Year: 2013

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iPhone urine micrographs

Calcium oxalate crystals
dirty granular casts indicative of ATN in a field of hematuria.
(The top left corner of the longer cast looks a little red cell cast-like)

Broad waxy cast, indicative of chronic kidney disease in a field of RBCs

New Nephrology merit badge for successfully using your iPhone to make a urine micrograph.

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How do you determine the severity of SIADH? Updated with Video

There are a number of ways to grade the severity of SIADH. The most obvious is to look at how low the sodium is. The problem with this is that it largely depends on how much water a patient is drinking and is not solely dependent on the severity of the SIADH. A patient with mild SIADH that is started on hypotonic fluids will have a much lower sodium than a patient with severe hyponatremia who is adherent with her water restriction and urea tablets.

I assess the severity of SIADH by looking at the electrolyte content of the urine. Here is a doozy:

  • Urine sodium: 134
  • Urine Potassium: 62
  • Urine osmolality: 777
But this strategy suffers from a similar limitation, the urine electrolyte are affected by factors beyond the severity of the SIADH. Patients with SIADH are in sodium balance, that means that all the sodium they ingest is excreted. Increased sodium intake will be reflected by increased urine sodium, the same goes for dietary potassium and urinary potassium. The above labs came after the patient was given isotonic saline for 24-hours. The serum sodium fell from 128 to 117 with saline.
The true measure of SIADH severity probably is simply the urine osmolality.

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Creatine is not just Creatinine misspelled

A few years ago I had a pre-med student shadow me on the dialysis service for a week or two. I had a hard time teaching him because he was so early in his medical education. I had him investigate an issue that he had some personal contact with and I think he did a nice job. The question was, “Is creatine nephrotoxic (bad for the kidneys).”

From this commercial sight, their
information is pretty tight

Creatine is synthesized by the body from the amino acids arginine, glycine, and methionine. It is phosphorylated by ATP to form phosphocreatine which is stored in muscle cells and acts as an instant energy source. When exercise depletes ATP, phosphocreatine rapidly restores ATP from ADP. Skeletal muscles typically have 3 times as much phosphocreatine as ATP. After being used up creatine is excreted as creatinine (and you thought creatinine’s purpose was to measure renal function).

The student, DJ_Scary, put together the following presentation on the biology and nephrotoxicity of creatine.

Medicine tends to be pretty puritanical. If it feels good, don’t do it. If it it feels bad, do it more. Eat your vegetables. Exercise every day. Don’t drink. Don’t smoke, Eat less red meat. Don’t put so much salt on your food. When it comes to performance enhancing drugs, the knee jerk and conservative response is the same. Avoid protein supplements. Don’t use anabolic steroids. Creatine will damage your kidneys. Some of this advice is wise, Joshua Schwimmer showed that anabolic steroids can cause FSGS (anybody ever test Zo or Sean Elliott for steroids?).

Creatine can double, triple or quadruple a patients serum creatinine. The math on how that works is shown in the video.
Note for the equations to be valid the following assumptions and units need to be used:

  • CrCl: ml/min
  • Creatinine: mg per 24 hours
  • Serum creatinine: mg/dL

The point of the video is that creatine will increase your creatinine and not affect your creatinine clearance or GFR which are the important variables. This is a situation where one cannot trust the estimated GFR formulas.

The medical puritan tells patients not to use creatinine because it can damage the kidney. This is not true. There is no data, beyond some pretty sketchy case reports that creatine can damage the kidney. Long term follow up with medical use of creatine shows no harm (randomized, placebo controlled data!). It seem convincingly safe (Oh, you wanted a Cochrane Meta analysis, we got that here). It will always be safer and more conservative for physicians to tell patients not to take a substance. (One year follow-up too short for you, how does 5 years of follow-up taste?) Patients deserve honest, unbiased answers about what different substances and behaviors do to their bodies and if physicians provide them with the same, old, predictable, puritan, advise, they will bypass doctors and we will lose our role in health advice.

To see a range of nephrologist views on creatine, take a look at the replies to this tweet.

Creatine: Bad for the kidneys or just bad for the kidney test (creatinine)?
— Joel Topf (@kidney_boy) March 5, 2013

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Awesome kidney video

From the website Laboratory equipment.

