How serious is nephrotic syndrome? What are the symptoms of nephrotic syndrome?

The kidneys are important organs in the human body. If there is a problem with the kidneys, it will affect the patient's physical health in many aspects and even affect the patient's sexual life. Therefore, nephrotic syndrome is a relatively serious disease. The main symptoms of nephrotic syndrome are: massive proteinuria, hypoproteinemia, edema, and hyperlipidemia. If these symptoms occur, active treatment is necessary to relieve the pain.

1. Heavy proteinuria

Heavy proteinuria is the main clinical manifestation of NS patients and the most basic pathophysiological mechanism of nephrotic syndrome. Heavy proteinuria refers to urine protein excretion >3.5 g/d in adults. Under normal physiological conditions, the glomerular filtration membrane has molecular barriers and charge barriers, which cause the protein content in the primary urine to increase. When it far exceeds the amount of reabsorption by the proximal tubule, a large amount of proteinuria is formed. On this basis, any factors that increase intraglomerular pressure and lead to hyperperfusion and hyperfiltration (such as high blood pressure, high-protein diet or large-scale infusion of plasma protein) can aggravate the excretion of urinary protein.

2. Hypoproteinemia

Plasma albumin dropped to <30 g/L. In NS, a large amount of albumin is lost in the urine, which promotes the increase of compensatory albumin synthesis in the liver and renal tubular decomposition. Hypoalbuminemia occurs when the increase in hepatic albumin synthesis is insufficient to overcome loss and breakdown. In addition, NS patients may suffer from gastrointestinal mucosal edema, which leads to decreased diet, insufficient protein intake, malabsorption or loss, which also aggravates hypoalbuminemia.

In addition to the decrease in plasma albumin, certain plasma immunoglobulins (such as IgG) and complement components, anticoagulant and fibrinolytic factors, metal-binding proteins and endocrine-binding proteins may also decrease, especially when there is massive proteinuria, severe glomerular pathological damage and non-selective proteinuria. Patients are prone to complications such as infection, hypercoagulability, trace element deficiency, endocrine disorders and immune dysfunction.

3. Edema

In NS, hypoalbuminemia and decreased plasma colloid osmotic pressure cause water to enter the tissue space from the vascular cavity, which is the basic cause of NS edema. Recent studies have shown that about 50% of patients have normal or increased blood volume and normal or decreased plasma renin levels, suggesting that certain factors originating from sodium and water retention in the kidney play a certain role in the pathogenesis of NS edema.

4. Hyperlipidemia

The cause of NS combined with hyperlipidemia has not yet been fully elucidated. Hypercholesterolemia and/or hypertriglyceridemia, increased serum LDL, VLDL and lipoprotein (α) concentrations, often coexist with hypoproteinemia. Hypercholesterolemia is primarily due to increased lipoprotein synthesis in the liver, but decreased breakdown in the peripheral circulation also plays a part. Hypertriglyceridemia is mainly caused by metabolic disorders, with increased hepatic synthesis as a secondary factor.