Pre-renal azotemia

[chromuffin]

Why does BUN reabsorption occur in prerenal azotemia? I think I may have read somewhere that BUN follows H2O via an unknown mechanism?

So then decreased renal blood flow leads to aldosterone release, leading to H2O reabsorption leading to BUN reabsorption leading to >15 BUN:Cr?

It's just hard for me to blindly follow that BUN is reabsorbed when H2O is reabsorbed. I need a mechanism!

---

Members don't see this ad.

 

[caxoo]

IIRC the mechanisms of absorption itself (if you're talking about transporters, specific solute gradients, etc) isn't what's important in prerenal azotemia. The mechanism to remember is that in prerenal azotemia, since reabsorption function is preserved (as opposed to the other azotemias), hypoTN -> more BUN reabsorption (in addition to Na/H2O reabsorption). It might seem like memorizing arbitrary details that you'll eventually forget, but after you run into your n-th question talking about renal function and BUN and Cr, it'll start to stick

But urea handling details about transporters and stuff might be important in other concepts, like urea recycling and establishing gradient, I just can't remember anymore lol...

 

[chromuffin]

Thank you! I do feel like it's just arbitrary facts. Understanding tubular function is intact makes sense. Thanks!