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1. Don’t plan too carefully; improv is the name of the game with technical talks.
2. Begin by thanking an enormous number of people, including blurry little pictures if possible. It comes across as humility.
3. Waste a lot of time at first on some small point, like the correct spelling of “Chebychev.” Whoever heard of running out of time? (See Rule 13.)
4. An elaborate outline of the talk to come, phrased in terms the audience hasn’t heard yet, really sets the stage, and saves saying “I’m going to present the beginning, the middle, and the end.”
5. Don’t give away your simple motivating example early on. That’s like stepping on your own punchline.
6. A good way to start is with the most general, abstract statement possible.
7. The best notation is the most complete notation — don’t skimp on those subscripts!
8. Blank space on the screen is wasted space. There should be an icon for everything — if you say the word “Apple” an apple should tumble in from the right, etc. And don’t forget to read every word on the screen out loud.
9. Humans are incredibly good at reading tables, so the more rows and columns the better. Statements like “you probably can’t make out these numbers but they are pretty much what I said” are audience confidence builders.
10. Don’t speak too clearly: it isn’t necessary for those in the front row.
11. Go back and forth rapidly between your slides. That’s what God made computers for.
12. Try to get across everything you’ve learned in the past year in the few minutes allotted. These are college grads, right?
13. Oh my, you are running out of time. Don’t skip anything; show every slide even if it’s just for a millisecond. Saying “This is really interesting stuff, I wish I had time for it” will make people grateful for getting “Chebychev” right.

From here, Hat tip to David Juurlink, author of this great potassium paper.

It was hard. It was harder than I expected.

The Test

Many of the questions were second derivative type questions. They would describe a renal disease and then ask a question that required you to know what the hidden diagnosis was and then some additional bit of knowledge about the disease, i.e. diagnosis, treatment or prognosis.

I felt the test was hard and initially complained that I thought it was unfair but with some more time I feel that it was actually a pretty fair test. One complaint I heard among my fellow test takers was that the test did not reflect their practice. There was essentially no peritoneal dialysis. There was very little chronic hemodialysis and I felt that chronic kidney disease was under emphasized. There was a lot of electrolytes, acid-base and secondary hypertension.

One aspect of the test that bothered me was how the test seemed to have no clue how a modern, networked, doctor actually works. For example, there were questions that asked about a specific drug look the correct dose up on my phone. I am not arguing that drug dosing in renal failure questions are irrelevent in the era of the networked doc but the relevent fact is not what the dose is, but which drugs need to be dose adjusted. Provide a list of drugs and ask me which ones need to be dose adjusted in renal failure. Give me a list of drugs and ask in which ones are drug levels not indicative of biological activity. Adapt the question to be relevant in today’s connected world.

Similarly, regarding rare diseases in nephrology. Do not ask me how to treat Fabry’s disease. I have never seen a case of Fabry’s. I need to be able to diagnose the condition, and then the correct next step is not to reach back in the recesses of your memory for how to treat this one in a million disease. The right answer is to hit the books and brush up on the disease. Recognizing the pattern of symptoms and making the diagnosis is what is important. Treatment can wait for the practitioner to review the latest data. The best time to get up to date on a disease is right when you suspect it so you have the latest knowledge. Forcing people to memorize treatments of rare conditions de-inforces the better habit of hitting the books when something rare comes up (and by books I really mean UpToDate).

Just saw my 6th case of Fabry’s disease. Still all of them are on board exams. #ASNBRC
— Dr. Matt Sparks (@eAJKD) August 10, 2013

The Prep

To prepare for the recertification test I put all my wood behind the ASN Board Review Class. My results are not back, so it may be a bit premature to make a recommendation but, as of today, I feel that it is an excellent way to prepare.

• The breadth and depth of the lectures was right in line with what I saw on the test.
• I feared that the ASN would try to get the biggest names in nephrology rather than an all-star bench of great teachers. They did not fall into this trap. They found some really big names in nephrology who are also really good lecturers.
• They provide a wealth of resources to help you extend your learning beyond the week at the conference.
• practice test
• paper syllabus with copies of all the slides
• CD-ROM with all the slides
• Audio synched to the slides for online review

I went to the lectures in Chicago and was an active learner by live tweeting the lectures for eAJKD (coverage provided by the excellent uKidney).

