Precious Bodily Fluids

Mark Parker, the chair of the ASN Workforce Committee, will be on Twitter next Tuesday to discuss the latest report. This report is the second done by Ed Salsberg and his colleagues at GWU. This report is all about the fellow experience in getting a job.

The report is available here.

Dr. Parker answered some questions to stoke the fires of discussion, that interview can be seen on Medium.

ASN Nephrology Workforce Report

The first workforce report stimulated some discussion on Twitter, that discussion is saved here:

A summary of the discussion about the second report so far is available here:

My summary of the report:

• The survey was distributed to 1,530 ASN Nephrology fellow and trainee members in June and July of 2014.
• 441 responded. Response rate of 28.8%.
• There are 930 fellows in ACGME accredited programs and they received 333 responses from this sub-group. 
• What is up with the 600 trainees not in ACGME spots? DO programs?

Interesting gender differences:

How about this eye opening stat:

USMGs had a median debt of $100,000 to $149,999. IMGs were significantly different with a median debt of $0 and 65% having no debt.

Career plans

Nephrology breaking barriers, has higher starting salaries for women compared to men:

Female respondents had a slightly higher median anticipated base income than male respondents, who had a median anticipated base income of $150,000 to $174,999.

Job hunting troubles were much more common among IMGs with only 22% finding a satisfactory job compared to 56% of USMGs. Visa problems and unappealing locations were leading problems in job hunting. 71% reported no or very few jobs within 50 miles of their training location.

Happily 72% of respondents indicated they would recommend nephrology to medical students and internal medicine residents.

It’s an interesting report, take a look and…

Please join Dr. Parker to talk about #NephWorkForce Tuesday, January 13 at 9pm

In February I’m giving grand rounds on the Potassium Wars (what, you didn’t realize we are in the opening stages of the potassium wars?). I was looking at the original research on Kayexalate from 1961 and came across this ad. Check out the doses of spironolactone they were slinging:

From the NEJM 2007.

Purple discoloration can occur in alkaline urine as a result of the degradation of indoxyl sulfate (indican), a metabolite of dietary tryptophan, into indigo (which is blue) and indirubin (which is red) by bacteria such as Providencia stuartii, Klebsiella pneumoniae, P. aeruginosa, Escherichia coli, and enterococcus species. The clinical course is benign, and the urine typically clears with resolution of the bacteriuria and acidification of the urine. 

H/T Life in the Fast Lane

A few pioneers at the intersection of social media and nephrology have banded together to create an internship in social media. The founding members of the loosely coordinated Nephrology Social Media Collective (logo pending, but it should be pretty cool) are:

• Myself
• Swapnil Hiremath, co-founder and brain child of NephJC
• Matt Sparks, savior of Renal Fellow Network and co-creator of NephMadness
• Kenar Jhaveri, blogger at NephronPower and editor of AJKDblog
• Paul Phelan, contributor to NephJC, Renal Fellow Network and AJKDblog
• Jordan Weinstein, creator of UKidney
• Edgar Lerma, creator of #NephPearls hashtag and serial author

Waiting for me in my inbox today:

Hello Dr. Topf, 

My name is Julia XXXXX, and on behalf of Keryx Biopharmaceuticals, I’d like to introduce Keryx as a resource for you as you develop content for your blog, Precious Bodily Fluids, given your commitment to advancing understanding of renal diseases. I’d like to periodically share updates from the company to keep you informed regarding its lead therapeutic product and commitment to patients on dialysis.

In fact, Keryx just announced it has begun shipping AURYXIA™ (ferric citrate) tablets to wholesalers in the U.S. Auryxia is approved for the control of serum phosphorus levels in patients with chronic kidney disease (CKD) on dialysis. Auryxia is the first and only absorbable-iron-based phosphate binder that is clinically proven to effectively control phosphate levels within the KDOQI guidelines range of 3.5 mg/dL to 5.5 mg/dL. The U.S. Food and Drug Administration approved Auryxia in September 2014. In addition, Keryx has created the “Keryx Patient Plus” program to assist with patient accessibility to Auryxia. 

For more information, please visit http://www.auryxia.com/. The full press release is below and includes additional information. 

If you are amendable, we will continue to reach out to share updates from Keryx and AURYXIA in the coming year that we hope will be useful for your readers and followers. 

Please feel free to reach out with any questions. 

