is because medical students are finding ways to learn that are better for them than sitting in a class room six hours a day. It’s more efficient to stream the lecture at 2x-speed with tabs open to other resources. If this is how they learn best, schools shouldn’t enforce inefficiency by making them attend lectures. Medical school deans should recognize how the material is going to be consumed and then develop curriculum around that consumption.
Every medical student, after paying tens of thousands of dollars for tuition, spends additional thousands of dollars on materials, tutorials, and videos to get ready for the big bad board exam at the end. What is the core competency of medical schools if it is not getting students ready to excel at licensing exams? Every one of those subscriptions is an indictment of the product that medical schools are providing their students.
Here is a list of vendors from the 2018 American Medical Student Association Convention. Check marks indicate vendors that provide services that medical students should be getting from their (wildly expensive) schools.
If we were to start from the position that students are going to consume every lecture on their own time on their own laptop, would we record the same slide show with the same talking head every year? No, that’s an absurd waste of the professor’s time to produce content that is not compelling or a good use of the medium. This is like the first movies, where directors would just film stage productions, ignoring the nature of the novel medium. Instead of seeing the empty lecture halls as a problem it should be viewed as the huge opportunity it is. The students have already moved to the new medium, it is time for medical schools to catch up.
It is time to turn those lecture halls into production studios. It is time to hire professional animators, artists, and video producers, and go from slide shows that need to be performed live every year to tightly produced educational shows that can be created once and shown many times. Let’s teach for the contemporary reality, rather than fight it with rules that serve to waste student’s and teacher’s time.
Kidney Week is my favorite week of the year. It’s Kidney Christmas. Kidney Week is the one week when all of the connections I make over direct message, e-mail, and text via the black rectangle in my hand transform into living, breathing people. If you are going to Kidney week, I’d love to meet you in real life.
Here is a rough itinerary
Pre-Conference
Tuesday and Wednesday
Fundamentals of Renal Pathology β Anthony Chang, MD, FASN, Lynn D. Cornell, MD, Mark Haas, MD, PhD
Conference
Thursday:
1:00 to 1:30 pm I’ll be at the ASN Community Booth discussing Leveraging Social Media for Your Career in Nephrology.
6:30-7:30 pm Nephrology Secrets Book Signing at the Elsevier booth (1119) during the ASN Welcome Reception
Friday
10:30am Join Cathy Quinlan and I on the NephJC Poster Tour. Meet at the Arkana booth (2515)
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!
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.
The learner really wants (or needs) to have a mechanistic understanding of why we do what we do then…
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.
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.
The nephrology fellow
Use the following:
Nephrology Secrets
Burton Rose’s electrolyte book
Daugirdas’ Handbook of Dialysis
All of the KDIGO clinical practice guidelines
A subscription to UpToDate
A subscription to Nature Reviews Nephrology
Attend every NephJC
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.
Although some of the information from this page may be 'Australia-centric', Kidney Health Australia may have some useful resources:https://t.co/recYxeLNjj
— Samuel Holland ππππ π¦₯ (@SEdwardHolland) October 15, 2019
There's heaps of free Fact Sheets, Books, and Brochures provided on the site. But as an example this is a link to one of their free ebooks, 'My Kidneys My Health' which aims to provide information to patients with early stage CKD.https://t.co/3FsYQtM6y4
— Samuel Holland ππππ π¦₯ (@SEdwardHolland) October 15, 2019
βHelp, I Need Dialysis!β Outstanding book. We buy them by the case and give to every CKD4-5 patient we see. Published by the MEI foundation, also through 3rd party sellers on amazon.
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.
What about feehally's comprehensive? Or henrich's dialysis?or daugirdas's ? As fellows when time is limited when and how do we benefit from these ones? Or not. Or the ones you mentioned are enough?
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:
reabsorption sodium down its chemical gradient through eNaC
The chemical gradient to allow sodium resorption is generated and maintained by the Na-K-ATPase
Movement of sodium without an anion(or a cation going in the opposite direction creates a negative charge in the tubular fluid which pulls potassium down an electrical and chemical gradient from the cells into the tubule. This occurs through ROMK and BIGK.
That is how potassium is excreted but, how is potassium regulated? There are two primary components to regulation:
Aldosterone stimulates the transcription of all three transporters (ENaC, Na-K-ATPase, and ROMK) as well as transcribing versions of the proteins which are more active.
Tubular flow. Increased distal sodium delivery provides plenty of sodium to be reabsorbed into the principal cell providing the negative charge, as well as washes away any secreted potassium to maintain the chemical gradient favoring potassium excretion.
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.
Internists know that eGFRs can not be used in AKI, that the formula requires the patientβs being in steady state. But fewer internists (and fellows) know that also applies to the protein to creatinine ratio (PCR). (1/10)
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.
Not the patient’s urine, but those are some nice muddy brown casts.
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:
Urinary protein to creatinine ratio
Intact PTH
The fallacy of the Protein Creatinine ratio was the subject of the afore mentioned tweetorial.
Some great comments and discussion from the tweetorial:
Wouldnβt the decrease of GFR also affect the proteinuria, decreasing the numerator and canceling each other out?
LOL I remember a case from fellowship, middle age guy w garden variety ATN. UP/Cr = 8g/g day 1 during midst of injury, less than 1g/g day 4 when he was recovering
No formula. No equation. No quantification. Do a global assessment. Examine the patient. Dip the urine to confirm proteinuria. Look for hematuria. Urine microscopy. Serologic work-up for GN (ANCA, Anti-GBM, ANA, C3, C4, etc). Consider kidney biopsy.
U make excellent points Joel. Personally, I wouldnβt be as radical as saying stop ordering UPCR in AKI. Iβd say in oligoanuric AKI definitely not a good idea. But in a non-oliguric AKI who reached a plateau Cr and I suspect a glomerular cause, it helps framing the case. 1/2
Had a case last week where the team ordered a PCR and it came back at 5. Did an actual urine protein collection to show them why it was wrong and it came back at 100mg/24 hours.
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.
A med student answered a question and was very nervous to say he learned it from UpToDate. He wasn't sure how I felt about UpToDate. He then pointed to this exchange from @OnlineMedEd where one of the teachers disparages UpToDate https://t.co/TQ42Bbsp0Epic.twitter.com/8zMK6uWsXl
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
Better than textbook (more likely to be…UpToDate) but narrative review not systematic review so you donβt know what you are missing. Great for next steps and MOC but not for prepping a talk.
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.
I've come a long way since this comment; it certainly could be worded better. Of course full context helps, but that aside I was not disparaging any one specific person. I find utd helpful for me, but not for students. And yes, there are problems with it. But that is universal
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.
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.
