Ant79 Forum Newbie
Topics: 2 Posts: 12
| | 04/22/08 - 01:11 AM  
 
   
 
|   #1 |
Please, explain why in nephritic syndrome there isn't significant proteinuria? If the glomerular filter permeable for RBCs it must be permeable for plasma and urine has to contain a lot of protein, isn't it? Thanks in advance.
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| mukho Forum Elite
Topics: 6 Posts: 300
| | 04/22/08 - 05:46 AM  
 
   
 
|   #2 |
not sure but maybe because the gross proteiuria seen in nephrotic is caused by the loss of negative charge on the basement membrane rather than just increased size of pores (which actually are large enuff to let albumin pass anyways) This is in contrast to nephritis where basement membrane damage from inflammation and immune complex deposition cause large defects to form, thru which RBC can pass but as the negative charge of basement membrane is intact it successfully repulses the negatively charged albumin....there seems to be a lot of controversy regarding pathogenesis of hematuria and especially proteinuria in various renal pathology...if u have the energy, u could skim thru the artical below, pretty detailed...sorry for not having a more definitive ans, but very interesting question! http://www.nature.com/ki/journal/v63/n3/full/4493...
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| drshvetasm Forum Elite
Topics: 19 Posts: 232
| | 04/22/08 - 06:08 AM  
 
   
 
|   #3 |
i agree with mukho, i think she's right...i its the whole charge business causing proteinuria in nephrotic against nephritic
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| Ant79 Forum Newbie
Topics: 2 Posts: 12
| | 04/22/08 - 08:44 AM  
 
   
 
|   #4 |
[mukho] Your explanation looks like logical, but membrane of normal RBCs has negative charge too.
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| mukho Forum Elite
Topics: 6 Posts: 300
| | 04/22/08 - 08:58 AM  
 
   
 
|   #5 |
yeah ur right bout that...there has to be some other basic explanation but i really cant think of one...will search and let u know if i find anything....weird i never thought of it when i was studying real good question though!
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| Ant79 Forum Newbie
Topics: 2 Posts: 12
| | 04/24/08 - 11:18 AM  
 
   
 
|   #6 |
I haveŃ an idea. In inflammation the hyperfibrinogenemia causes change of negative charge of RBCs (that is why ESR is increased). So they can pass through glomerular membrane (its charge remains negative), but not proteins, which still have negative charge. What do you think?
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