The Curbsiders' 'Hot Takes'

No Need to Dread Acute Kidney Injury

Matthew F. Watto, MD; Paul N. Williams, MD

Disclosures

July 23, 2020

Matthew F. Watto, MD: Welcome back. This is the Curbsiders. I'm Dr Matthew Watto, here with the great Dr Paul Williams.

Paul N. Williams, MD: I'm going to take the reins for a change. This is a recap of one of our Curbsider podcast episodes. Tonight we had the great fortune of talking to Dr Joel Topf (AKA @Kidney_Boy), a favorite guest of our podcasts — someone who always teaches us something important about nephrology. We'd like to share our favorite takeaway points from this episode about acute kidney injury. Matt, what did we learn?

Watto: The most helpful point that he made — one that will be burned into my memory, hopefully forever — is that 70%-90% of patients with acute kidney injury have either prerenal azotemia or some sort of postrenal cause. Giving fluids and inserting a Foley will handle those issues.

Another 5% of patients have acute tubular necrosis , which gets better no matter what you do. As long as you don't tank the blood pressure or throw a bunch of nephrotoxins at them, they are going to get better in days or weeks. So around 90% of the time, you don't really have to do much except give fluids, make sure there's no obstruction, and just wait. That's great news, because only about 5% of the time do we have to think about things like biopsy and sending all these weird studies — that whole panel of labs and urine studies that nephrology asks you to get.

Williams: It was hugely comforting (as someone who is a little afraid of the kidneys at baseline) to hear that you have limited options. If you have even a vague sense of what's going on, your interventions are limited as well: lactated Ringer's, urinary catheter, observation, and see what happens. Most of the time it's going to get better, which should be encouraging to some interns who are terrified at this point in their career.

Watto: And attendings.

Williams: As someone who lives with terror, it was helpful for me, too.

Watto: Speaking of terror, seeing patients with an elevated creatinine level and thinking about this contrast issue — what did you make of Joel's take on that?

Williams: The point he makes is that there are no randomized controlled trials with a strong signal that there is such a thing as contrast-induced nephropathy. It's important to emphasize that this is his expert opinion, but he has looked at a lot of literature about that.

The medical community came to a group consensus because it's such an iffy thing. Everyone sort of dreads it but no one has been able to prove it.

The point he makes, and I think it's important, is that the risk of contrast-induced nephropathy shouldn't be the determining factor in deciding whether to get a test or not. If you need help to make a prompt diagnosis, you should get that test and not be as worried about contrast-induced nephropathy.

Dr Topf raised the point that if the patient's renal function is incredibly tenuous, it might give you pause, but by and large, it should not be the determining factor in test selection if someone truly needs a prompt diagnosis and workup.

Watto: Absolutely . If you think a patient is having a stroke, and you need to give them contrast and might be doing a thrombectomy, you just have to do the study and deal with whatever happens to the kidneys.

It's really complicated. There are so many patient factors and confounders in acute kidney injury, which is part of the point he is making.

Williams: Right. Many patients end up with acute renal insufficiency just because of the hospitalization, even in the absence of contrast. It's hard to know what's to blame and what isn't, because randomized trials are hard to perform.

Watto: A big-ticket item on my list of questions is acute interstitial nephritis because I had a suspicion that I was missing it. Of course, that's not the case because it's not that common. That's one of those diagnoses that I throw in there but I'm not really sure about, because urine eosinophils is a terrible test. One of my favorite things that Joel told us on this episode was that acute tubular necrosis, rather than acute interstitial nephritis, is actually a more likely reason that someone would have eosinophils. Every board question would have you think that if someone has urinary eosinophils , then slam, dunk: It's acute interstitial nephritis .

You should think about acute interstitial nephritis when a patient has a lot of white and red cells in their urine. About 95% of the time it's going to be acute tubular necrosis, prerenal or postrenal. If it doesn't seem like it's either of those things and the whole picture isn't quite making sense, then you have to think about exposure to drugs (NSAIDs or PPIs) or antibiotics. Beta-lactams are the classic antibiotics that people think of in association with a fever and a rash, but that's not the majority of patients. If you don't think this is acute tubular necrosis and it's not one of those other situations, then acute interstitial nephritis is something you can think of.

That's all we have time for. This was a huge discussion with Dr Joel Topf . It's packed with pearls. I highly recommend that you check it out.

Click to hear the full episode of Acute Kidney Injury — Myths & Musings, or find the Curbsiders podcasts on iTunes.

The Curbsiders is a national network of students, residents, and clinician educators from across the country, representing 15 different institutions. They "curbside" experts to deconstruct various topics in the world of medicine to provide listeners with clinical pearls, practice-changing knowledge, and bad puns. Learn more about their contributors and follow them on Twitter.

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