My favorite way to lecture is to pass out a personally written chapter on the subject and then collectively read the hand-out. I call this lecturing “Seder-style” named after the ritualistic dinner of the Jewish holiday Passover.
The booklets have four pages on each sheet of paper but you need a computer program to reorder the sheets so the booklets come out right. I used to have a print service that did this for me but it stopped working when I upgraded to Snow Leopard. I found this web service BookletCreator which does a great job with this.
Last week at the end of a morning conferance there was an impromptu discussion of the problem of residents ordering IV contrast for patients with acute kidney injury. The residents see a patient on dialysis and feel that its open season for contrast.
As part of the discussion one of the attendings mentioned this is also a problem with his PD patients with residual renal function and the residents need to know that contrast should be avoided in these patients to preserve residual renal function. I mentioned that actually the data doesn’t support the common sense notion that contrast accelerates the loss of residual renal function. Immediately all eyes were on me and the consensus was that no one else had seen that data and that I was way off the reservation. Pretty uncomfortable place to be.
I had buttoned holed Paul Palevsky at the 2006 ASN Renal Week after a talk on contrast nephropathy and in that hallway conversation he had mentioned that he had just finished research on this vary question. he only reason I remember it was that the results were so counter intuitive. Contrast has no measurable affect on residual renal function. I had actually never seen the article but now I had put up or shut up.
After the conference I had to run to an outside hospital but I stopped at a Tim Hortons (the best thing to come out of Canada since Douglas Coupland) and fired up PubMed on Tap (PMT).
PMT is an app dedicated to adapting the PubMed database to the constraints of a mobile platform. I used an app by the same name on my old Treo. Adding Palevsky as author, and then contrast and residual renal function as text words.
I especially love the two Nobel prizes in the top corner. Pauling is one of only four people to win two. In an alternate universe Linus got a couple of breaks to beat Watson and Crick to the structure of DNA. In that universe he has three Nobels and walks around like Michael Phelps.
As we come to the end of the naughts, we naturally reflect back and think about how far we have come from in the last ten years. Here is my quick list:
MYH9 gene for ESRD
The failure of the normalization of hemoglobin and the wholesale reevaluation of ESAs
The rise of aldosterone and its importance in hypertension and renal disease
the failure of dialysis dose to improve out come in both chronic (HEMO) and acute dialysis (ATN).
FGF-23, hey a whole new hormone and a major advancement in renal physiology
Re-emergence of home dialysis
Problems with the definition of CKD and the problems with eGFR
discovering the antigen in idiopathic membranous nephropathy
I want to do a longer article about this but I’m sure I’m missing some stuff. I don’t have a transplant subject, seems like vitamin D belongs up there, what about the phos binder wars? Bundling? What about MMF in lupus nephritis and every other GN?
I saw the highest glucose I can remember in a patient without ESRD. I have seen the glucose go over 2,700 in a patient with the misfurtune to have both DKA and anuric ESRD. Without the osmotic diuresis to lower the glucose the glucose can shoot the moon. This patient had HyperOsmolar Non-Ketotic Coma (or HONK as my fellow calls it, love that) and baseline Cr of 0.83 and a peak glucose of 1,600 mg/dL.
I love the twin graphs showing the falling glucose and the simultaneous resolution of the pseudohyponatremia. The patient had enough pre-existing osmotic diuresis to cause hypernatremia which was masked by the hyperglycemia. As the glucose comes down the sodium goes up from 136 to 162.
Calcium The other crazy number was the most severe hypercalcemia I have ever seen. The calcium was 18 mg/dL with an albumin of 3.7 g/dL. The patient is a kidney transplant recipient who was recently seen in the outpatient clinic with hypocalcemia. His calcium was 6.5 and his calcitriol was increased from 0.5 mcg to 1 mcg twice daily. He was also continued on his calcium carbonate.
