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Pathophysiology of nephrotic syndrome

Dec 26, 2016
A large amount of proteinuria in normal physiological conditions, the glomerular filtration membrane with a molecular barrier and charge barrier barrier effect, especially when the charge barrier damage, glomerular filtration membrane of plasma protein (with albumin based) permeability increase in protein content in urine increased, when more than the proximal tubule back to the absorption, the formation of proteinuria. On this basis, every increase in glomerular pressure and lead to high perfusion, high filtration factors (such as hypertension, high protein diet or massive infusion of plasma protein) can aggravate urinary protein excretion.

Two 、 when plasma protein changes nephrotic syndrome, a lot of albumin is lost from the urine, which promotes the compensatory synthesis of albumin in liver and increases the decomposition of renal tubule. Hypoalbuminemia occurs when albumin synthesis is not sufficient to overcome loss and breakdown. In addition, patients with nephrotic syndrome due to gastrointestinal mucosal edema leading to poor appetite, insufficient protein intake, malabsorption or loss, also aggravate hypoproteinemia.
Three, edema nephrotic syndrome when hypoalbuminemia, plasma colloid osmotic pressure decreased, so that water from the blood vessels into the interstitial space, is the basic cause of nephrotic syndrome edema. Recent studies show that approximately 50% of patients with normal or increased blood volume, plasma renin levels normal or decreased, suggesting that sodium and water retention factors of some primary in the kidney play an important role in the pathogenesis of edema in nephrotic syndrome.
Four, hyperlipidemia high cholesterol and (or) hypertriglyceridemia, serum LDL\, VLDL and lipoprotein (a) concentration increased, often with hypoalbuminemia coexist. Its mechanism is related to the increase of hepatic synthetic lipoprotein and the decrease of lipoprotein decomposition, and the latter may be more important reason for hyperlipidemia.

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