Nils Lindstrom, from the Univ. of Edinburgh, earned third place honors at the Small World in Motion Photomicrography Competition with his video, “Growing complexity in the kidney.”  Lindstrom’s research is focused on understanding how the kidney and nephrons are patterned during embryonic development. His image, captured as part of his ongoing research on that topic, shows a metanephric kidney, cultured in vitro and imaged over four days.
Lindstrom submitted the time-lapse video because it’s such a striking example of how a kidney starts from a simple structure and gradually becomes a highly complex collecting duct system in a matter of days. He says that how tissues are structured and patterned is a fundamental aspect of kidney development.

Tat tip Joshua Schwimmer

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Bracketology: Vicki Ivancevic

I first Twitter met vicki a couple of months ago. The Armstrong thing was blowing up. I made a joke

“@kidney_boy: When I need to order Epo, I just tell the nurse to give them a full Armstrong.” I only wish epo worked that well for me
— Vicki Ivancevic (@VIvancevic) January 17, 2013

The story of my frantic run with Lance.

I was a real admirer of Armstrong and I lost countless hours listening to Bob Roll and Phill Liggett as US Postal and then Radioshack preyed on the Peloton in the Alps and Pyrenees  When the myth of Armstrong finally collapsed it stung.

A month later I posted a picture of my dietician’s phosphorous jail. Our unit was having trouble with phosphorous, so our new dietician was throwing some creativity around. If your phos was at goal you got out of Jail, otherwise, you were doing time. In real jail you bust rocks, in our jail your arteries turn to stone.


While not loved by all:

@kidney_boy Phos jail? Seriously? As a pt, I despise being treated like a five year old. But I guess it’s what motivates some, just not me.
— Vicki Ivancevic (@VIvancevic) February 27, 2013

I thought it was valuable to get a patient perspective. It can be hard to motivate patients. Techniques that work for some are pejorative or childlike to others.

The technique seems to be working, our unit numbers are improving.

On a whim I sent Vicki a #NephMadness invitation. No one needed personal invitations to play, but I can see a patient being intimidated by a doctor gag like NephMadness. I was delighted to see her enthusiasm:

@kidney_boy honored you would ask. I tried but will need to really study. I’m just a lowly patient. But I will give it a go!
— Vicki Ivancevic (@VIvancevic) March 20, 2013

With no further ado:

Hello Dr. Topf!

Here are my NephMadness brackets. It was very interesting to read the descriptions of the “teams” on the blog and make the correlations to my experiences with dialysis and my nephrologist (Dr. Hsien-Ta Fang from Edward Medical Group in Naperville, IL). I am going to bring a copy of my bracket to him on my next appointment and see what he thinks 🙂  

I filled out the bracket completely from my experience and what has helped me the most as I have navigated this disease and its treatment options. This is why, for example, I chose EPO as the winner of the Loop of Henle bracket as it is EPO that keeps my hemoglobin in some sort of decent range. And since I have already gotten two calls for a transplant plus had many living donors tests (and unfortunately fail), this is why I chose Transplant as my overall NephMadness champion.

Thank you again for suggesting that I fill this out!

Vicki Ivancevic

And one final bit of VikWhit

@kidney_boy @eajkd my bracket is bleeding more than an infiltrated fistula#nephmadness
— Vicki Ivancevic (@VIvancevic) March 22, 2013

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Updates and reader feedback

was updated with a letter from a reader describing how important Myron Miller was to their decision to be a nephrologist and some insight in to teaching Na and water.

Dialysis for cast nephropathy

In that post I mention my frustration with a Springer Paywall, in the days after I pushed that out, four different readers sent me the pdf. Awesome. There are advantages to living in the ivory tower.

Another letter, this one about the Fluids book

I’ve written in on your blog before thanking you for your book. It was the singular great read of my undergraduate medical education nearly 15 years ago. I recommend it to my trainees regularly, and like you, alternate between despair and hope that they’ll “get it.” I’m writing to encourage you to release an updated version soon. The motivation for me is that Clinical Physiology of Acid-Base and Electrolyte Disorders will be updated this spring after a 13 year hiatus. Your Companion is about as old as the 5th edition of Clinical Physiology and offers a more tractable entry point for medical students and resident physicians.

I am an endocrinologist with a basic science laboratory. I would be happy to provide some input (no desire for credit solicited by this offer) on topics to include. Off the top of my head, discussion of TTKG, expansion of adrenal steroids and evaluation of hypermineralocorticoid states ranging from congenital adrenal hyperplasia syndromes to adult exotica (e.g., deoxycorticosterone tumors, ectopic ACTH syndromes, and expansion of licorice poisoning and related molecular disorders).