Admission labs:
The other pertinent calcium labs:
PTH: 3.2 pg/mL
Vit D 1,25 dihydroxy: 36 pg/mL
SPEP/UPEP: unremarkable
PTHrp: pending
I think this is milk-alkali syndrome from the calcium carbonate exacerbated by the calcitriol. One supporting string of evidence supporting this is the fact that his calcium came down and has not reoccurred. If it was hypercalcemia of malignancy I would have expected his calcium to be resistant to conservative therapy.
Does removal of the light chains with plasmapharesis reduce the severity of cast nephropathy? We know that renal failure is a terrible prognostic factor in multiple myeloma so fixing acute renal failure is important.
Though not randomized this recent article from KI should be of interest (Thanks Kyste):
Leung et al. Improvement of cast nephropathy with plasma exchange depends on the diagnosis and on reduction of serum free light chains. Kidney Int (2008) vol. 73 (11) pp. 1282-8.
I was scheduled to give a talk on disorders of sodium and water to the fellows yesterday. We have a particularly clever cohort of fellows this year and I really couldn’t give them a warmed over version of my resident and student sodium lecture so I put together this talk which looks five different issues with hyponatremia and some data regarding them:
mannitol induced pseudohyponatremia
TURP syndrome
uremia and propensity for myelinolysis
exercise induced hyponatemia
differentiation of salt delpetion from SIADH with FENa, FEUrea and FE Uric acid with a couple of slides on treating SIADH with saline
Remember, downloading the native Keynote file will give you animations and a better looking experience.
Last Thanksgiving weekend, many bloggers participated in the first documented “blog rally” to promote Engage With Grace – a movement aimed at having all of us understand and communicate our end-of-life wishes.
It was a great success, with over 100 bloggers in the healthcare space and beyond participating and spreading the word. Plus, it was timed to coincide with a weekend when most of us are with the very people with whom we should be having these tough conversations – our closest friends and family.
The original mission – to get more and more people talking about their end of life wishes – hasn’t changed. But it’s been quite a year – so we thought this holiday, we’d try something different.
A bit of levity.
At the heart of Engage With Grace are five questions designed to get the conversation started. We’ve included them at the end of this post. They’re not easy questions, but they are important.
To help ease us into these tough questions, and in the spirit of the season, we thought we’d start with five parallel questions that ARE pretty easy to answer:
Silly? Maybe. But it underscores how having a template like this – just five questions in plain, simple language – can deflate some of the complexity, formality and even misnomers that have sometimes surrounded the end-of-life discussion.
So with that, we’ve included the five questions from Engage With Grace below. Think about them, document them, share them.
Over the past year there’s been a lot of discussion around end of life. And we’ve been fortunate to hear a lot of the more uplifting stories, as folks have used these five questions to initiate the conversation.
One man shared how surprised he was to learn that his wife’s preferences were not what he expected. Befitting this holiday, The One Slide now stands sentry on their fridge.
Wishing you and yours a holiday that’s fulfilling in all the right ways.
Turns out that seemingly sound advice will kill’ya.
Headlines from this week:
Any drinking lowered the risk of heart disease but the more patients drank the greater the protection. And the amount they drank was pretty staggering:
light drinking, about a glass of wine or 1.5-beers per day,reduced risk by 35%
moderate drinking, 2 glasses of wine or 2-3 beers reduced the risk 51%
Moderate and heavy drinking, 5+ glasses of wine or 7+ beers, resulted in 54 and 50% risk reduction.
The health benefits of alcohol were touched upon in ths prior post.
Not only did the patients randomized to folic acid + B12 have a higher rate of developing cancer, they had a higher cancer mortality. Most of the cancer mortality came from excess lung cancer in the folic acid + B12 group. This was despite the fact that there were more smokers in the placebo group (38% vs 40% p=0.01). (JAMA)
The fall of folic acid was touched on in this prior post.
So parents, remind your kids to drink their beer and forget their vitamins.
My favorite way to lecture is to pass out a personally written chapter on the subject and then collectively read the hand-out. I call this lecturing “Seder-style” named after the ritualistic dinner of the Jewish holiday Passover.
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