A recent study published in Nature Medicine reveals some very interesting findings. The researchers in Alabama showed that glomerular expression of angiopoietin-like-4 (Angptl4), a secreted glycoprotein, is glucocorticoid sensitive and is highly upregulated in the serum and in podocytes in experimental models of minimal change disease and in the human disease. Podocyte-specific transgenic overexpression of Angptl4 (NPHS2-Angptl4) in rats induced nephrotic-range, and selective, proteinuria (over 500-fold increase in albuminuria), loss of glomerular basement membrane (GBM) charge and foot process effacement, whereas transgenic expression specifically in the adipose tissue (aP2-Angptl4) resulted in increased circulating Angptl4, but no proteinuria. Mice with no Angptl4 had no proteinuria.
This is exciting in many ways: This might suggest that this specific protein might be the type of nephrotic syndrome that responds to steroids, so if you have elevations of this protein in your urine or blood you have a certain nephrotic syndrome that will respond to steroids and decrease proteinuria. Lets see what this pans out in human studies. Great work by the scientists at Alabama on this breakthrough discovery. Check out the link below.
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