After the week in Chicago I carefully went through the practice exam provided by the ASN BRC. One hundred fifty questions with answers and good explanations. I loved this tool and only wish they were a bit more indulgent with the answers (in other words love it, just give us more). I feel that questions and answers I think are one of the best ways to prepare for the test.

In the weeks leading up to the test I listened to hours of the ASN BRC lectures on my computer. The online component has audio synched to the slides, so it really is a way to relive the Chicago experience. The site is a bit balky to navigate but this resource is worth its weight in gold. Tremendous value.

You know how you memorized all the fibrillary diseases as a fellow. Here’s a great chart to memorize it again. Joy.

From the ASNBRC who got it from Brenner and Rector*.

* I do not know who the Rector from that duo is but I do wonder if he gets a lot of “Rector? I barely met her!”

In terms of the quality of the lectures, I am a connoisseur of good lectures and a lecture snob when it comes to poor lectures. When I go to Kidney Week or other conference I usually feel that most lectures are actually pretty bad. However, ASN BRC broke mold with excellent lecture after excellent lecture. They had had a few clunkers and the bade ones looked even worse because the bar was set so high by the other speakers. What a crew they assembled.

The one weak point of the course is when the organizers tried to provide some alternative learning strategies. The organizers were not very forthcoming with the motivations for the afternoon interactive sessions but my guess is it goes something like this:

Every year the primary criticisms they get when they look at feedback is the sheer number of hours in lecture is both mind and butt numbing.

The directors response to this is small group, interactive learning sessions. An attempt to flip the class room. Their attempt at this was stymied either by poor planning or limited by physical space. They were able to divide the 500 odd participants into a group of about 100 and a group of 400. Neither of these qualifies as small groups. They did some case based questions but they really were just lectures in disguise. The professors read a question, did the audience-response thing, then proceeded to give a short lecture, sometimes with up to a dozen slides.

Despite inviting audience interaction there was not enough time or an appropriate venue for meaningful audience participation.

A small black mark on an otherwise impressive and highly recommended nephrology review.

This tweet came through my time line yesterday:

Fav pearl 3: Does contrast induced AKI even happen with IV contrast? Recent meta analysis suggests NO. http://t.co/rDiApxCG8W #NACCT13
— Bryan D. Hayes (@PharmERToxGuy) September 28, 2013

You really should check out the tweet on twitter to see all of the discussion it generated (I sampled some of the best tweets in the Storify below).

I skimmed over the full text article and it is not very convincing. The study is a meta analysis of 13 non-randomized trials that compared iodinated contrast imaging to non-contrasted imaging. I suspect most of the imaging was CT scans. No intra-arterial contrast was allowed, this eliminated all of the cardiac cath data (though the idea of a non-contrasted cardiac cath is ludicrous).

Before I started reading the article I suspected he would be pulling lot’s of old studies form the early days of iodinated contrast, I mean who today is questioning the existence of contrast nephropathy. Wrong:

Red: contrast causes renal failure Blue: contrast protects from renal failure

not determining if the contrast itself was safe. Looking at the references it becomes clear why I hadn’t been familiar with this supposed controversy, this stuff is not published in general medicine or nephrology journals. All doctors live inside specialty defined bubbles and, besides a single negative study published in Archives of Internal Medicine, none these articles pierced the bubble.

The thrust of the article is that renal dysfunction following IV contrast administration is no more common than renal dysfunction without contrast administration. If one looks at placebo (or placebo-like) controlled studies there was no signal that contrast increased the risk of acute renal failure:

AKI

Contrast: 6.4% (1004 of 15582)
No contrast: 6.5% (675 of 10368)

Death

Contrast: 2.4% (178 of 7359)
No contrast: 6.7% (81 of 1216)

Dialysis 

Contrast: 0.3% (24 of 7270)
No contrast: 1.2% (15 of 1214)

From Tepel. NEJM 2000. Shows NAC not only prevents CN but lowers creatinine.

