July 1st approaches, it’s new fellow season

I remember the first days of nephrology fellowship. It was exhilarating. It was terrifying. All through residency, when you came across a patient that had you stumped you could just call the consultant. Now I was the last line of defense. I was on the receiving end of that phone call and I did not feel up to the task. I remember those months as being among the most stressful of my career. I started carrying around a small bottle of Pesto-Bismol to fight the stress induced gastritis.

I felt like a drunk, walking out of the ICU to take little nips from “my little helper.” It’s a lot of self induced pressure to battle the imposter syndrome inherent in being a new fellow, especially one coming from an outside institution.

One of my first consults was a transplant patient. The patient had acute kidney injury (AKI) and hyponatremia. She had recently received IVIG and I was so excited that I figured out that her hyponatremia was due to pseudohyponatremia from the IVIG. (See

this letter to the NEJM). So it was particularly disheartening when the transplant surgeon was not impressed pseudohyponatremia diagnosis especially since I had not been able to make any heads or tails regarding the AKI. He made his displeasure quit clear. I felt pertty humbled going to my attending, Patrick Cunningham, but he said, “Let’s walk through the case” and quickly, and humanely, pointed out the possibility of osmotic nephrosis from the same IVIG I had already blamed for the hyponatremia.

Fellowship is hard. Be humble. Try hard. Read as much as you can. Ask for help. Every person we graduate is a competent nephrologist. You will be one too. Trust the system. Together we’ll get you there.

The failure of creatinine as a marker of AKI

  • If you went to a national nephrology meeting in the 2000’s and walked into a lecture on clinical AKI there were two obligatory sections that would be part of the talk.
    1. The first would be how poor creatinine was as a marker for AKI. The expert at the front of the room would explain that creatinine was a lagging indicator and that by the time the creatinine had begun to climb the injury was yesterday’s news. Identifying AKI by a bump in the creatinine would force you to always be reactive rather than proactive. This discussion would then lead to a plea for better markers of AKI, followed by descriptions of NGAL, KIM-1, and other promising AKI assays of the future.The second would be a complaint about the lack of a consensus definition of AKI. The speaker would point to 35 different definitions of AKI in the literature, from highly sensitive (25% bumps in serum creatinine) to perfectly specific (need for acute dialysis during the hospitalization).
Oh 2002, how I miss you… (https://www.ncbi.nlm.nih.gov/pubmed/12454534)

Depending on the exact year of the talk, they would then talk about the RIFLE criteria, or to the AKIN modifications to the RIFLE criteria, or to KDIGO’s modifications to AKIN. The speaker would always point to a future where we had a consensus definition of acute kidney injury so that we could start to move forward with a cohesive literature where one paper could be compared to another. What was always odd about these talks was that the second part of the lecture, about the emerging creatinine-based consensus definitions of AKI must have been browsing Facebook during the earlier part of the lecture about the futility of creatinine-based definitions of AKI.

But the consensus did emerge. Despite all the experts warning us about the problems with small changes in creatinine defining AKI, that is the world we live in. One problem with this definition recently emerged in a discussion of cardiorenal syndrome. This article by Testani et al found that:

The group experiencing hemoconcentration received higher doses of loop diuretics, lost more weight/fluid, and had greater reductions in filling pressures (p<0.05 for all). Hemoconcentration was strongly associated with WRF (OR=5.3, p<0.001) whereas change in right atrial pressure (p=0.36) and change in pulmonary capillary wedge pressure (p=0.53) were not. Patients with hemoconcentration had significantly lower 180 day mortality (HR=0.31, p=0.013). This relationship persisted after adjustment for baseline

We should not have a situation where increased risk of AKI (yes, I know the definition of worsening renal function, WRF, does not perfectly overlap with Stage 1 AKI, but work with me) is also associated with improved 180 day mortality. By defining AKI around changes in AKI we have deputized nephrologists to be the creatinine police and make decisions on treating patients based on what effect it has on short-term changes in GFR which may or may not have anything to do with long-term outcomes. In the above study, using serum creatinine to guide therapy leads to insufficient diuresis, poor fluid removal, and poor 180 day outcomes.

The Twitter discussion about this was particularly enlightening. Take a look.

Citrate or Heparin for CRT

As part of my other blogging job (eAJKD) I had the opportunity to interview Drs. Mei-Yi Wu and Ka-Wai Tam who performed a meta-analysis looking at anticoagulation. They examined filter life and other complications of CRT. The interview was conducted by Facebook IM, which was pretty cool and helpful with a significant language and time-zone barrier.

Check out the interview and the article.

By the way Jhaveri, Sparks and the rest of the team have been killing it at eAJKD and have really built a solid blog. Amazing how far they have come in a couple of months. Solid work.

second lecture of the year: acute kidney injury

This is a significant upgrade from the version I posted a couple of years ago. I put the lecture together right before the ATN trial was published. I finally got around to updating the presentation to include that data. I also updated the NGAL section and added some data on avoiding volume overload.

I used a number of the posts on the blog to allow me to rapidly update the presentation. I was pleased with how well my ATN commentary/review stood up.