The future of nephrology

Super fun discussion on Twitter that has spilled out over the last few days. It began with this tweet about Nayan’s take on the latest MRI imaging during dialysis.

The original article is here and I’m a bit embarrassed about my sensationalization being a bit overwrought.

Forunaltely, it did trigger a great rolling conversation about the future of dialysis and by extension, nephrology. It may be difficult to recreate the discussion from that original tweet, so here are some key tweets:

In the midst of this discussion I broke the thread and added novel tweet asking people to place a bet on the future of transplant.

But this prognostication is focused on emerging transplant technologies and fails to capture the full breadth of nephrology transformation that we are seeing. With the emergence of Flozins, GLP1 agonists, MRAs (both steroidal and non-steroidal) as well as the increased interest and development of novel treatment targets, it is not a leap to say that nephrology in 10 years will look very different than it is today.

How will we mark that development? My poll of when will more than half of transplants come from non-human sources is a specific and quantifiable time that will represent a sea change in transplant. A marker that represents a change not in potential but in delivery. So how will we mark that moment in nephrology at large? I would argue that it happens when we see consistent year over year fall in the number of prevalent dialysis patients (in-center and home) for four consecutive years.

So how long until the combination of slower CKD progression, increased transplantation, and, unfortunately part of the equation, continued stagnation in dialysis longevity, result in consistently falling dialysis prevalence?

The magic of treating minimal change disease

I had this patient come to me with miserable nephrotic syndrome. Following a biopsy that revealed minimal change disease (MCD), I started her on prednisone and BOOM she got better.

A few months later I tweeted (since deleted, don’t ask) these pics with the caption:

If all I could find a job where all I did was treat minimal change disease all day long, I would sign up in a heart beat.

The point was that MCD is one of the most rewarding diseases nephrologists get to treat. The patients are miserable, you give them the medicine, and they get better. Yes, I know there is a terrifying relapse rate, and high dose steroids are no walking the park, but compared to the disease we typically treat in nephrology, this one is particularly rewarding.

Teaching on Two Ell: Acute Renal Failure and GFR

Yesterday we discussed the problem with the curvilinear relationship between gfr and creatinine and how the MDRD equation dispenses with this problem. Today we will go over a handout introducing GFR, MDRD and how to manage them, including referral to a nephrologist.

Additionally I want to do my canned acute renal failure lecture. This lecture has been made obsolete by the recent ATN data and data from Vanderbilt so it will need to be revised.

ARF No ATN Data

View SlideShare presentation or Upload your own. (tags: arf atn)

Teaching on 2 Ell, the second week

On Monday one of our interns gave a lecture on the range of renal pathology possible found with lupus nephritis.

Lupus Nephritis

View SlideShare presentation or Upload your own. (tags: sle pathology)

This was a follow up on her lecture on the renal manifestations of lupus nephritis by WHO criteria. After her lecture we went down to bowels of the hospital to look at the kidney biopsy we had done on Friday on one of our patients with lupus.

On Thursday we began interpretation of Acid-Base disorders.
Also on Thursday I lectured the house staff on Nephrogenic Fibrosing Dermopathy, Acute Phosphate Nephropathy and Contrast Nephropathy. Renal adventures in imaging.

On Friday the 13th we completed Acid-Base disorders. As part of acid-base we talked about the anion gap. This article in CJASN on the anion gap was wonderful.

Rhabdomyolysis

Just got my second rhabdomyolysis patient in the last 2 months. Both had anuric acute renal failure and both had CPKs over 100,000.

In fellowship, the dogma was that sodium bicarbonate was ineffective and could do harm. The reasoning was that alkalinizing urine made calcium-phosphate less soluble, increasing the likelihood of calcification in the tubule extending the renal damage.

Recently, I found a paper from the Journal of Trauma 2004 by Brown and Rhee (Alternative) which showed compelling trends for improved outcomes with mannitol and bicarbonate. What was so impressive to me was that as the disease got more severe (higher CPK) the experimental group appeared to do relatively better. The authors were prevented from reaching a significant p value primarily by having too few patients with severe rhabdo.

I will use the handout from a prior morning report on the subject for the teaching session on Monday.

Rhabdo for Morning Report

Two Ell

This month I’m attending on the renal ward at Saint John Hospital and Medical Center. I have a huge team: one fellow, one second year resident, three interns (2 categorical and one ER resident) and two medical students. I have been having a blast teaching them.

I am going to track all of the teaching I do this month here.

So far this is the formal (as opposed to bedside) teaching we have done:

Monday June 2: Introduction to Two-Ell
Tuesday June 3: Nephrotic Syndrome
Wednesday June 4: Dialysis basics and Anti-hypertensive agents saves lives
Thursday June 5: Renal Adventures in Imaging (the nephrologic implications of Gadolinium and NFD, phosphate nephropathy as a complication of colonoscopy prep, and contrast nephropathy)

Adventures in Renal Imaging

More to come.