These justifications are just another way of pointing out the problems that come from a lack of randomization and secondarily a lack of blinding. These methodology shortcomings are not solved by a meta-analysis. 

This is obviously an important question, but in my mind, and by my experience it is one that has already been solved. I have seen contrast nephropathy with my own eyes and I would need to see pretty compelling data to change that fact, and this study isn’t it.

UPDATE: My resident just pointed out that two of the authors have received money/grants from GE Healthcare, a manufacturer of CT scanners and iodinated contrast.

Here are some of the responses from Twitter

Note: My first grand rounds after finishing fellowship was on contrast nephropathy. I think it was the first time I used Keynote, way back in 2004. When I look at most of my presentations from that era I usually cringe but I think that old presentation holds up pretty well.:

Every year the National Kidney Foundation of Michigan’s Scientific Advisory Counsel puts together the Ronald Easterling Memorial Lecture. Ronald Easterling was a Michigan nephrologist who was instrumental in the establishment of dialysis. He worked for years at the University of Michigan and kept meticulous records of dialysis patients which became the prototype of the USRDS. His namesake’s lecture is a fund raiser for the NKF of Michigan.

This year I had a role in lining up the speaker and we hooked Dave deBronkart, i.e. ePatient Dave. Dave just recently spoke at MedX and you can get a feel for his view on medicine from his TEDx talk (yeah, we got a TED-level speaker for the Easterling!)

It should be hugely entertaining. If you are interested in the intersection of social media, patients and medicine I would highly recommend you come to the Easterling at Townsend in Birmingham, Michigan.

When the economic stimulus package passed and the basic blue print for meaningful use started to be hammered together, my practice committed to making the jump from paper to an EMR. Through blood sweat and tears (mostly tears) we implemented an EMR program in the first year that funds were available and we successfully qualified for meaningful use. We threw off the shackles of our paper chart and embraced the shackles of our EMR system, Allscripts (in case you wanted to follow us down this boondoggle).

It is hard work moving a large, multi-site practice across this chasm and the federal money really helped because it was expensive, more expensive and more complex than just about anything else our practice has accomplished, i.e. we did a heart transplant on our out-patient practice without taking taking a day off work.

After qualifying for Meaningful Use Part One for two years we were well on our way to qualifying for meaningful use Part Two when we hit a massive speed bump.

I maintain the medical records on the patients I see in clinic. I contribute to but do not maintain the medical records of the patients I see in the hospital. Those are maintained by the hospital. It makes sense for the hospital to take charge of the medical record and because I am only one of many doctors taking care of each patient. In addition to doctors there are pharmacists, nurses, physical therapists, etc that all share the medical record. So when meaningful use tracks how compliant I have been in using my EMR, they wisely don’t include the patients I see in the hospital as part of the denominator:

I also see a lot of my patients in the dialysis unit. Part of the reason so many of the visits are in the dialysis unit is that the federally implemented a payment structure encourages four visits a month. So I strive to go four times a month. These dialysis visits represent a large proportion of my monthly non-hospital-based patient encounters. Dialysis is truly the third leg that supports our practice.

Note: the feds look like they are right on this one with improved outcomes seen with longer time spent with the patient.

Just like in the hospital, I contribute to the medical record in the dialysis unit but I do not control it. It is a shared resource used by the nurses, dietitians, social workers and technicians, who all contribute to patient care and the medical record. This medical record is newly electronic. I work in Davita facilities
and I have been blown away by the simplicity, speed, and ease of use of their Falcon EMR. (I was not paid to say that, though I jointly own a dialysis unit with Davita.)

Unfortunately, that EMR is not certified for Meaningful Use, so not only do I not get credit for using it, all of those patient encounters are counted in my denominator against my office use of the EMR dragging me down so even with 100% compliance in the clinic I am unable to qualify for Meaningful Use. I not only forfit the incentive money but I will start to be penalized for not adopting an EMR. I will be punished despite, investing in and using an EMR for all of the outpatient visits in my clinic. The only outpatient visits that I don’t use the EMR for, are the dialysis visits, and even in that situation I use an EMR.