Best, 

Julia

My reply

Julia,

Thanks for reaching out. I’m glad there is a new phosphate binder available for dialysis patients. I was wondering if you have any data that shows Auryxia reduces any patient oriented outcomes (e.g. hospitalization, mortality, fractures, morbidity)? And if not, is Karyx planning on doing such a study? And if not, why not?

Joel

Fingers crossed but with a skeptic’s scowl

PDF | Powerpoint

The colours in the table are not explained anywhere. I am guessing “green”means statistically significant, and “orange” means… a decline in posts over time? Maybe that could be mentioned in the main text at the left. 

The table is big and dense. Again, I wonder if it could be simplified, either graphically (first step: remove the vertical gridline!) or even removed. If I’m reading it right, some of the information in the table is repeated in the graphs to the right of the table. 

The last line of the table – “Totals” – appears to be incorrect. It looks like most of those entries are means, not totals. 

Also, the text mentions 30 blogs, but only 22 are plotted.

I have a patient with CKD stage four, diabetes and hypertension. In fact, I have a hundred patients with CKD stage four, diabetes and hypertension. However, this patient had uncontrolled blood pressures. Here is the nomogram from her home blood pressures:

She was taking once daily furosemide and we changed it to torsemide, for better pharmacokinetics. She returned a month later and her blood pressure was fixed, systolics equally distributed between the 120s and 130s. So a win for Torsemide, or maybe not…

She was excited because she had been reworking her diet and was no longer drinking pop. She was eating more home-cooked meals and really focusing on eating more vegetables and fruits. She was also being more conscious of her sodium intake.

I remember a time when I thought the treatment of chronic SIADH was going to be revolutionized by the vaptans. These small molecular ADH antagonists would interrupt the disease the precise mechanism of disease. I expected a Banting and Best like revolution. (If you have not seen the story of the discovery of insulin take a moment to watch the movie, Glory Enough for All, especially if you thought the greatest thing to come out of Canada was Tim Horton’s)

The initial data was promising with convincing studies on conivaptan and tolvaptan, but something happened on the way to SIADH nirvana.

First the EVEREST trial went sideways. In heart failure:

• Angiotensin 2 is elevated and blocking it prolongs life
• The sympathetic nervous system is up-regulated and blocking it prolongs life
• Aldosterone is elevated and blocking it prolongs life
• ADH is elevated and blocking it doesn’t do a damn thing

With no hope for a heart failure indication the drug was marketed solely as a treatment for hyponatremia where it was shown to be effective. The pitch was that doctors should not discharge people with hyponatremia and tolvaptan was faster and more effective than the previous standard of care. The drug was priced for short-term inpatient use at $300 a pill tolvaptan was a non-starter for chronic outpatient SIADH.

So generous of Otsuka to make the 30 mg dose the same price as the 15 mg

The side effects reported for demeclocycline and lithium were such that we recommend not using them for any degree of hyponatraemia.

Fluid restriction, the cornerstone of therapy, is difficult to maintain and in severe cases is insufficient to correct hyponatremia (I’m thinking of patients with negative free water clearance). Urea has a good track record but I have not heard of it being used in the United States. Salt tablets can help, but often are inadequate to correct the hyponatremia.

On the list of possible treatments are loop diuretics. I have tried loops in hyponatremia on a number of occasions and though the math works, in my hands I have not found them to be effective. In the past, I have used loops in hospitalized patients with hyponatremia. The results have been underwhelming. But I know have a loop diuretic success story in a patient with significant but stable outpatient hyponatremia.

+1 “@medicalaxioms: Nothing aggravates a nephrologist like a kidney that refuses to obey the math.”
— Joel Topf (@kidney_boy) March 31, 2014

I met the patient when he was admitted to the ICU with mental status changes due to a sodium south of 120. This was not his first episode of hyponatremia. We corrected the sodium and restored normal mentation. We did a thorough work-up, looking for the etiology of the SIADH and despite some promising leads that turned into blind alleys, I am quite confident, now, that this is idiopathic SIADH.

During subsequent outpatient follow-up he had persistent hyponatremia with sodiums running in the high 120’s. During this time, treatment consisted of salt tablets and fluid restriction. A couple of visits ago I added torsemide, and boom the two sodiums since have been 138 and 134.

Here is the sodium and urine osmolality over time. It plummets after the torsemide is started. This increases the free water clearance.