Confusing Terms: Cardiorenal...also...Pre-Renal vs. volume loss ATN

[Redpancreas]

Two terms which confuse me are "cardiorenal" and "volume loss ATN".

Cardiorenal: I was talking to other interns who felt Cardiorenal just meant pre-renal AKI. I was under the impression it could be a fluid underload, overload and could be renal or cardiac in origin. Any good sources to iron out all the mechanisms and what to do in each case?

Volume loss ATN: So my impression was volume loss in an acute bleed for example would lead to a pre-renal AKI. However, I literally read this in a note today. "Random urine sodium and creatinine showed pre renal, volume loss ATN most likely based on microscopy"..so I thought ATN was a intrarenal cause of AKI which is a different entity. I know lack of perfusion leads to necrosis physiologically, but if someone could clarify the terms, that would be great.

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[skyuppercutt]

Pre-renal is a broad term for not enough blood getting to the kidney. It can be from dehydration, bleeding, or being intravascularly dry. Cardiorenal is pre-renal but basically sheds light on the cause of the pre-renal, which in this case, is because the heart isn't functioning well, as in CHF where you are intravascularly dry. You can still be fluid overloaded in CHF or cirrhosis (think edema), but the fluid isn't where you want it to be (in the blood vessels), it's outside the blood vessels in your legs. In that way you can be volume overloaded, but also "Dry" at the same time. Sometimes in CHF you have too much fluid in the blood vessels, so the heart doesn't pump is as effectively think of cardiomyocytes being super stretched. in that case because the heart isn't pumping well, you don't get enough blood to the kidney --> pre-renal (specifically cardio renal)

ATN basically means the kidney is damaged and you're right that it is a "renal" cause of AKI. THe thing with ATN is that one of it's causes is a pre-renal AKI. If you have a pre-renal AKI and you get fluids to correct it quickly often times the kidney recovers really fast. If you don't get to it in time, then the actual kidney gets damaged, which is called ATN). If you look at the urine, you can see urine sodium is low indicating not enough perfusion to the kidney. If you then look under a microscope and see "muddy brown casts" then you now know that the AKI was so significant/prolonged that the actual kidney got damaged too, which means it'll probs take longer to recover (if at all)

 

[whoknows2012]

I’d also add that a more in depth explanation involves renin angiotensin activation due to “perceived” volume depletion, exacerbating the whole process, creating a feedback loop

 

[IMreshopeful]

Cardiorenal is a very complex thing and there are several causes and types

There’s chronic which is usually due to long-standing volume overload causing renal congestion (also can be acute) and due to long-standing poor cardiac output and low renal perfusion. This causes the chronic elevated Cr. So basically the preload is so high that renal perfusion pressure is compromised and to boot in low EF you have low stroke volume.

Acute can also overlap with ATN in cardiogenic shock... severe impairment in renal perfusion leads to necrosis and requirement for RRT

Making all this worse in heart failure is that your adrenergic neurohormonal stuff is all hyperactive so you get systemic - and this renal - vasoconstriction and low GFR

Plus there’s just the unfortunate fact that diuretics lead to increased volume loss and worsen vasoconstriction by activating the neurohormonal axis to some degree. So some of it is drug induced

There’s some good review articles on it

Acute cardiorenal syndrome: Mechanisms and clinical implications

Cardiorenal syndrome in heart failure: A cardiologist’s perspective