Ok so the point that is confusing me, which neither Kaplan nor EK went into detail about, is GFR. Can you explain what happens with decreased gfr step by step? All I know is that you get less urine output and more reabsorption.
With a damaged kidney, as it is in this case, how does a decreased gfr translate into fluid accumulating in the interstitium.
Is it because solute concentrations in the interstitium increase relative to the capillary, thereby increasing the fluid left in the interstitium? This doesn't really make sense though, since the capillaries would have a higher oncotic pressure.
Or is it because, like sodium, when urea is getting reabsorbed in larger quantities, water follows it. And if water is following the urea then the hydrostatic pressure (due to blood pressure) will increase? This would make sense to me in the context of an edema