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Pathophysiology of nephrotic syndrome

Jan 31, 2017

As the permeability of the glomerular filtration membrane changes, the protein swim through the increase in the formation of large amounts of proteinuria. Glomerular filtration membrane permeability changes, in addition to pathological changes, but also with the glomerular epithelial cell membrane surface charge changes. Normal membrane surface protein sialic acid, with a negative charge, and albumin molecules in ph7.4 on the negatively charged, due to homosexual repulsion, so that albumin is not easy filtration, simple nephrotic protein decreased sialic acid. Thereby increasing the protein filtration.

A large number of proteinuria leading to hypoproteinemia, especially albumin decreased plasma colloid osmotic pressure, water and electrolyte leakage from the blood vessel to the interstitial space, coupled with increased secretion of secondary aldosterone, antidiuretic hormone secretion increased. Reduced natriuretic factor and other factors, further aggravating edema.

Hypercholesterolemia, the main reason is due to increased liver compensatory synthesis, followed by reduction of lipoprotein catabolism.

The disease has a variety of pathological types, of which the most common small lesions (about 80%); simple nephropathy is mainly of this type, followed by focal segmental glomerulosclerosis and membranoproliferative glomerulonephritis. A few were mesangial proliferative or membranous nephropathy, such lesions more performance for nephritis nephropathy.

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