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Acute kidney injury

Acute kidney injury

InjuryWikipedia

Search complete. 175 mentions across 39 episodes found for "Acute kidney injury".

Sep 18, 2026

John MandrolaHOST
21:07
The primary endpoint was death, MI, stroke, or ischemia-driven revascularization.
John MandrolaHOST
21:11
The primary safety outcome was a composite of contrast-associated AKI, acute kidney injury, or major bleeding.
John MandrolaHOST
21:20
And all this seems reasonable on the surface, doesn't it? But it assumes that complete revascularization is the strategy of choice.
John MandrolaHOST
21:28
And I've talked about this issue a lot, so I'm not going to go on forever, but I do think that we need to talk about it a little.
John MandrolaHOST
24:45
All components of the primary outcome except stroke, which was rare in both arms, was lower in the physiology-guided arm.
John MandrolaHOST
24:53
Safety, too, was impressively lower.
John MandrolaHOST
24:55
Both bleeding and AKI were lower with the physiology-guided approach, and the authors concluded that physiology-based PCI was better.
John MandrolaHOST
25:03
Of course, it's the only conclusion you can make from this trial.
Josh WeitzmanPANELIST
17:09
Well, and
Melanie HonigPANELIST
17:09
maybe you have a little AKI.
Juan Carlos VelezPANELIST
17:11
Yeah.
Juan Carlos VelezPANELIST
17:12
Is your patient in clinic, does the patient have chronic kidney disease? No.
Joel TopfHOST
20:28
And this is consistent with my experience.
Joel TopfHOST
20:30
My CKD stage four patients don't get hyponatremic.
Joel TopfHOST
20:33
It's that patients that are either already on dialysis that typically run hyponatremic or people that are getting real close to that or advanced AKIs, you're managing them.
Joel TopfHOST
20:44
Anybody else have any thoughts on renal failure, kidney failure?
speaker_3HOST
23:21
Well, to wrap up our deep dive today, I want to leave everyone with a broader concept to analyze on your own.
speaker_3HOST
23:27
Think back to our 68-year-old man who induced acute kidney injury simply by sweating in a 105-degree garage.
speaker_4HOST
23:33
Yeah, poor guy.
speaker_3HOST
23:34
Right.
Tim SmeetsGUEST
24:22
Only I think the important thing to To think about this for medazolam, especially this, we talked about it earlier, this last metabolite is normally radially cleared.
Tim SmeetsGUEST
24:36
And there's also some evidence, especially in AKI and CRT, this last metabolite, which is also almost 10% active.
Tim SmeetsGUEST
24:48
that can accumulate highly during AKI and on CRT.
Tim SmeetsGUEST
24:55
So probably during your midazolam infusion, you don't see this very good.
Tim SmeetsGUEST
25:02
But when you want to switch and do sedation stops and do a neurological adjustment, then it makes it very hard to make good judgments directly after your midazolam sedation stop.
Adam ShehataHOST
35:17
But was and remain amazed at how difficult it is when you have more than one patient, because in anesthesia, often we just have one patient at a time, more often, not always.
Adam ShehataHOST
35:27
then if you're a hospitalist, then if you're an emergency physician, to keep track of your patients and know what the next thing is that's coming up for them, but also when are they deteriorating? And I think if you had asked any of these physicians towards the end of this patient's care when they were clearly sick, If you had just jumped them in right away, they would have said, oh, this is a patient with sepsis or whatever the issue was and AKI, et cetera.
Adam ShehataHOST
35:49
They would have been able to deal with that in a reasonable way.
Adam ShehataHOST
35:51
But if you give them the patient three days prior and give them 29 other patients and then have them go through with limited nursing because they're always short-staffed, you can see how the situation arises.
AndrewHOST
0:04
Welcome back to the One Stem at a Time podcast, where we go through one clinical vignette at a time.
AndrewHOST
0:10
Today we're talking about acute kidney injury.
AndrewHOST
0:13
AKI is incredibly high yield because questions often give you a rise in creatinine and then ask you to determine where the problem is and what's occurring.
AndrewHOST
0:22
Is the kidney not getting enough blood flow? Is the kidney itself damaged? Or is the urine unable to get out? That gives us the classic framework of pre-renal, intrinsic, and post-renal AKI.
AndrewHOST
0:33
But before we get into those, let's start with a question.
AndrewHOST
0:40
A 72-year-old man presents to the emergency department with weakness and decreased urine output for the past two days.
AndrewHOST
1:14
Which of the following best explains this patient's renal dysfunction? Is it A, acute tubular epithelial cell injury, B, decreased renal perfusion with intact tubular function, C, immune-mediated inflammation of the renal interstitium, D, bilateral obstruction of urinary outflow, or E, immune complex deposition within the glomerulus? Take a few minutes to think about your answer.
AndrewHOST
1:45
And the correct answer is B, decreased renal perfusion with intact tubular function.
speaker_2SOUNDBITE_SPEAKER
61:39
This is perhaps the single most critical safety intervention on our entire list.
speaker_2SOUNDBITE_SPEAKER
61:44
A systematic review published in the British Medical Journal investigated cases of acute kidney injury, or AKI, in extreme endurance events.
speaker_2SOUNDBITE_SPEAKER
61:51
The researchers isolated 27 severe cases where runners suffered complete renal failure requiring hospitalization and temporary dialysis.
speaker_1SOUNDBITE_SPEAKER
61:58
27 cases?
Dennis KimGUEST
30:04
It also reduced ICU length of stay without an increased risk for renal failure or the need for renal replacement therapy.
Dennis KimGUEST
30:12
And I think the last part matters, and that's where a lot of our earlier fears were, is that if we start to diurese them too early, we might be contributing to AKI or acute kidney injury.
Dennis KimGUEST
30:23
And the FACT trial says that fear is not really something we need to worry about.
John McClellanHOST
30:27
about.All right, now how do we bring this into our clinical practice?

