Acute kidney injury

We see this acutely with the kidneys.

Cancer patients are three times more likely to experience acute kidney injury, or AKI, compared to non-cancer patients.

And one of the most dangerous metabolic emergencies driving complications here is hypercalcemia, right?

Exactly.

or that they have a biliary tract complication, whether it be obstruction, perforation, fistulization, bilomas, what have you.

And then renal, obviously you want to make sure they're not developing a post-procedure AKI, but that's less about the tips itself and more about just cirrhotics having a very lack of reserve within the milieu of their renal pathology.

All right, getting closer to the end here, we've got some pearls, key takeaways, and then some practice questions.

So some pearls specific to emergency critical care when it comes to TIPS is TIPS treats portal hypertension.

You always want to know what the precipitant is because a patient with cirrhosis and confusion may have a lot of different things going on.

And you always want to think about, is there a precipitant that is causing hepatic encephalopathy, or is there confusion going on that is actually not hepatic encephalopathy? So anytime you see someone with cirrhosis or liver disease who is confused, you want to think about normal causes of confusion.

Are they septic? Do they have GI bleeding, hypovolemia, AKI, electrolyte derangements, hypoglycemia? Do they have a structural lesion in their brain, stroke, hemorrhage? People with cirrhosis are slower to clear some drugs.

So is there some buildup of polysubstances that are causing confusion? Is there alcohol withdrawal, SBP, acute liver failure, acute and chronic liver failure, right? So is there a precipitant causing hepatic encephalopathy? Is there confusion that is not hepatic encephalopathy? And this is a difficult question to to answer sometimes, right? So we want to stabilize the patient, we want to search for precipitants, we want to treat reversible triggers, and then that'll help guide us in terms of where this patient can be dispositioned as well as what the next best steps in management are.

I am Benedetta Bussolatti from the University of Turin and today I will be discussing our study entitled Urine and Plasma Extracellular Vesticle Analysis for Monitoring Urinary Recovery after Acute Kidney Injury.

Acute kidney injury is a very common complication in hospitalized patients.

Although we often think of AKI as an acute and potentially reversible event, we now know that recovery of kidney function does not necessarily mean complete biological recovery of the kidney.

This creates an important clinical problem.

At-hospital discharge, serum creatinine, and the estimated glomerular filtration rate tell us about kidney function.

They carry a signature, such as proteins, lipids, nucleic acids, that reflects the identity and physiopathological state of the cells that release them.

And therefore, EVs present in biological fluids can potentially be used as a sort of liquid biopsy.

The aim of this study was therefore to investigate whether combining these two sources of information, urinary and plasma EVs, could help us monitor renal repair after AKI and to identify patients with different trajectories of kidney function recovery.

And I do want to mention though, phosphate is going to get its own episode later in this series.

And if you have listened to the recent episodes on kidney disease, so episodes 126 on CKD and 127 on AKI, we have chatted a bit about phosphate recently.

So some of this will be familiar.

And because phosphate and calcium are linked when we're chatting about phosphate, calcium, of course, comes into play too.

Question one.

A child develops acute kidney injury while receiving a renally cleared antibiotic.

Which change most directly affects the maintenance dosing requirement? A, increased volume of distribution, B, reduced clearance, or C, reduced

oral bioavailability? This is a good question, and I can guarantee you such questions will be on the boards, Rahul.

Loading dose mainly depends on the volume of distribution and the peak concentration we want to achieve.

That's why we call it a loading dose.

So acute kidney injury doesn't automatically mean the initially loading dose should be smaller.

Clinically, at the bedside, that distinction matters.

And that was a decision that we thought very carefully about.

And part of it was in discussion also with our colleagues, some colleagues with decades of experience in treating PKD patients, the concern that adding this glycosuric drug on top of a profound aquaretic drug of Tlobaptin could lead to very severe volume depletion and even AKI.

Almost all of our patients, however, were on a RAS inhibitor, which is consistent with the current treatment guidelines by KDGO.

And we also excluded patients who were on loop diuretics, for the same reason, concern about severe volume depletion.

So being able to use this stress test to determine which kidney would be better to take out to improve patient outcomes for living donors.

And in addition to this, for determining whether a patient undergoing cardiovascular bypass surgery is more likely to develop AKI.

So I think some papers have shown that evaluating kidney functional reserve can be predictive of this.

So this kind of like allows a more comprehensive assessment.

Thank you very much for this opportunity today.

This is a really interesting paper and we always see casts.

We see them in the urine when patients have AKI and we see them on the kidney biopsy.

And one of the things I always look at and said, well, it's mostly uromodulin.