I get nervous when I need to dialyze someone who is severely hyponatremic. Dialysis has the power to change the sodium concentration very fast. Patients with chronic, compensated hyponatremia need their sodium corrected slowly. Experts recommend increasing the sodium by less than 12 mEq/L/day and to actually undertarget only 6 mEq/L/day to give you some margin for error.
Over the week-end we were consulted on a patient with a sodium of 106 and acute renal failure. By the time we were forced to dialyze the patient the sodium was up to 112. To do this safely we selected CVVHD and then diluted our dialysate down to 120 mEq/L.
The movie available for download is very high quality. Below is a YouTube conversion of that video to save you the 118 mb download.
This is some serious Sodium Jujitsu and I awarded my team the first Nephrology Merit Badge: Sodium Ninja (pages | pdf). Designed for Avery 5163 2×4 labels.
Nephrology Merit Badge, updated for the 21st century as a sticker for your iPad
The first time PBFluids was referenced in the medical literature was in Matt Sparks’ article on nephrology internet resources.
Today I received an e-mail from Tom Oates. Apparently, when he is not researching the unique genetic predisposition of the WKY rat to crescentic glomerulonephritis he is an avid reader of both Hemodialysis International and PBFluids. He sent me this article in Hemodialysis International regarding the highest creatinine ever. The key sentence in the article:
Extremely high levels of serum creatinine have been reported in the literature.3 The highest level of serum creatinine reported was 37 mg/dL.3
So what is the highest previous creatinine reported in the literature? Well according to the author, Said Abuhasna, it’s 37 from this post at PBFluids. Nice to see blogs being included in the canon of medical literature. Though it would be even nicer if they spelled my name right.
“Can anyone tell me what MobileMe is supposed to do?” Having received a satisfactory answer, he continues, “So why the f*** doesn’t it do that?”
He then picked another executive to run the project on-the-spot. Ultimately, this resulted in the service being shuttered and replaced with iCloud.
I never had any problems with MobileMe; it always worked fine for me. However, I foolishly relied on it to host files for PBFluids. This includes all of the presentations and handouts that are the highest trafficked pages of the site. Well, MobileMe stopped accepting new subscriptions a year ago and as of June 30th the hosted files are no longer accessible. I have downloaded all of the material and will start re-uploading the files to DropBox. The problem is rewiring all of the past links to the new file locations. This will take some time.
As I looked through the collection of files that used to be hosted at MobileMe I found a lot of journal articles and other copyrighted works. I have no idea how popular these links were but I remember when I uploaded them, PBFluids was a lonely backwater, where I was the sole source of traffic. I put the files the files online for my own use in teaching and on rounds. I don’t plan on replacing these files.
Update:
7/3/12 Lecture tab is ported to DropBox
7/3/12 Handout tab is ported to DropBox through Adventures in Renal Imaging
For the past few years I have had the honor of giving the July 1st morning lecture for the internal medicine residents at St John Hospital and Medical Center. Unfortunately, July 1st was a Sunday and Monday mornings are dedicated to a formal sign out rounds in our division. So July 3rd was my first lecture.
I gave my Fluids, Diuretics and Sodium for the Terrified Intern lecture. You can down load it here:
It was dramatic and there was a lot of buzz among the kidney folk on Twitter about this. You can read some of the coverage here. It was exciting but it tasted too much like a publicity stunt for my taste. The counter argument, of course, is that raising the profile of living unrelated donors increases the likelihood that people will come forth and donate and I should just swallow my distaste and be supportive of the outreach effort.
We need more living donors.
We need more deceased donors.
We need more kidney donors.
As part of the Twitter publicity campaign, IU_health tweeted various facts about transplant. This one seemed wrong to me:
One every twenty minutes
Three an hour
Seventy-two a day
26,280 deaths a year
That’s a lot
That’s too many
When I first read the tweet I read it as “1 American dies every 20 minutes waiting for a kidney transplant.” Twenty-six thousand deaths out of the ninety-thousand people on the wait list seemed like a very high mortality rate, higher than the dialysis morality rate. A quick check in the USRDS Atlas revealed the mortality rate to be only 7% on the wait list.
When I went back and read the tweet again I saw that they were talking about people waiting for all transplants. This seemed more than a bit disingenuous because when we encourage people to become living donors we are only talking about kidney transplants (in 2008 there were only 250 living partial liver transplants). I assume that IU is not encouraging living donors for hearts and lungs.
In 2008 there was only 4,638 deaths among people waiting for a kidney transplant. For all organs it was only 7,182 deaths. These numbers are from Health Resources and Services Administration. Similar data can be found in USRDS Atlas Volume 2 Chapter 7 (PDF).
We need more kidney donors and social media is a great tool to unlock the thousands of spare kidneys Americans carry around with them but the great need does not justify spreading lies and misinformation.
Literally minutes after I posted this I received the following tweet:
Kudos for IU Health in coming clean. Also Hat tip to Sunny Gill, one of our first year fellows for finding the HRSA website.
Endobible arranges a database of endocrine diseases in widely searchable manner. They lead physicians through the diagnosis, work-up and treatment of most endocrine diseases. They skip diabetes, but outside of that is looks awesome. Nice reminder that endocrine is more than diabetes.
I perused the Conn’s Syndrome section (primary hyperaldosteronism). The history and physical were great. The work-up was less impressive. They don’t advise saline loading and they still recommend stopping ACEi and beta-blockers before performing a Aldo Renin Ratio. Good luck keeping a resistant hypertension patient from stroking while you wash all those drugs out for 4 weeks.