This feels incredibly stupid, mean spirited and counter productive. Please Davita, get Falcon approved for Meaningful Use ASAP so this mindless punnishment does not befall all neprhologists. Please CMS grant nephrologists hardship exemptions so that dialysis unit visits are excluded from the denominator calculation just like hospital and emergency room encounters are.

BTW: I have been told that Fresenius’s in-house EMR is likewise not approved for meaningful use. Lunacy.

Awhile ago I posted this tweet to twitter:

RT if you have ever given a patient money so they can buy their medications.
— Joel Topf (@kidney_boy) March 7, 2013

It received 24 retweets and a lot of twittversation around it. A number of doctors give money to patients when they are in need. Too many times the safety net is porous or too difficult for unsophisticated patients to navigate. This week-end I saw this tweet:

Great article in JAMA by physician reprimanded for giving $ for Rx to patient who couldn’t afford to pay http://t.co/7zIchqb1W7 #meded
— Margaret Chisolm (@whole_patients) September 28, 2013

The article is really good and is worth a read.

When I was just out of fellowship I saw a young patient in the emergency department with hypokalemia and severe hypertension. We sent an aldo and renin and treated her blood pressure with a number of medications but not spironolactone. I was sure he was going to have primary hyperaldosteronism and starting an aldosterone antagonist would complicate getting selective adrenal vein sampling to diagnose an adrenal adenoma. I set her up for a follow-up appointment and discharged him. He never made it to the follow-up visit. I didn’t see him again for years but when he re-presented he still was hypertensive but his kidney’s were thrashed. Half a decade of uncontrolled hypertension had taken their toll.

I asked him about why he didn’t follow-up. Turns out he lost his job a few weeks after being discharged and didn’t have any medical insurance. I regret not giving him the spironolactone prescription.
I know that for $0.13 a day I could have had better blood pressure control than with whatever concoction anyone else threw at him.

He eventually went become one of my dialysis patients. He was morbidly obese and was rejected by the transplant team for that reason. We were discussing what to do next. I was trying to convince him to take charge of his life and lose the weight. He kept making excuses about why he couldn’t. At one point he said that he didn’t have enough money for a treadmill. I pulled up Craig’s List and found a an $80 dollar treadmill for sale I told her her could probably buy it for $40 and gave him $20 to get him halfway there. I know my guilt from the earlier miss influenced my behavior but mainly I was trying to shake him out of dialytic nihilism.

Soon after that, either I switched shifts or he changed units and we lost contact.

The other day I was talking to our transplant nephrologist and he told me that the patient was touched by that gesture. The act of pulling out my wallet and throwing down some cheddar made him feel that he needed to recommit and give a full throated effort to lose weight.

He was successful. He lost the weight, received the kidney and is off dialysis.

Best $20 I ever spent.

I gave my fructose and uric acid lecture yesterday. Here are the slides from that lecture.

Is it just me or does the science seem to be moving slow in this field. Where are the interventional trials with febuxostat? Where are the larger trials on allopurinol with more than 50 people in each arm?

PDF (47 mb)
Keynote presentation (78.1 mb)

Nice update from twitter:

2. @kidney_boy. ..The CKD-FIX trial will have N = 620; https://t.co/snyFTHyxxm
— swapnil hiremath (@hswapnil) September 28, 2013

For the second year I attended Med 2.0. Just like last year I covered the conference for eAJKD. It is a fascinating look at the influences of social media, the internet and mobile technology on medicine and health. Please take a look at these posts:

• Why Medicine 2.0
• Susan Michie and the science of changing behavior
• Twitter: listening to a million conversations at once
• My very short time on stage at Med 2.0
• Technology for the elderly
• Closing Keynote, the present and future of sensors

Great blog post with video of Sherry Pagoto’s talk, Hashtag your way to Health.

The best way to revisit the conference is through the twitter stream. Symplur has all the tweets archived here.

