Thursday, October 9, 2014

Ever heard of Chinese Restaurant Syndrome?

From a letter in the 1968 NEJM:


Friday, October 3, 2014

Questioning Medicine, sweet podcast.

This morning I received this tweet:
Somehow it reminded me of an email I once received from Nigeria:
REQUEST FOR URGENT BUSINESS RELATIONSHIP 
FIRST, I MUST SOLICIT YOUR STRICTEST CONFIDENCE IN THIS TRANSACTION. THIS IS BY VIRTUE OF ITS NATURE AS BEING UTTERLY CONFIDENTIAL AND 'TOP SECRET'. I AM SURE AND HAVE CONFIDENCE OF YOUR ABILITY AND RELIABILITY TO PROSECUTE A TRANSACTION OF THIS GREAT MAGNITUDE INVOLVING A PENDING TRANSACTION REQUIRING MAXIIMUM CONFIDENCE. 
WE ARE TOP OFFICIAL OF THE FEDERAL GOVERNMENT CONTRACT REVIEW PANEL WHO ARE INTERESTED IN IMPORATION OF GOODS INTO OUR COUNTRY WITH FUNDS WHICH ARE PRESENTLY TRAPPED IN NIGERIA. IN ORDER TO COMMENCE THIS BUSINESS WE SOLICIT YOUR ASSISTANCE TO ENABLE US TRANSFER INTO YOUR ACCOUNT THE SAID TRAPPED FUNDS. 
THE SOURCE OF THIS FUND IS AS FOLLOWS; DURING THE LAST MILITARY REGIME HERE IN NIGERIA, THE GOVERNMENT OFFICIALS SET UP COMPANIES AND AWARDED THEMSELVES CONTRACTS WHICH WERE GROSSLY OVER-INVOICED IN VARIOUS MINISTRIES. THE PRESENT CIVILIAN GOVERNMENT SET UP A CONTRACT REVIEW PANEL AND WE HAVE IDENTIFIED A LOT OF INFLATED CONTRACT FUNDS WHICH ARE PRESENTLY FLOATING IN THE CENTRAL BANK OF NIGERIA READY FOR PAYMENT. 
So I hid my checkbook before I went and checked out the podcast. No worries, they never asked me to send any money to complete the download or authorize my listening. It was just a great medical podcast. The two hosts have excellent chemistry and the discussion was astute and evidence based. I highly recommend it.


You can find Questioning Medicine in iTunes.

Wednesday, October 1, 2014

Kidney Transplant Report Cards are Out

The Information from the Scientific Registry of Transplant Recipients (SRTR) publish transplant statistics for every transplant center. 7/2/12 – 6/30/13

Here are the results from Michigan. St John's is doing a great job!


Monday, September 22, 2014

Pentoxifylline in renal disease, a tour through the literature

Tomorrow is another exciting edition of #NephJC. We will be discussing pentoxifylline in diabetic nephropathy. There is a summary of the article at NephJC.com.

In support of that article and to aid the discussion, Christos Argyropoulos has stepped up to the blogger plate to provide some color on pentoxifylline.

Joel

+++++++

In wild anticipation of next week’s #NephJC on Pentoxifylline (PTX)  let’s go over some of the known facts about the drug:
  • It is a non-selective phosphodiesterase inhibitor.  PDEs are enzymes that inactivate cyclic nucleotides and have been organized in 11 families (Table 1 [1]) based on sequence, structural and pharmacological considerations. Inhibition of PDE4 by PTX (Figure 1) [1] increases cAMP & stimulates PKA activity. 
  • Activation of PKA leads to phosphorylation of the cAMP response element binding protein (CREB) which in turn leads to suppression of the TNF-a[2,3] synthesis at the transcriptional level
  • Inhibition of cAMP production by these phosphodiesterases has a broad range of immunomodulatory effects (Table 2[1])
  • The drug also affects red cell deformability and favorably affects microcirculatory blood flow
  • “Mainstream” indications: intermittent claudication, vascular dementia, sickling crises, acute alcoholic hepatitis
  • Figure 1: Pentoxifylline (white) complexed with PDE4 (ribbons). Also shown are the Mg2+ and Zn2+ cofactors of PDE4 (spheres)
  • Pharmacokinetics: bioavailability (10-30%), elimination (mostly renal as 50-80% of the drug is recovered in the urine), half life (24-48 mins)

Sunday, September 21, 2014

Is this the best review on treating hypertension in pregnancy? Updated

Note: this is a living post that is growing as I brush up on preeclampsia

From Hypertension:

Update on the Use of Antihypertensive Drugs in Pregnancy

Free PDF FTW!

