What is the role of lipid metabolism in the pathophysiology of pediatric nephrotic syndrome?

Updated: Mar 04, 2020
  • Author: Jerome C Lane, MD; Chief Editor: Craig B Langman, MD  more...
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INS is accompanied by disordered lipid metabolism. Apolipoprotein (apo)-B–containing lipoprotein levels are elevated, including very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL), and lipoprotein(a), with resultant increases in total cholesterol and LDL-cholesterol. The level of high-density lipoprotein (HDL) cholesterol is normal or low. Elevations in triglyceride levels occur with severe hypoalbuminemia.

The traditional explanation for hyperlipidemia in INS was the increased synthesis of lipoproteins that accompany increased hepatic albumin synthesis due to hypoalbuminemia. However, serum cholesterol levels have been shown to be independent of albumin synthesis rates.

Decreased plasma oncotic pressure may play a role in increased hepatic lipoprotein synthesis, as demonstrated by the reduction of hyperlipidemia in patients with INS receiving either albumin or dextran infusions. Also contributing to the dyslipidemia of INS are abnormalities in regulatory enzymes, such as lecithin-cholesterol acyltransferase, lipoprotein lipase, and cholesterol ester transfer protein. [32, 33]

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