kidney question

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Hordin

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Why, if there is increased permeablility of the glomereolus to plasmaproteins, will edema (overload of fluid in tissue) result? I would have thought that there would just be an increase in urine volume to balance out the increased solute that is now in the filtrate (i.e. lower reapsorbtion).

Also, is low osmolarity the same thing as hypotonic?

Thanks!!!
AHHHH 1 week....🙂
 
Why, if there is increased permeablility of the glomereolus to plasmaproteins, will edema (overload of fluid in tissue) result? I would have thought that there would just be an increase in urine volume to balance out the increased solute that is now in the filtrate (i.e. lower reapsorbtion).

Also, is low osmolarity the same thing as hypotonic?

Thanks!!!
AHHHH 1 week....🙂


First, lowER osmolarity = hypotonicity .. they are relative measures. B/t 2 things the lower is HYPO and the higher is HYPER...

For ur glomerular Q, do you mean that plasmaproteins are EVER permeable to the endothelial membrane?? I thought they were NOT hence they importance as osmoregulators???
 
Remember that proteins play a very important part in maintaining oncotic pressure. This is the pressure that opposes hydrostatic pressure (which pushes fluid out of capillaries) and causes reabsorption to occur.

If you lose plasma proteins due to kidney damage and increased permeability, then you're losing proteins. So, the hydrostatic pressure remains the same (because most of the fluid filtered is reabsorbed) but the oncotic pressure decreases. If oncotic pressure decreases, there's less of a reabsorptive force. And if there's less reabsorptive force, fluid stays in the interstitial space rather than being reabsorbed into the capillaries. Thus, you get edema (which is the accumulation of fluid in interstitial spaces). Hope this helps.

Edit: Bernoulli, you're right that normally, plasma proteins do not get filtered. Various pathologies can cause an increase in the permeability to proteins though.
 

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