Another great article:

New aspects of pre-eclampsia: lessons for the nephrologist

Also with a free PDF. Thanks NDT.

+++++++++
Although these renal changes in general are believed to resolve completely after delivery, recent evidence suggests that pre-eclampsia may leave a permanent renal damage.
CKD is a risk factor for pre-eclampsia in advanced CKD 3-5, weak evidence
the risk for pre-eclampsia and other pregnancy complications is sub-stantially increased in women with chronic kidney disease (CKD) stages 3–5 
 CKD 1-3 is not a risk factor unless the woman also has hypertension, higher quality evidence.
but these women were not at increased risk for pre-eclampsia. However, there was a significant biological interaction between eGFR and hypertension making eGFR 60–89 ml/min per 1.73 m2 a risk factor for pre-eclampsia if the women were also hypertensive.
Pre-eclampsia increases the risk for subsequent kidney biopsy and subsequent ESRD:
In the first study, women with pre-eclampsia in their first pregnancy had a considerably increased risk of developing kidney disease that needed investigation with a kidney biopsy [Adverse Perinatal Outcome and Later Kidney Biopsy in the Mother in JASN]. 
women who previously had pre-eclampsia had a four to five times increased risk of later end-stage renal disease, independent of primary renal disease [Preeclampsia and the Risk of End-Stage Renal Disease in NEJM]. Women with recurrent pre-eclamptic preg- nancies and women who gave birth to offspring with low birth weight had an even higher risk. The increased risk remained significant throughout the follow-up period of nearly 40 years. 


 In regards to the natural history of pre-eclampsia:
It should also be kept in mind that although the extensive glomerular changes during pre-eclampsia are believed to completely resolve after pregnancy [The Glomerular Injury of Preeclampsia in JASN], no studies have routinely performed a kidney biopsy months after the pre-eclamptic pregnancy. The fact that as many as 20–40% have microalbuminuria after a pre-eclamptic pregnancy may argue for a permanent glomerular damage in a great proportion of these women [Microalbuminuria after pregnancy complicated by pre-eclampsia in NDT, Blood pressure and renal function seven years after pregnancy complicated by hypertension].
Warning about these conclusions regarding pre-eclampsia causing CKD:
When interpreting the studies of pre-eclampsia and later kidney disease, it should be remembered that pre-eclampsia might unmask asymptomatic or undiagnosed CKD, a disease that might have been present also before pregnancy. A pre-pregnancy eGFR >60 ml/min per 1.73 m2 measured at screening was in a population-based sample associated with future pre-eclampsia risk in hypertensive women [Kidney function and future risk for adverse pregnancy outcomes in NDT]



This article by Eiland, Nzerue, and Faulkner in PubMed Central does a nice job reviewing the pathogenesis of the preeclampsia.


Friday, September 19, 2014

ACEi talk.

A pharmacist from Blue Cross, Kim Moon, sent me an e-mail and told me she was a fan of the PBFluids and my and twitter. That, of course, instantly made her my newest bestie. She then asked me to do a webinar addressing common issues that prevent primary care doctors from prescribing ACEi/ARB to patients with diabetes. I agreed, anything for a fan of the blog.

A couple of months ago and long before the lecture was written she needed a title, so I threw out, "ACE inhibitors, the good, the bad, and the ugly"


Then I saw this tweet:
How embarrassing. Well, here's the show:

Link to video (740MB)
PDF (52.4MB) 
Keynote (132MB)


Streaming the video from google drive seems to be broken. Here is a forum describing the problem, and Google's lack of response to the issue. My work around has been to pony up the $60 and join Vimeo plus.


