Clinical manifestations of nephrotic syndrome

The basic features of NS are massive proteinuria, hypoproteinemia, edema, and hyperlipidemia, a group of clinical syndromes characterized by the so-called "three highs and one low" and other metabolic disorders.
1. massive proteinuria
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 albuminuria refers to the amount of >3.5g/d excreted by adult urine. Under normal physiological conditions, the glomerular filtration membrane has a molecular barrier and a barrier to electricity, resulting in an increase in protein content in the urine and a large amount of proteinuria when the absorption capacity of the proximal convoluted tubule is much higher than that of the proximal tubule. On this basis, all factors that increase glomerular pressure and lead to high perfusion and high filtration, such as hypertension, high protein diet or massive infusion of plasma proteins, can increase urinary protein excretion.
2. hypoproteinemia
Plasma albumin decreased to <30g/L. At NS, large amounts of albumin are lost from urine, contributing to albumin, hepatic compensatory synthesis and increased renal tubular decomposition. Hypoalbuminemia occurs when albumin synthesis in the liver increases and is insufficient to overcome loss and breakdown. In addition, NS patients due to gastrointestinal mucosal edema leading to poor appetite, insufficient protein intake, malabsorption or loss, also aggravate hypoproteinemia.
Besides the reduction of plasma albumin, some plasma immunoglobulin and complement components (such as IgG), anticoagulation and fibrinolytic factors, metal binding proteins and endocrine hormone binding protein can also be reduced, especially the large amount of proteinuria, glomerular pathological damage and non selective proteinuria is more significant. Patients are prone to infection, high coagulation, lack of trace elements, endocrine disorders and immune dysfunction.

3. edema
At NS, hypoalbuminemia and the decrease of plasma colloid osmotic pressure cause the water to enter the interstitial space from the lumen of the blood vessel, which is the basic cause of NS edema. Recent studies have shown that approximately 50% of patients have normal or increased blood volume and normal or decreased plasma renin levels, suggesting that certain primary sodium and water retention factors play a role in the pathogenesis of NS edema.
4. hyperlipidemia
The reason why NS is associated with hyperlipidemia has not yet been fully elucidated. High cholesterol and / or hypertriglyceridemia, increased concentrations of LDL, VLDL, and lipoprotein (alpha) in serum, often coexisting with hypoproteinemia. Hypercholesterolemia is mainly caused by increased lipoprotein synthesis in the liver, but reduced catabolism in the surrounding circulation also plays a part. Hypertriglyceridemia is mainly caused by catabolism, and liver synthesis is a secondary factor.