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Recipe for IV Fluids

Normal Saline

1 tsp salt = 2,300mg sodium = 100 mmol sodium

1 gallon = 3.78 liters
1 liter of NS has 154 mmol of sodium
1 gallon need 582 mmol of sodium (154 * 3.78)
582/100 = approx 6 tsp of sodium

3% Saline

1 tsp salt = 2,300mg sodium = 100 mmol sodium

1 gallon = 3.78 liters
1 liter of 3% has 513 mmol of sodium
1 gallon need 1,939 mmol of sodium (513 * 3.78)
1,939/100 = approx 20 tsp of sodium

D5W

1 tsp sugar = 4.2 g sugar

1 gallon = 3.78 liters
1 liter of D5W has 50 g of sugar (glucose)
1 gallon needs 189 g of sugar (50 * 3.78)
189/4.2 = approx 45 tsp of sugar or 15 tablespoons
Anyone want to check my math?

IV fluid taste testing at McLaren Macomb Hospital

@kidney_boy Your math is correct, of course depending on the size of a table spoon http://t.co/OvkVzDoWMJ. In netherlands 1tsp = 10g NaCl
— Martijn vd Hoogen (@MWF_vd_Hoogen) August 13, 2014

@kidney_boy would be good to say glucose instead of “sugar”
— Lewis (@Lewis_Lab) August 14, 2014

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Just saw a heart failure patient in follow-up

We had a patient, who had been healthy until he ran into some a-fib. He then began a months long descent into the depths of decompensated heart failure. His dry weight prior to decompensation was 208. On admission to the hospital he was 262.

It took over a month of acute and sub-acute care, a failed cardioversion, a pacer, and a cardiac ablation, but he ultimately emerged from his heart failure. He is now back to his dry weight. He went from 208 to 262 pounds to 208 pounds’  That is 54 pounds of water weight. My understanding of heart failure is this excess fluid is almost entirely extracellular.

Think about how much water and sodium that is:

  • 54 pounds = 24.5 kg of 24 liters of water
    • Total body water of an average adult is 42 liters
    • Extracellular volume is a third of that, or 14 liters
    • at 208 pounds his total body water is only 47 liters
  • 24.5 kg of water with a sodium concentration of 140 = 3,430 mmol of sodium. 
    • For comparison the total body sodium for a 70 kg man is around 2,200 mmol
Incredible.
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Addendum to Hypokalemia

I can’t post to Vimeo until next week. So google docs once again.

The hypokalemima section did not cover vomiting, so I added this addendum.

Part 3 is uploading right now so the final pots with all three parts and the keynote and PDF will be available tonight.

Addendum to Part 2

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August is aPLA2R month

For decades we have known that membranous nephropathy was an antibody induced glomerulonephritis, we just didn’t know what the antigen was. Then, in 2009, Beck et al. rocked nephrology by discovering the antigen, Phospholipase A2 antibodies were detracted in 70% of patients with membranous nephropathy and no patients with either secondary membranous, other proteinuric glomerulonephritis or normal controls. Since then there has been a steady stream of positive trials showing tight association with aPLA2R antibodies and disease activity in idiopathic membranous nephropathy.

Panel H illus­ trates the domain structure of PLA2R, which is composed of an N­-terminal cysteine­rich domain (Cys­R), a fibronectin type II domain (FNII), eight CTLDs, a transmembrane domain (TM), and a short intracellular C-­terminal tail (IC). The blocking fragment used in the experiments consists of CTLDs 4, 5, and 6 of a recombinant rabbit PLA2R.

This month both CJSAN’s eJC and #NephJC will be going deep with studies that examine the state of the art in aPLA2R research.

This month CJASN’s online journal club is doing an interesting article looking at aPLA2R status at the beginning and end of therapy and its ability to predict long-term outcomes. It is a unique study with multiple titers of aPLA2r over the course of time matched with 5 years of follow-up. Though it is not the biggest trial of aPLA2R in some ways it is the best and it is an important step in understanding how to use this new tool in the management of membranous nephropathy.

Every month eJC has a sponsor, this month that sponsor is my home institution St John Hospital and Medical Center in Detroit. My fellow and I reviewed most of the key studies in aPLA2r and provided a helpful summary of this study. Check out our background post at Medium and then participate in the forum.

#NephJC will be shortly announcing its article for discussion and then have a twitter discussion on August 12th at 9pm EDT.

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World’s Best Potassium Lecture part 1 of 3

Once agin I have the honor of teaching the second year medical students at Oakland University William Beaumont School of Medicine. I have 4 points of contact with the students:

  1. I get to run the first TBL of the renal section. It is on sodium and water
  2. I get to run an Acid-Base workshop
  3. I get to deliver a traditional Acid-Base lecture
  4. I get one hour to do potassium. Last year I tried to squeeze potassium, metabolic alkalosis and secondary/monogenic hypertension into that one hour. What a disaster. So this year I am going to flip the class took so that the students can learn the basics of potassium on their own and then do an interactive case based approach to the more advanced concepts. We’ll see if I get better ratings this year.
The lecture is mostly done, but not quite ready to be posted for download. However I did record the first segment. You can see that here.
I should have the other two segments online soon and when I do the lecture will be available as a PDF and a Keynote 2014 file.
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cJASN is building an open access renal physiology text book

One of the surprising things about nephrology fellowship is how far separated renal physiology is from the day to day work of nephrologists is. Kind of by definition we are called in when the kidneys aren’t working so we don’t get normal physiology thrown in our face. But that doesn’t mean we don’t need to know it. One of the important jobs of the nephrologist is to keep this knowledge alive and be experts in the internal workings of the kidney. I am a disciple of of Burton Rose, others carry the generation before me used Brenner and Rector and before that Guyton and before that Homer Smith. Who will the next generation of nephrologists look to enlighten them in the ways of the kidney?

CJASN is making the argument that they will. Mark L. Zeidel, Melanie P. Hoenig, and Paul M. Palevsky have started a renal physiology course that is open access and will come serially every month like Dickinson novel.

Take a look at the editorial describing the project and the first chapter which is just an introduction to the main course. The introduction is the subject of this month’s eJC. Here is what I wrote in their forums:

I am so excited about this series. Fellowship application season is upon us and I have already heard rumblings that this year will be even worse than the devastating match results from 2014.  

The work-force task group from the ASN has been focusing on developing nephrology mentors to increase interest in nephrology. This is a great idea, but the mentor that inspired me to become a nephrologist was not made of flesh and blood but of ink and pulp. 

I am a nephrologist because I was inspired by the brilliant prose of Burton Rose in the yellow edition of Clinical Physiology of Acid Base and Electrolyte Disorders. But times have changed and residents no longer read books. I applaud this series and hope it will serve as a contemporary inspiration for medical students and residents to pursue the noble and fascinating field of nephrology. 

I also tip my hat to the editors of CJASN for making the series open access. A resource this valuable should be shared with the world.  

Bravo.