Thursday, September 18, 2014

Imagine if the wards were really like the boards

1. You have a new patient with a drug you've never heard of before. Your next step is to:

  1. Look it up on your phone.
  2. Ask a colleague what the drug is.
  3. Take a careful look at the patients medical history and try to figure out the purpose of the drug from the context. Hopefully it won't be relevant to the question you are asked.

2. The patient develops an infection and ID suggests adding clarithromycin. The patient is on a number of cardiac drugs and you are worried about QT prolongation. You should:

  1. Look up the possible interactions on your phone.
  2. Depend on your memory of potential drug-drug interactions. Because, though you hate to brag, you did pretty good in medical school and have a keen mind.
  3. Give the clarithromycin, but also order telemetry for the patient, because you are a careful doctor.

3. A patient presents for confusion and is found to have hyponatremia. She has the following labs:

  • Urine Na 80
  • Urine K 40
  • Serum Na 105
  • Urine output 600 mL over the last 18 hours
Calculate the electrolyte free water clearance.
  1. Don't worry that you are bad at math, this is probably SIADH so just prescribe tolvaptan.
  2. I can't remember the equation, but this just smells like an experimental question. I'm sure I can take care of the patient without this calculation. Let's look at the possible choices and I'll take a logical guess.
  3. Fire up MedCalc, put in the values. Out comes the answer.

4. The biopsy comes back for a patient with proteinruia. The Pathologist calls it dense deposit disease. You have never seen a patient with this before but you did do presentation on MPGN type two 11 years ago in fellowship.


  1. Perfect, you've got this. This is nephrology, there's no way the standard of care has changed in the last decade.
  2. Hit the computer and look it up on UpToDate and do a quick lit search focusing on the top nephrology journals. Consider eculizumab.
  3. Review KDIGO GN clinical practice guidelines. Scream out loud when you find that it is not covered. Fall back on answer 2.

Tuesday, September 16, 2014

New neph blog: UC Kidney Stone Program

Fred Coe and the crew from University of Chicago have started a kidney stone blog. This is the most prominent nephrology scientist to stick his toe in the blogging world. Dr. Coe was one of my teachers when I was at the University of Chicago (I blogged about him here and here). Dr. Coe has been instrumental in establishing the foundations of kidney stone science and continues to move field forward. He was a category in 2014's NephMadness:
(5) Dr. Charlie Pak versus (4) Dr. Fred Coe 
Charlie Pak and Fred Coe are the Bob Knight and Dean Smith of kidney stones. Not only did they dominate the field and do the pioneering work establishing the fundamental discoveries of the field, but they also trained the next generation of stone scientists that are currently leading the field. 
To this day the centers where Pak and Coe worked are world leaders in the field. In a plot twist, that would most likely happen in a comic book origin story, they were classmates at the University of Chicago Medical School, class of ‘61, and then were residents together at U of C. 
Dr. Coe remained at University of Chicago but Pak went elsewhere to established the Clinical Research Center and a new Division in Mineral Metabolism at University of Texas Southwestern Medical Center at Dallas. 
They even jointly won the Belding Scribner Award from the ASN in 2000.  
Intellectually they have staked out differing areas of excellence, Dr. Coe has focused on the the importance of the earliest stones to be anchored to the kidney. The location for these tiny early stones is Randall’s Plaques. The theory is that these tiny crystals form in the interstitium adjacent to the thin limb of the loop of Henle, they grow and eventually erode into the renal papilla. There, they are in contact with  supersaturated urine which can deposit calcium oxalate (or other other types of stones?). The plaques can be seen on cystoscopy and their presence predicts stone formers. Stone formation correlates with the degree of plaque coverage.
The blog is full of scientific and practical advice about kidney stones. His first post about why a blog is particularly insightful. 
A blog post is not a book chapter, a review article, a scientific article, or even a newsletter but something else entirely. It is the exact right size to convey one point and no more. It has no room for ornament or circumlocution, for fuzziness or indirection or even for two different points. You cannot avoid that moment when the main point must ring out clearly.
And this paragraph is just so Coe:
Being a singular, real, and immediate focus of attention, a point is something to work with. We can debate it, dissect it, even dismiss it if evidence permits or its logic is flawed. If a point appears to be sound, people can accept it as true for the moment, as an element that can be put together with like elements to make a picture of reality for this one disease. It is a picture that is true for the moment, arising as it does from science, just as the moment caught up in the pointillist net of Georges Seurat’s exquisite Sunday Afternoon on the Island of La Grande Jatte, being great art, will be true forever.