Thanks,

Amnon Schlegel, MD, PhD
University of Utah

I told him that I am reworking the fluids book for a second edition and he had these insights on the state of medical education:

I claim no expertise in marketing; however, my interaction with our second year medical students (I give a 3 hour marathon on everything lipid, and one hour on mineralocorticoids) and residents (one hour of triglycerides alternating yearly with one hour on mineralocorticoids) suggests that they don’t read anything outside testable material. The motivated residents buy MKSAP early and wade through it. The students buy assorted review books, but read only if the lectures are presented poorly. I see Rose’s 5th edition languishing on our book store’s shelf (along with many others).

My lectures get very high reviews because I’ve given up: I stuff the .pptx files with long comments beneath each slide that restate what I lectured using stiffer sentence structure.

Our nursing and pharmacy students buy and read books. Your strategy might meet that need and have a spill-over to medical students.

I think your target to below 500 pages is feasible: the first 100 about water can be condensed, as I’m sure you’re thinking. Similarly, the Winter’s formulae can be presented more briefly. Consider how terse A.B. Anup’s Arterial Blood Gas Made Easy is in this regard: it’s under 100 (small 5¼” x 8½” ) pages and is mostly quiz ABGs to practice with.

What prompted my writing you is the obtuse manner in which our house staff evaluate electrolytes. I do 2 weeks of ward attending per year, and no one knows anything about sodium. Your book will not cover loop diuretic pharmacology, but in my fortnight of explaining seemingly trivial things about oral bioavailability of furosemide, torsemide, and bumetanide, I saved the government tens of thousands of dollars by discharging fluid over-loaded patients quickly by switching to torsemide and bumetanide whenever possible. Similarly, in my capacity as the endocrinology consultant (again, not full-time like you: merely 6 weeks per annum), I try to get the residents to realize that clear understanding of physiology will help in evaluation of electrolyte disorders: in the past I was asked to see a severely hypertensive and hypokalemic man 5 days after the renal service had. They’d ordered appropriate 24 hour urine collections for aldosterone and cortisol, but these are slow-turn around test. When I saw him, the terrible hyperglycemia, thin skin, and big bruises at phlebotomy sites had me steer them to ACTH-dependent Cushing syndrome as the unifying diagnosis with more rapid blood tests (the urine aldosterone was 0 mcg/24 hours, eventually).

Your book would certainly help them think more broadly and order tests more gracefully. Similarly, vaptans are here and your deep familiarity will strengthen the water metabolism aspects.

Wow, great thoughts.

In a final addendum he wrote:

That patient ended up having small cell lung cancer (the first “Liddle syndrome” since Grant Liddle described non-pitiutary ACTH syndrome in 1962 and coined the term “ectopic ACTH syndrome” in 1963, while  his eponymous syndrome was reported in1963).

  • Meador CK, Liddle GW, Island DP, Nicholson WE, Lucas CP, Nuckton, JG, Luetscher JA. Cause of Cushing’s syndrome in patients with tumors arising from “nonendocrine” tissue. J Clin Endocrinol Metab. 1962 Jul;22:693-703.
  • Liddle GW, Island DP, Ney RL, Nicholson WE, Shimizu N. Nonpituitary neoplasms and Cushing’s syndrome. Ectopic “adrenocorticotropin” produced by nonpituitary neoplasms as a cause of Cushing’s syndrome. Arch Intern Med. 1963 Apr;111:471-5.
  • Liddle GW, Bledsoe T, Coppage W. A familial renal disorder simulating primary aldosteronism but with negligible aldosterone secretion. Trans Assoc Am Phys 1963; 76:199-213.
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Duty hour limitations

Latest headline regarding duty hour limitations:

There was no improvement in residents’ reported sleep and general well-being in 2011, however, and the proportion of medical trainees who said they’d made a serious error in the past few months rose from 20 to 23 percent. (Desai, JAMA 2013;173(8):649-655)

Well I’m glad we trashed decades long tradition and culture of medicine for that. One of the most important lesson I learned in medical school was from Ron Trunsky, a psychiatrist and medical sage,

“Medicine is not like selling shoes.” 

He would say that when ever there was patient care to be done but someone wanted to go home. Medicine is important. Medicine is hard. Medicine requires a commitment not found in regular jobs. Patients’ needs do not fall between the hours of 9 and 5 but around the clock. Part of residency is training you to accept that. Part of residency is turning normal people into physicians.

Working insane hours during residency was the forge that allowed me to be cast me into a physician. Like boot camp in the military, long residency hours broke you down and reformed you into a specific type, the physician.