I love it when I have a clinical question and I’m able to find a well executed study that’s exactly fits my question. It’s like fitting the last piece of a puzzle.
A year ago I was referred a patient with heavy proteinuria. Initial assessment showed 7 grams of proteinuria, a cholesterol over 300, edema and an albumin of 0.7. Classic nephrotic syndrome.
Before he returned for his first follow-up appointment disaster struck. He developed chest pain and shortness of breath from a pulmonary embolism. This was a patient my age, two kids, professional. Looking at him was like looking in the mirror, but for the grace of G-d that could be me sitting in that exam chair.
black arrow points to tubuloreticular inclusions seen in SLE and HIV.
After a month of anti-coagulation I was able to convince pulmonology and hematology to reverse the Coumadin for a few hours to get a kidney biopsy. It was membranous nephropathy with endothelial tubuloreticular inclusions. Along with consistent ANA and DS DNA we made a diagnosis of SLE WHO V and began mycophenolate mofetil. We titrated the MMF up to 3g a day and after 6 months he was in remission.
After a few months of sub nephrotic proteinuria, a normal albumin and a year of anti-coagulation he stopped his Coumadin. He has weaned his prednisone to 10 mg every other day and stopped the alendronate and rosuvastatin. Now he wants to get off the mycophenolate. Given how frightening the PE was, my preference would be to treat him forever. I casually surveyed my peers and got answers as varied as:
I never lower the MMF, every time I do the patient relapses
I taper it off after 6 months of remission
When I consulted the literature to look into this I found this paper:
Bingo. They maintained patients on MMF for 3 years at 2 grams a day with excellent results.
Importantly there were no deaths, only 10% had serious infections and no cases of cancer occurred with the mycophenolate.
Looks like an acceptably benign therapy with good outcomes.
Aside: While looking up how to spell endothelial tubuloreticular inclusions, I came across this paper (how I love you so Google) showing a significant number of patients with endothelial tubuloreticular inclusions that did not have lupus or HIV. I was taught that these EM findings were essentially pathognomonic for lupus. Interesting.
UPDATE: a second trial, the MAINTAIN trial (PDF), showed almost identical results. Included for completeness.
This post on BuzzFeed makes me so glad I never suffered the indignity of on-line dating. My favorite is this guy:
What are the odds he has Bartter’s or Gitelman’s. Every patient I have encountered with Bartter’s or Gitelman’s has admitted to drinking pickle juice, so it’s sensitive but I don’t know how common this is among norms so its specificity has yet to be determined.
I interviewed Allen Nissenson for eAJKD. He wrote a great review of his knowledge and experience with accountable care organizations and how they will affect nephrology. The best part of his article was when he discussed his experience working on a pilot project for CMS demonstrating benefits to dialysis patients using an integrated care model. This project showed a survival benefit not by changing the dose of dialysis, or giving additional drugs. The improved outcomes came simply from better communication and organized, systematic care. Eye-opening stuff.
The question that the investigators were examining was, “Is uric acid a cause of hypertension?” The data supporting this is largely epidemiologic, with a smattering of interventional trials. The largest criticism of the epidemiological trials has been the issue of causality and directionality, i.e. does the hypertension cause the high uric acid or does high uric acid cause the hypertension?
this is how I show the directionality debate in my presentation
Previous interventions involved using allopurinol to decrease uric acid. However there are questions of whether allopurinol may have some magical anti-hypertensive effect outside of its ability to lower uric acid. The investigators discovered a cohort of Amish with a variant of GLUT9, a urate transporter. This variant, an ILE for VAL at amino acid 259, lowers the uric acid level by about 0.5 mg/dL in women and 0.25 in men. The lowered uric acid is likely due to enhanced renal clearance.
The authors used Mendelian Randomization to see what the effect of a lower uric acid has on developing hypertension.
Mendelian randomization (MR) is a concept I had not come across before. Here is a video of Wayne State University researcher, Dr Anthony Ference, who used MR to study LDL. He does a nice job of describing the concept.
The authors of the uric acid acid trial describe mendelian randomization thusly:
The mendelian randomization principle relies on the tenet that alleles, and hence genotypes, are randomly assigned during gamete formation. The main advantage of this method is that gamete formation occurs before birth and is therefore unaffected by traditional confounders that occur after conception, such as diet, socioeconomic status, access to healthcare, and all other environmental factors. Because relationships between genotypes and outcomes have only limited susceptibility to confounding and are not subject to reverse causality, genetic variation may be used to establish directionality and infer causality between a certain gene product and a specific outcome. Therefore, Mendelian randomization is akin to a randomized trial design, inheritance of the GLUT9 ILE allele would be analogous to randomly being assigned probenecid, a uricosuric agent, from birth, whereas inheritance of the wild-type genotype would be analogous to receiving placebo.
The cohort was a group of 868 participants of the HAPI (Hereditary and Phenotype Intervention) study. Ninety-eight of these people had GLUT9 variants. Patients’ blood pressures recorded in clinic on a liberal (standard) diet and then checked with 24-hour ambulatory monitoring following a week on a high-sodium diet (280 meq/day) and again after a week on a low-sodium diet (40 meq/day). The diets had fixed carbohydrates and potassium.
The blood pressure spread is impressive and statistically significant in both the high- and low-sodium diets. The authors summary was for every 1 mg/dl decrease in uric acid the systolic blood pressure fell by 3-5 mmHg.
I thought this study was an original approach to the question of fructose and uric acid. They found an experimental method that allowed them to look at different levels of uric acid without confounding the results with the pleiotropic effects of allopurinol.
