COMMENTARY

The Significance of the 'Creatinine Bump'

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

Disclosures

July 13, 2022

This transcript has been edited for clarity.

Matthew F. Watto, MD: Welcome back to The Curbsiders. I'm Dr Matthew Watto, here with my great friend, Dr Paul Nelson Williams. Paul, how are you doing today?

Paul N. Williams, MD: I'm great. We're talking kidneys, we're talking heart. I mean, what more do you want?

Watto: That's right. We're going to talk about an excellent episode from NephMadness: Cardiorenal Syndrome. Expert cardiologist Dr Sadiya Kahn, and everyone's favorite nephrologist, Dr Joel Topf, talked to us about the physiology and the ins and outs of treating patients with both cardiac and renal disease.

The first big revelation for me was that I had always been told that poor forward flow was the main reason for the bump in creatinine seen in patients with heart failure. But actually it seems that it's venous congestion — right-sided heart failure building up the pressure, and that puts pressure on the kidneys. That seems to be the bigger issue. It's not just that the kidneys are underperfused; it's that there's just too much venous pressure on them.

A caveat is when the patient is frankly hypotensive. In that case, it might be more of a forward flow problem. Many of these patients aren't hypotensive but their creatinine is up. We think this is related to venous congestion.

Williams: Dr Kahn makes the point that the cardiac index is, by and large, commonly preserved. These patients are not presenting in cardiogenic shock. That equals poor forward flow, a preserved index with volume overload. The venous congestion element makes a lot more sense to me now.

Watto: Whenever we treat heart failure in or out of the hospital, we worry about the creatinine bump. What should we do with that? Their answers were really helpful. First, if the patient is significantly volume-expanded, that will dilute and probably hide the patient's true serum creatinine level. As you diurese the patient, the hemoglobin level might change, and you can see a similar change in the creatinine level, much like you see in a patient who is volume-expanded or volume-contracted. I never thought of it that way, but both Dr Khan and Dr Topf suggested that it's not surprising to see a little bit of a rise in creatinine as you're administering a diuretic.

Furthermore, these experts said to pay close attention to how the patient is feeling. What's happening with their body weight? Are they decongested? Those are the things that will make the patient feel better. We might have to accept a small rise in the creatinine level. In fact, in the DOSE trial, in which they used very high-dose diuretics for patients with acute decompensated heart failure, they found that the patients who had a bump in creatinine did better, and they speculated that it was probably because they did a better job aggressively diuresing those patients. That was always something that gave me anxiety when treating patients with heart failure.

Williams: It was nice to get the reassurance that we should just pay attention to the patient. You made the point that the real goal is to get them back to their baseline and not to follow the specific numbers so much. As Dr Topf said, we're treating the patient, not the numbers, and trying to make the patient feel better. If we don't get them as dry as we can, then we haven't succeeded.

Watto: Right. If you discharge the patient as soon as they have a slight bump in creatinine, you probably haven't gotten them back to their dry weight. Probably they're not fully decongested. And if you discharge them, that's going to lead to a worse outcome in the long term.

Let's think about this. I always prescribe furosemide and I don't see any difference between furosemide and bumetanide or torsemide. Am I wrong? It's okay if you tell me I'm wrong; I can take it.

Williams: I use furosemide as my father did before me, and his father did before him — three generations of furosemide use. Part of the discussion that I enjoyed was when we compared the different types of diuretics.

Among the loops, we talked about the difference between furosemide and bumetanide, because they are the most commonly used. There's a lot of institutional variation, but where I trained, we reached for furosemide first. But for a couple of reasons, bumetanide might be a little bit better. It has better oral bioavailability than furosemide, if you don't need to use IV diuretics. Even if there is a little bit of gut edema, it's probably a better agent. The bioavailability of furosemide is hugely variable, but bumetanide is pretty consistent. It's about 97%, and the levels are not as affected by changes in GFR. So you don't have to make these gigantic dose adjustments to get patients diuresing appropriately. You can make relatively minor changes and feel a bit less terrified in terms of dose tweaking with bumetanide. In comparing the two agents, bumetanide might be more consistent. Is that your practice now?

Watto: Yes. I learned about the varying absorption rates within the past couple of years, and that was through doing our podcast. I will consider using bumetanide if I'm worried about gut edema. Of course, we are talking about oral bioavailability here. The bioavailability of furosemide doesn't vary when given intravenously.

Paul, maybe I'll be wrong again here. I'm admitting a patient with heart failure to the hospital. They have a slight elevation in troponin and their BNP is elevated. This is probably because they have chronic kidney disease, right? I don't really have to worry about those biomarkers. They are always elevated with chronic kidney disease, and they have no prognostic value. Am I correct or horribly wrong?

Williams: I might suggest that if you're checking biomarkers that you're going to completely ignore, they might not be the right biomarkers to follow, but that is not to say that they're without value. We often hear that an elevated troponin level is probably because they have chronic kidney disease and they're not "clearing it."

It turns out that isn't entirely correct. It's a relatively bad prognostic indicator if a patient with renal insufficiency has an elevated troponin. It doesn't mean the patient needs to be rushed off to the catheterization lab. It may not be something that you directly intervene on, but it does risk-stratify the patient in a way that is meaningful and a reminder that the number-one cause of death in patients with chronic kidney disease is cardiovascular.

An elevated troponin is something that you really have to take seriously and be nervous about, even though you may not be doing anything in the moment about that number. And the BNP may be chronically elevated with renal insufficiency, but you can look at the relative changes in the same patient to give you a sense of volume status as well. So the BNP level in isolation may not be very helpful, but if you have multiple points in time where a BNP was checked, that might actually have real value in terms of helping to determine the patient's volume status, which can be challenging.

Watto: We've talked about many great pearls from Dr Topf and Dr Kahn. Certainly we couldn't cover them all in this short video, but if you want to hear the full conversation, then click here. This has been another episode of The Curbsiders. Until next time, I've been Matthew Frank Watto.

Williams: And I remain Dr Paul Nelson Williams. Thank you and goodbye.

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