I was hoping I could ask you a few questions. I’m finding there is a lottttt of contradictory information.
- According to starling forces, decreased plasma oncotic pressure should increase GFR, but according to nephrotic syndrome, decreased albumin will cause edema and overall decrease GFR. Which one should I believe?
- In general, it’s said that AT2 at low levels dilates the afferent arteriole to increase GFR, but at high level it constricts both efferent and afferent to decrease GFR. However, the SNS, which stimulates renin, constricts all arterioles in the body as well as activates the RAAS system. How does that work? Is the SNS more immediate until the aldosterone system is ready to say okay go ahead and dilate the afferent I’m ready to take up the water anyway?
- This is a very basic question but sometimes I have moments of self doubt and this is one of them: So we always say edema is fluid buildup in ISF due to increased hydrostatic or decreased oncotic pressure (like nephritic syndrome hypoalbumineia) right? So why does fluid build up in ISF as opposed to go inside the cell where I guess technically there is more stuff to pull it in?
- How does K suppress ammonia genesis?
Thank you very much!
Nephrotic syndrome and GFR. Don’t connect those neurons. Proteinuria does not cause an immediate and hemodynamic change in GFR that is clinically meaningful. Yes, you are right that lower oncotic pressure should increase GFR, but those increases in GFR will be trimmed by tubuloglomerular feedback so that in the end there is not a meaningful change in GFR. Likewise the nephrotic syndrome will cause fluid to leak from the blood vessels decreasing effective circulating volume lowering renal plasma flow. However, once again these changes in volume are small enough that the kidney easily compensates with changes in AT2, PGE, filtration fraction, etc so that GFR remains stable.
Over a long time, proteinuria causes chronic kidney disease and decreases renal function, but not by the mechanisms you described.