19 MINS LATER

Dennis KimGUEST
49:20
Certainly, patients, their ARDS may have started with a pneumonia, and certainly they're gonna be at risk for hospital-acquired or ventilator-acquired pneumonia as well.
Dennis KimGUEST
49:30
We've talked about the widespread systemic effects of ARDS.
Dennis KimGUEST
49:34
And so not surprisingly, a lot of these patients may develop an AKI.
Dennis KimGUEST
49:39
But I think the one thing that we always wanna think about is the impact on hemodynamics, because the physiologic link between our right ventricle and lung injury really impacts our ventilator choices.
AniHOST
0:20
We will be discussing another important topic in relation to the MRCP, which is when to suspect intrinsic renal disease.
AniHOST
0:32
AKI is something we frequently encounter in clinical practice.
AniHOST
0:37
Often, there's an obvious prerenal cause, such as infection, sepsis, or a postrenal cause such as urinary tract obstruction.
AniHOST
0:47
However, one of the challenges is recognizing when the problem may actually be within the kidneys itself.
Shahryar KhanGUEST
1:22
Hi, Ani.
Shahryar KhanGUEST
1:22
Thank you so much for inviting me on the podcast and happy to be here, uh, you know, back here for the second time.
AniHOST
1:29
When we approach AKI, we divide the causes into prerenal, intrinsic renal, and postrenal disease.
AniHOST
1:35
What exactly do we mean by intrinsic renal disease, and what clinical features should make us suspect an intrinsic renal cause of AKI rather than a prerenal or postrenal cause?
Lance WheelerHOST
16:10
Temperature above this range can cause cellular oxygen consumption to exceed oxygen delivery, leading to cellular dysfunction and injury.
Lance WheelerHOST
16:19
Above 107 degrees Fahrenheit, we worry about DIC, thrombosis, bleeding, cerebral edema, confusion, delirium, obtundation, seizures, coma, arrhythmias, hypoglycemia, hyperbilirubinemia, GI epithelial desquamation, endotoxin absorption, GI hemorrhage, AKI, hypoxemia, hyperkalemia, skeletal muscle cytolysis, tachypnea, metabolic acidosis, tachycardia, and hyperventilation.
Lance WheelerHOST
16:47
Environmental heat stroke and malignant hyperthermia can also cause severe rhabdomyolysis, hyperkalemia, hypocalcemia, myoglobinemia, myoglobinuria, and increased creatinine phosphokinase.
Lance WheelerHOST
17:01
I've seen plenty of true fevers in the 106.5 to 106.9 range, but I've never seen a true fever at or above 107 degrees Fahrenheit.

39 MINS LATER

Lance WheelerHOST
55:53
Water and caloric requirements increase by 7% for each 1°F or 0.6°C above normal.
Lance WheelerHOST
56:02
Most fevers are not immediately life-threatening unless temperature exceeds 107 degrees Fahrenheit or 41.6 degrees Celsius.
Lance WheelerHOST
56:10
Temperatures above 107 degrees Fahrenheit or 41.6 degrees Celsius can cause DIC, neurologic injury, arrhythmias, GI injury, AKI, mods, and death.
Lance WheelerHOST
56:21
A closed car in direct sun can exceed 120 degrees Fahrenheit or 48 degrees Celsius in less than 20 minutes when outside temperature is 75 degrees Fahrenheit or 24 degrees Celsius, and death can occur in less than an hour.

29 more episodes mention Acute kidney injury.

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