Welcome to the blogosphere Dr. Coe, we look forward to your posts. Your blog has earned a spot on my list of Notable Nephrology and Medical Blogs.

Sunday, September 14, 2014

Lecture on modern strategies to keep up to date in the medical literature. #FOAMed at Work.

I love it when fellows turn the tables on their attendings and school them on how the kids do it today.



Kamran Boka is currently a critical care fellow at Henry Ford Hospital but when he was a wee resident he worked with me at St John Hospital. This is an excellent lecture, make sure you check it out. Boka is fully engaged in the 21st century medical infosphere:


Check it out. He has important lessons for everyone.


Thursday, September 4, 2014

Urine specific gravity, not that great at estimating osmolality

I have a clinic patient with SIDAH and until the FDA regains some sanity and Otsuka provides a more rational price this will continue to be a frustrating battle. This patient had some pretty typical labs for a patient with SIADH, except for the specific gravity. I don't remember seeing such a discrepancy between the Sp Grav and osmolality before.




One of the sharpest nephrologists on twitter, Christos Argyropoulos, replied with this reference:




The conclusions from the abstract:
RESULTS: This study demonstrated that USG obtained by both reagent strip and refractometry had a correlation of approximately 0.75 with urine osmolality. The variables affecting the correlation included pH, ketones, bilirubin, urobilinogen, glucose, and protein for the reagent strip and ketones, bilirubin, and hemoglobin for the refractometry method. At a pH of 7 and with an USG of 1.010 predicted osmolality is approximately 300  mosm/kg/H(2)O for either method. For an increase in SG of 0.010, predicted osmolality increases by 182  mosm/kg/H(2) O for the reagent strip and 203  mosm/kg/H(2)O for refractometry. Pathological urines had significantly poorer correlation between USG and osmolality than "clean" urines.

Here is a table I made from the conclusions:

Tuesday, September 2, 2014

Sodium, in the spotlight for next week's #NephJC

In August, the NEJM pushed out three articles examining the role of sodium in human disease. These are the subject of September 9's #NephJC.

The first article is the Association of Urinary Sodium and Potassium Excretion with Blood Pressure. This question used the large epidemiologic study, Prospective Urban Rural Epidemiology (PURE) to answer the question.

PURE enrolled 157,543 adults age 35 to 70 from 18 low-, middle-, and high-income countries on 5 continents.

The study collected 102,216 fasting first morning urines. The authors used the Kawasaki formula to extrapolate 24 hour urine sodium and potassium from the samples. They collected 24-hour samples on 1,000 patients and found that they over estimated sodium intake by about 7%:


The mean sodium excretion was 4.9g and the mean potassium excretion was 2.1 grams.
It was difficult for me to understand the difference between the Observed excretion and Usual excretion but the authors seemed to reference the Usual excretion as the definitive curve.

Sodium excretion was higher in rural areas and in lower income countries. The reverse was true for potassium, higher in cities and higher in higher income countries.

The meat of the paper was the positive association between sodium intake and blood pressure. For every additional gram of sodium excretion the systolic blood pressure went up 1.46 mm Hg and the diastolic rose 0.54 mm Hg (P less than 0.001). Statistical mumbo jumbo increased those numbers to 2.11 systolic and 0.78 mm Hg diastolic. This relationship was non-linear with increased blood pressure effect as the sodium excretion rose over 5 grams.

Potassium had the opposite effect with systolic blood pressure falling 0.75 systolic (1.08 after statistical adjustment) and diastolic dropping 0.06 (0.09 adjusted) mm Hg for every gram increase in potassium excretion. 

Older people showed larger changes in blood pressure with increased sodium excretion.

The sodium effect on blood pressure was a lot larger that the 0.94 mmHg systolic and 0.03 mmHg diastolic found in the landmark INTERSALT study but still seems like a pretty small effect given the difficulty in getting to a low a salt diet. Look at the bell curve showing only 0.2% of samples hitting the WHO goal of less than 2.3 g a day.
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