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Transcript

Hi everyone, let’s review some key takeaways from our episode about cardiorenal considerations.

So what causes cardiorenal syndrome? Think of your collective glomeruli as the coils of a garden hose, where the water supply is the incoming blood (from the afferent arteriole) and the outlet is the outgoing blood (the efferent arteriole).

Cardiorenal syndrome typically involves two main mechanisms at the ends of this hose:

The first is a low-flow state, where the heart is sick and is not getting enough blood to the kidney, so your water supply is not adequate.

The second, and probably more important mechanism is renal venous congestion, where the exit for the water is all jammed, like someone is clamping the nozzle of the hose. This also makes the flow through the hose stagnant and your kidney/glomeruli not as happy.

This second situation is our classic “warm and wet” heart failure patient, where total volume overload is jamming up the hose nozzle.

It is very important to think broadly as patients with HF and kidney disease often are sick and can have many reasons to have an AKI aside from cardiorenal syndrome. Here is a different framework to think about AKI with a focus on hemodynamics, in both a cardiac but really any patient.

On the inflow or water supply side, you have anything that affects blood getting to your kidney – this includes your classic prerenal/hypovolemia, hypotension, or conditions like cirrhosis where other factors impact your renal perfusion. On the outflow or nozzle side of the hose, you can have things like a renal vein thrombus or more rarely, an abdominal compartment syndrome that jams up your exit. Certainly, we should note that volume overload and cardiac issues are by and large the most common cause of an exit jam. All of these “hemodynamic” issues are what we traditionally call “prerenal AKI”, but some of them really involve the outflow of blood too.

Of course, you can also have your usual intrinsic and post-renal causes of AKI like ATN, AIN, a glomerular process, or urinary obstruction that you should keep in mind.

The urinalysis can be helpful. In pure cardiorenal syndrome, your urine dipstick should be “bland”—no protein, blood, or signs of white cells— because it’s the hemodynamics in the kidney that are not ideal and the blood flow that’s mucked up, rather than actual tissue damage. On microscopy, you will not see any cells or cell casts, though you may see some hyaline casts. You should be careful interpreting some of these markers in patients with baseline CKD as they often will have protein and maybe blood in the urine (because they always do). The key is to make sure there is no new or worsening protein, blood, or cellular casts that may indicate a more acute intrinsic kidney injury.

When you send the urine down for chemistry, often your urine sodium in cardiorenal syndrome will be low because your kidney wants more blood flow and turns RAAS on. Of course, all of the hemodynamic causes of AKI that we discussed can do this to your urine sodium too. And caution interpreting this study if the patient just took diuretics! That will make the urine sodium look higher too.

Thanks for listening! Stay tuned for Part 2: Our Diuretic Toolkit and check out the full Cardiorenal: 5 Pearls episode for more nuances and expert insights!