There is a lot to criticize about this system, but it was an important part of the physician ecosystem and it irresponsible to trash one component of that system without doing prospective studies on what will happen. Now, 9 years later what are supposed to do with this data. Apparently working 30 hours in a row was a key part of reducing medical error and made no difference in the hours slept or resident depression.

This agrees with my experience. Reduced duty hour requirements is forcing residents to spend more and more of their time watching the clock, filling out attendance records, missing lectures and skipping rounds. Trading improved fatigue for less investment in patients was a terrible bargain.

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NephMadness

I spend some of my blogging time at AJKD’s blog, eAJKD. We have just launched what I think is the most ambitious project the nephrology blogosphere has seen. It is an NCAA-style tournament of the biggest ideas in nephrology.

Get PDF and PPT versions of the brackets at eAJKD.com

On the surface, it is simply a set of brackets that pit 64 different ideas, projects, discoveries and drugs against each other. But what makes this important are the descriptions of all 64 entities. The National Cooperative Dialysis Study was published in 1981, the year my fellows were born. They have no knowledge of these landmark moments in dialysis. The 8 posts which describe all 64 concepts can be found here:

Some of the descriptions of the match-ups are awesome. Top notch blogging. Definitely worth perusing through.
I had my partners and fellows fill out brackets today. They all had a lot of fun doing it. There is something light and joyful pitting these heavy topics against each other in totally absurd ways. Take a crack at it, have fun. Post your brackets to twitter with the hashtag #NephMadness or email them to nephmadness@cluemail.com.
Here are some of the highlights from today. 
Dr. Steigerwalt

Dr. Steigerwalt is a hypertensive specialist and a big proponent of ACEi/CCB combination so I was sure she was going to select ACCOMPLISH over ALLHAT. Interesting that she went the other way and brought ALLHAT all the way to the Final Four. When she first glanced at the brackets she told me how couldn’t ESRD Medicare Benefit win it all? Well, she answered her own question because in the face of the RCT, even the Medicare ESRD benefit falls. Rounding out her final four is kidney transplant and UpToDate.
Keith Bellovich, Fellowship Director
Dr. Bellovich and I are are on very similar wave lengths and I agree with finals matchup and a lot of his early round choices. His Final four are: ESRD Benefit, Transplant, FGF-23, and NephSAP. His Cinderella team, the NCDS, going all the way to the Elite 8! He also has the TTKG making an improbable run to the sweet 16.
Three fellows filled out brackets. I will protect the innocent and just summarize their choices:
Fellow 1
  • Final Four
    • Randomized Controlled Trial
    • FGF-23
    • UpToDate
    • Kidney Transplant
  • Cinderella: Burton Rose Clinical Physiology of Acid Base… going to the sweet 16 from a 13 seed
Fellow 2
  • Final Four
    • Randomized Controlled Trial
    • ACCOMPLISH
    • Transplant
    • UpToDate
  • Cinderella: ACCOMPLISH, a 12 seed advancing to the final 4. Honorable mention the U/A and Rose’s book both to the Sweet 16.
Fellow 3
  • Final Four
    • Randomized Controlled Trial
    • FGF-23
    • UpToDate
    • Kidney Transplant
  • Cinderella: Burton Rose’s Clinical Physiology of Acid Base, and Rituximab… going to the sweet 16. And the DOPPS study (which has not been getting any love in the brackets I have looked at) going to the Elite 8!
Since I have a role running the tournament I will keep my brackets secret until a winner is declared.

Update:

Graham Abra, of the Renal Fellow Network was doing what all bracketologists do, trash talking other people’s brackets. This is what he had to say:

@kidney_boy FGF-23 in 2 of 3 fellow final 4s!? Sooooo you like surrogates? Surrogates in BMD? Where no rx impacts ANY hard outcome?;)
— RenalFellowNetwork (@RenalFellowNtwk) March 19, 2013

Here is my fellow’s reply:

I liken FGF-23 to the Gonzaga of college basketball.  It shows up whenever you talk about MBD-CKD (as the bball team makes it to the bracket almost every year)  you know it has a huge impact but not sure how much to apply it to clinically taking care of patients, but you are just waiting for the time that it all fits (aka Gonzaga wins the championship)

My reply:

@renalfellowntwk Also the idea that there is a new hormone central to phosp regulation that went undiscovered for so long is kind of sexy
— Joel Topf (@kidney_boy) March 19, 2013