Tuesday, July 31, 2012

Clinical Case 59: Answers and Summary


In nephrotic syndrome(albumin 2-3 range), VLDL produced by the liver are rapidly metabolized so that the LDL concentrations rise whereas VLDL remain normal (13%)
Cholesterol increases but TG remain normal(30%)
With severe nephrotic syndrome, < albumin 1.0g/dl, VLDL accumulate and LDL decline and TG start rising (21%)
When proteinuria is massive, the apoprotein CII are lost and contribute to accumulation of VLDL as well (43%)
No consistent pattern of HDL serum conceontrations has been identified in nephrotic syndromes(26%)

Under normal circumstances, VLDL produced by the liver is hydrolyzed to IDL and HDL by lipoprotein lipases situated in a number of extrahepatic sites including endothelium and adipose tissue.  IDL then gets converted to LDL by the liver. In nephrotic syndromes with moderate hypoalbuminemia (2-3g/dl), VLDL produced by the liver is rapidly metabolized so that the LDL concentrations rise whereas VLDL remain relatively normal.  Cholesterol increases and TG might stay normal.  With severe hypoalbuminemia(<1g/dl), VLDL accumulate and LDL concentrations fall and hence TG rise higher.  This might be because inhibition of lipoprotein lipase is seen by free fatty acids that normally bind to albumin and accumulate in adipose tissue as albumin falls. When there is massive amounts of proteinuria, apoprotein CII, a normal component of VLDL and stimulator of lipoprotein lipase may also contribute in accumulation of VLDL. 
What about HDL? Since HDL have molecular sizes comparable to albumin, it may be reduced in nephrotic syndrome due to urinary losses. Also, accumulation of unbound lysolecithin may decrease the synthesis of HDL. Even with these two mechanisms, one would predict low HDL levels but mixed patterns have been noted in nephrotic syndromes. 

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