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submitted by โˆ—brolycow(33)
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He has heart failure which leads to a decrease in renal blood flow and prerenal azotemia. In prerenal azotemia, BUN:Cr ratio is >= 20; Activation of the RAAS system due to the prerenal azotemia means that the spec grav is high at 1.025 and he is holding onto sodium so urinary sodium will be low (<20, FENa <1%).

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figprincess  did you figure out the the ratio by actually divding out the numbers since the q didn't give it as a ratio? also what resource tells us what prerenal spec gravity should be? +
brolycow  I just usually remember from class that spec grav 1.001-1.010 is considered dilute urine, and anything 1.025 and above is concentrated. For this question specifically, I think I remember there only being one option that even had the ratio >=20, all of the others were like 15 or less, so just have to rule them out. +10
benzjonez  Very helpful video for acute kidney injury: https://www.youtube.com/watch?v=bMp6IxDKK2Q +11
notadoctor  Another explanation that helped me is that inability to concentrate the urine means something is wrong with the kidneys. If you have dilute urine, or the spec gravity is between 1.001-1.010 in someone with low urine output it suggests something is wrong with the concentration mechanisms of the kidney. Because this person had congestive heart failure we were already looking for something that matched up with prerenal azotemia so we can pretty much get rid of all the answer choices that suggest other azotemias. Then finally to get the precise answer I looked at the BUN/Cr ratio which you would expect to be high(>= 20). +
mikay92  Would fully recommend the OnlineMedEd video on AKI. Goes through the differential, lab results, treatment, etc in a very clear and concise manner. +
drdoom  @mikay92 is this the OnlineMedEd video you're referring to? -> https://youtu.be/EWFgzVtMN50 +1
drdoom  aha! there is an updated AKI video but you need an OnlineMedEd (free) account to view it: https://onlinemeded.org/spa/nephrology/acute-kidney-injury/acquire +
popofo  I understand that BUN:Cr > 20 if renal perfusion is repaired, but in heart failure wouldn't there be increased secretion of ANP/BNP from the atria that pushes up the sodium excretion? +
an1  what about ANP/ BNP? if CHF is present won't these down regulate RAAS, leading to less ADH and a more dilute urine? I understand this q says the urine output has decreased so this wouldn't be the case here. But when would we know that they want the ANP/BNP theory? +



 +1  upvote downvote
submitted by lostdinosaurs(1)
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Hey can someone explain the renal findings? Physio is definitely not my strong suit.

Is it because he has fluid/Na+ retention that his specific gravity and Na+ are so low? Is there a reason for those specific BUN/creatinine over the others?

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brolycow  He has heart failure which leads to a decrease in renal blood flow and prerenal azotemia. In prerenal azotemia BUN/Cr ratio is >= 20; Activation of the RAAS system due to the prerenal azotemia means that the spec grav is high at 1.025 and he is holding onto sodium so urinary sodium will be low (<20, FENa <1%). +7
mousie  Agree with above, HF and not taking meds would increase or activate RAAS = increase ATII and Aldosterone which leads to body retaining Na and H2O so the urine concentration of Na will be low and the urine will be very concentrated i.e. high SG. I didn't think about the BUN:Cr > 20 but this would have also narrowed it down! +2



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submitted by โˆ—haozhier(23)
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I chose C because I thought it has been four weeks so it must have been acute tubular necrosis. Can anyone explain? Thanks!

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miriamp3  @haozhier if you are deciding to think that he had a ATN because of the 4 weeks.. then he should be by now in the recovery phase(polyuria, Bun/cr fall) But he is with HF and his urine output has progressively decrease. So AKI prerenal HF Bun/cr >20. the only one is D. Don't get confused with the rest of the information. +
jesusisking  I thought the same thing so chose C as well! +



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submitted by โˆ—imgdoc(183)
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If you were like me and were thinking that this is acute tubular necrosis because the UW tables/FA passage mention HF as a cause of ATN, then read below.

You have to understand that acute kidney injury exists on a spectrum when it comes to renal blood flow decreases. If you have a patient who is oliguric and who has had renal blood flow loss (due to excessive diuretic overuse, HF, hemorrhage, ischemia of basically any cause) the first thing to happen is PRERENAL AZOTEMIA. Afterwards, you progress to acute tubular necrosis, where you will get the classic decreases urine osmolality, urine Na+ decreases, FeNa+ increase, and serum BUN/Cr decreases.

Remember this is a spectrum for renal blood flow decreases, the more severe the more chances it will progress to ATN. In this case, its prerenal azotemia, so only choice D makes sense.

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submitted by โˆ—handsome(3)
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fa 2020 pg 601 tHERE'S a table about values . exemplified by the question and the etiology of pre renal azothemia as seen in the patient -HF.

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