Hyperlipidemia in nephrotic syndrome

[MudPhud20XX]

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Kaplan explains this it's because the liver starts throwing out lipid to compensate the loss of protein due to nephrotic syndrome. To me this doesn't really make any sense. Lipid breakdown via beta-oxidation will generate ATP that can be used for gluconeogenesis, but w/o glucogenic amino acids, gluconeogenesis won't work. So what is the point of releasing lipid into the blood stream if you are losing your protein in nephrotic syndrome?

Can anyone explain the hyperlipidemia in nephrotic syndrome?

Many thanks in advance.

 

[Transposony]

Two mechanisms:
1. Reactive production of lipoproteins by liver in response to hypoproteinemia.
2. Decreased plasma lipoprotein lipase to catabolize lipids.
Both will lead to hyperlipidemia and lipiduria causing oval fat bodies in the urine as plasma apolipoproteins levels are also affected.

Body can't think of the logic, it can only react !

 

[ulikedaggers]

Two mechanisms:
1. Reactive production of lipoproteins by liver in response to hypoproteinemia.
2. Decreased plasma lipoprotein lipase to catabolize lipids.
Both will lead to hyperlipidemia and lipiduria causing oval fat bodies in the urine as plasma apolipoproteins levels are also affected.

Body can't think of the logic, it can only react !

I agree, though we learned in biochem that LPL is a membrane protein on the luminal surface of capillary beds. Are there also plasma isoforms?

 

[ChessMaster3000]

I agree, though we learned in biochem that LPL is a membrane protein on the luminal surface of capillary beds. Are there also plasma isoforms?

I would guess that decr apolipoprotein synthesis causes decreased activation of LPL on membrane surface (doesnt apoC activate it?), instead of directly decreasing amounts of LPL. whether or not that is what actually happens, I think that is an appropriate way to think about it for test purposes.

 

[Transposony]

I agree, though we learned in biochem that LPL is a membrane protein on the luminal surface of capillary beds. Are there also plasma isoforms?

You are right. Plasma lipase is sometimes used to describe LPL. Endothelial Lipase would be a more appropriate term.
As Chessmaster 3000 pointed out, LPL would have difficulty in doing it's job in deficiency of Apo C II & Apo E since it can't be activated and anchored to the Chylomicrons. It looks like there is both quantitative & qualitative deficiency of LPL in Nephrotic syndrome.

On a side note: Lipolysis does cause some of the LPL to dissociate from the cell surface (reason why plasma LPL is correlated with plasma free fatty acid levels).
But I don't think this is relevant for the boards.