The twitter analytics are mind blowing:

Compare that to Kidney Week ’12 which felt about 10 times the size of Med 2.0:

Gr8 quest! Lets ask @kidney_boy @deanoburns “When following UO in morbidly obese&using 0.5ml/kg/hr do U use actual,ideal or adjusted weight?
— Haney Mallemat (@CriticalCareNow) August 29, 2013

The short answer is just use the patients mass. No need for ideal or adjusted weight.

The long answer follows: To answer this I’m gonna to proceed from first principles. Why do we measure urine output? It is the most fundamental and basic measures of renal function. Before there were MDRD, creatinine or a Chem-7 we could measure the urine output. A biochemical urinalysis meant tasting it.

Oliguria means the urine output has fallen below the minimal healthy amount. (NEJM Review) So how much urine do people need to make to stay healthy? The flippant answer is enough, enough for what? Enough to stay in balance. Enough that every drop of water that is ingested is then excreted. Enough that every microgram of solute is excreted.

In regards to water, some will be lost with respiration, some in stool and some through the skin, but whatever is left over must be excreted by the kidneys. If water is not excreted and accumulates patients develop hyponatremia.

In regards to solute, proteins, electrolytes and minerals are constantly being absorbed by our indiscriminate digestive tracks. All of them most be accounted for and must either be incorporated into the body (growth) or cleared out, most of this work devolves on the kidney. If solute is not excreted it will accumulate and we will see increases in BUN from protein, edema from salt accumulation and other symptoms from the infinite variety of solutes we take in.

Obviously, accumulation of solutes is the factor whose symptoms better correlate with out definition of renal failure, so oliguria should be defined as the urine output, below which, people begin to accumulate solute. This volume is highly dependent on the diet. If the patient is eating a tiny amount of solute they will be able to have a very low urine output without beginning to accumulate solutes.

But the definition of oliguria is not built for these edge cases, it is designed to answer the question, what is the minimum amount of urine a person could make and still get rid of all the solute of a regular diet.

This math is pretty straight forward:

The definition of oliguria is 400 or 500 mL per day. The 583 on a normal diet is pretty close. If acutely ill patients decrease solute intake their minimal urine volume will creep down to the established 400-500 mL limits.

But this sets up the question, “Does urine output matter? Is it superior to biochemical assessments of renal function? Does the fact that I can order a serum creatinine every 12 hours make following hourly urine output unimportant?”

The answer is No. Urine output provides additional information on renal function that can not be seen with serum creatinine. Urine output increases the sensitivity of the RIFLE and AKIN definitions of AKI without compromising specificity. Increased sensitivity means that when combing through a cohort of patients, the addition of urine output will roughly double the number of patients flagged with AKI. Maintaining specificity means that clinical outcomes of these patients will be roughly identical to patients who meet AKI criteria due to changes in creatinine.

Sensitivity data: the use of oliguria roughly doubled the incidence of AKI from 24 to 52% of this cohort. While specificity was maintained:

In this multi-center, prospective study, however, they found differing conclusions. Though oliguria was associated with AKI from Cr, the relationship was to lose to be clinically useful. Oliguria was frequent, they found it in one third of ICU days. This resulted is a high false positive rate of AKI. They also found that half of patients who develop AKI by creatinine did not have oliguria for 4 or more hours the day prior and a quarter did not have oliguria at all. Only when they increased the duration of oliguria to at least 12 hours did the likelihood ratio rise above 10 (necessary for a clinically useful test) but this dramatically dropped the specificity of oliguria to the point that it would miss over half the cases of AKI.

So the addition of oliguria does add sensitivity without additional loss of specificity but in no way can oliguria displace creatinine as a reliable and early detector of AKI.

Looking through the data collected on using urine output to define AKI and predict outcome, they do not use ideal weight or adjusted weight, just straight mass. It would be interesting for someone to re-run the analysis on the previously collected data using ideal or adjusted weight and see if oliguria became a better biomarker of acute kidney injury.

What a crappy text book, it doesn’t even have “oilguria” in it. Who wrote this piece of…? oh. pic.twitter.com/U1JRBLji89
— Joel Topf (@kidney_boy) September 6, 2013