A large amount of proteinuria
A large amount of proteinuria is the most important clinical manifestation of NS patients, and it is also the most basic pathophysiological mechanism of nephrotic syndrome. A large amount of proteinuria refers to the amount of urine protein excretion in adults>; 3.5g/d. Under normal physiological conditions, the glomerular filtration membrane has a molecular barrier and a charge barrier, resulting in an increase in the protein content of the original urine, which forms a large amount of proteinuria when it far exceeds the absorption of the proximal convoluted tubule. On this basis, any increase in glomerular pressure and high perfusion, high filtration factors (such as high blood pressure, high protein diet or a large amount of plasma protein infusion) can aggravate the discharge of urinary protein.
Hypoproteinemia
Plasma albumin decreased to <; 30g / L. At the time of NS, a large amount of albumin is lost from the urine, promoting the compensatory synthesis of albumin liver and the increase of renal tubular decomposition. Hypoalbuminemia occurs when the increase in liver albumin synthesis is insufficient to overcome loss and breakdown. In addition, patients with NS due to gastrointestinal mucosal edema caused by diet, insufficient protein intake, malabsorption or loss, is also a cause of aggravation of hypoalbuminemia. In addition to plasma albumin reduction, certain immunoglobulins (such as IgG) and complement components, anticoagulant and fibrinolytic factors, metal-binding proteins and endocrine-binding proteins in plasma can also be reduced, especially large amounts of proteinuria, glomeruli. Significant pathological damage and non-selective proteinuria are more pronounced. Patients are prone to complications such as infection, hypercoagulability, trace element deficiency, endocrine disorders and immune dysfunction.any question , you can contact with us
emai:fatimahmomo@gmail.com
whatsapp:008613048787911
Edema In the NS,
hypoalbuminemia and plasma colloid osmotic pressure decrease, so that water enters the interstitial space from the vascular lumen, which is the basic cause of NS edema. Recent studies have shown that about 50% of patients with normal or increased blood volume, plasma renin levels are normal or decreased, suggesting that some of the primary in the kidney sodium, water retention factors play a role in the mechanism of NS edema.
Hyperlipidemia
The cause of NS with hyperlipidemia has not yet been fully elucidated. High cholesterol and/or hypertriglyceridemia, increased concentrations of LDL, VLDL, and lipoprotein (α) in serum, often coexisting with hypoproteinemia. Hypercholesterolemia is mainly due to an increase in hepatic synthetic lipoproteins, but a reduction in decomposition in the peripheral circulation also plays a part. Hypertriglyceridemia is mainly caused by catabolic disorders, and increased liver synthesis is a secondary factor.
A large amount of proteinuria is the most important clinical manifestation of NS patients, and it is also the most basic pathophysiological mechanism of nephrotic syndrome. A large amount of proteinuria refers to the amount of urine protein excretion in adults>; 3.5g/d. Under normal physiological conditions, the glomerular filtration membrane has a molecular barrier and a charge barrier, resulting in an increase in the protein content of the original urine, which forms a large amount of proteinuria when it far exceeds the absorption of the proximal convoluted tubule. On this basis, any increase in glomerular pressure and high perfusion, high filtration factors (such as high blood pressure, high protein diet or a large amount of plasma protein infusion) can aggravate the discharge of urinary protein.
Hypoproteinemia
Plasma albumin decreased to <; 30g / L. At the time of NS, a large amount of albumin is lost from the urine, promoting the compensatory synthesis of albumin liver and the increase of renal tubular decomposition. Hypoalbuminemia occurs when the increase in liver albumin synthesis is insufficient to overcome loss and breakdown. In addition, patients with NS due to gastrointestinal mucosal edema caused by diet, insufficient protein intake, malabsorption or loss, is also a cause of aggravation of hypoalbuminemia. In addition to plasma albumin reduction, certain immunoglobulins (such as IgG) and complement components, anticoagulant and fibrinolytic factors, metal-binding proteins and endocrine-binding proteins in plasma can also be reduced, especially large amounts of proteinuria, glomeruli. Significant pathological damage and non-selective proteinuria are more pronounced. Patients are prone to complications such as infection, hypercoagulability, trace element deficiency, endocrine disorders and immune dysfunction.any question , you can contact with us
emai:fatimahmomo@gmail.com
whatsapp:008613048787911
Edema In the NS,
hypoalbuminemia and plasma colloid osmotic pressure decrease, so that water enters the interstitial space from the vascular lumen, which is the basic cause of NS edema. Recent studies have shown that about 50% of patients with normal or increased blood volume, plasma renin levels are normal or decreased, suggesting that some of the primary in the kidney sodium, water retention factors play a role in the mechanism of NS edema.
Hyperlipidemia
The cause of NS with hyperlipidemia has not yet been fully elucidated. High cholesterol and/or hypertriglyceridemia, increased concentrations of LDL, VLDL, and lipoprotein (α) in serum, often coexisting with hypoproteinemia. Hypercholesterolemia is mainly due to an increase in hepatic synthetic lipoproteins, but a reduction in decomposition in the peripheral circulation also plays a part. Hypertriglyceridemia is mainly caused by catabolic disorders, and increased liver synthesis is a secondary factor.
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