Pre-renal AKI: Diagnosis and Treatment

00:01 So, when our patients present to us with a pre-renal picture, we want to really be able to diagnose them.

00:08 We wanna be able to do our diagnostic workup.

00:11 So, as a good detective as we are as internist, we're going to want to take our patient history and chart review and really look and see if that patient has had any significant history consistent with this.

00:22 Have they been having emesis, diarrhea, things that would make us think about a gastroenteritis, any history of GI bleeding, or do they have a known history or are we diagnosing them with heart failure, liver failure or portal hypertension and sepsis.

00:39 On physical exam, there's some signs that can be very helpful to us.

00:43 Does our patient have orthostatic hypotension or skin tenting, dry mucous membranes? These tells us that the likelihood of hypovolemia is very high.

00:52 How about our patients who have a low effective arterial blood volume but their total ECF is expanded? These are our edematous states.

00:59 This is a beautiful picture of our patients, who have heart, a patient with heart failure who has an elevated jugular venous pressure.

01:07 That's really indicative of a patient having something like heart failure.

01:12 So, how about a laboratory workup? It's important for us to look, there are some clues that are very simple on labs that can help us to determine whether our patient might be more suggestive of a pre-renal hit.

01:26 This includes looking at our BUN and creatinine and the BUN to creatinine ratio.

01:32 So when we see a BUN to creatinine ratio of greater than 20 to 1, then that really indicates that perhaps this patient has a pre-renal hit.

01:41 And a reason why that happens is because remember, this is a reversible injury, our tubules are still working.

01:47 And because you have a reduction in GFR, you've got stasis of urine, so you're really able to reabsorb more urea and so you tend to have a higher BUN to creatinine ratio.

02:00 The urine osmolality tends to be high - greater than 500 mosm/kg.

02:04 Why is this? We just said that remember, autoregulation is really helping us by enacting ADH.

02:12 We wanna conserve our volume as much as possible.

02:15 So ADH is going to be active allowing us to reabsorb waterin order to expand that vascular space and in so doing, leaves us with a very high urine osmolality.

02:25 Our urine sodium is going to be very low as well as urine chloride.

02:29 Why is that? Because remember, we just talked about how the RAAS system, Renin-Angio-Aldo system is activated.

02:37 Angio II is activating not only at the efferent arteriole but also, it's having an effect on increase in sodium reabsorption.

02:45 Aldosterone is being activated in order to increase sodium reabsorption and again we're doing this so that we can really preserve our vascular volume, leaving us with a very low urine sodium chloride.

02:57 On urine analysis, we'll see a high specific gravity, no protein or blood or white blood cells.

03:04 And as a nephrologist, when you have me consult on your patient, then I will actually look at the urinary sediment and I will see that it shows nothing significant, there are no casts and no cellular activity.

03:18 And just aside so you'd understand what that means is that, when patients develop any kind of kidney injury, it's important for a nephrologist to take a look at that urinary sediment underneath the microscope.

03:29 There are so many different clues that are very helpful on the diagnosis of a lot of different diseases.

03:35 So essentially, we take 10 ml of urine, we spin it in a centrifuge at 3000 rpm, we then take the supernatant, decant it and then resuspend that pallet and using a transfer pipette, we can look at that underneath the microscope at both 10x and 40x magnification.

03:56 And there are many clues in there whether they are casts or cells that can lead us to a correct diagnosis with our patients.

04:06 Another helpful test in the diagnosis of our patients with pre-renal disease is something called the fractional excretion of sodium or FENa.

04:14 FENa measures the percent of filtered sodium excreted in the urine and it's really used to differentiate between pre-renal disease and acute tubular necrosis.

04:24 And I wanna just take a moment to really underscore that and say that one more time, it's used to differentiate between pre-renal disease and acute tubular necrosis.

04:33 It is not used to differentiate between pre-renal disease and all intrinsic renal diseases or post-renal.

04:40 It is really just between pre-renal and ATN, so please keep that in mind when you're using this formula.

04:47 It's estimated by simultaneously obtaining the urine and plasma specimens of sodium and creatinine and you can see the formula there in which we use in order to actually obtain FENa.

04:58 But really what's important for you is to understand that a FENa of less than 1% in pre-renal diseases indicates that the patient most likely will be responsive to volume or correcting their hypovolemic state.

05:14 A FENa that's greater than 2% is going to be most common in ATN and we're going to talk about that in just a moment.

05:22 Another thing to keep in mind is that this is best to use when patients are oliguric because that's really what this test was predicated on when it was first developed.

05:32 So, when our patient comes to us and we've diagnosed them with pre-renal disease, how do we treat our patients in order to return their kidney function back to normal? In a sense of true volume depletion, it's fairly easy and intuitive.

05:45 We simply want a volume expand them and we can do this if they have true volume depletion with a crystalloid, something that's isotonic to their osmolality.

05:54 So normal saline would be great or lactated Ringer's which is a little bit more physiologic.

05:59 We can use both of those fluids to correct their hypovolemia.

06:02 In a situation where our patient has a decrease in effective arterial blood volume, remember that's those edematous states that we were talking about earlier.

06:11 It's really important to target the underlying condition.

06:15 So in this situation of our patient who has heart failure, we really wanna correct their cardiac hemodynamics and we can do this with diuretics and if our patient is so volume overloaded with their heart failure, that they're off of the Starling curve, the heart really can't pump effectively, we can actually mobilize volume off their body with diuretics and we can actually get an increase in the ejection fraction.

06:38 So that can be very helpful.

06:40 We wanna perhaps treat those patients with vasodilators and afterload reducers.

06:44 And again, if our patient has an organ perfusion that's impaired, using something like inotropes would be very important.

06:52 In our patients who have portal hypertension and liver failure, we wanna provide them with some kind of oncotic pressure like albumin in order to help again with renal artery perfusion.

07:02 Because they have splanchnic dilatation and they have a decrease in peripheral vascular resistance, it's also important to use things like midodrine or norepinephrine if our patients are in the ICU and that really helps with their systemic hemodynamics.

07:16 And then finally in our septic patients, we really wanted to treat them with goal-directed therapy.

07:21 So we want to volume resuscitate them with crystalloid usually at 30ml/kg within the first 3 hours and then we want to use broad spectrum antibiotics and vasopressor support in order to again support their hemodynamics and increase renal artery perfusion.

07:36 Okay, so we just finished pre-renal disease and the take home points that I'd like you to remember is that this is a reversible injury that can get better once you increase renal perfusion back to the normal state either with volume or by correcting the underlying cause.