PART1: What You Need To Know About Nephrotic Syndrome

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1. What is Nephrotic Syndrome?

Answer: Nephrotic syndrome is a disease mainly caused by glomerular basement membrane disease due to various reasons, and it is a group of symptoms manifested in glomerular diseases. It is characterized by a marked increase in the permeability of the glomerular capillary walls to plasma proteins. With or without glomerular inflammatory changes. (Hematuria, proteinuria, leukocyte casts, renal insufficiency.

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2. What are the clinical manifestations of nephrotic syndrome?

A: The main manifestations are high body edema, severe proteinuria (≥3.5 g/24 hours), hyperlipidemia, and hypoproteinemia.

(1) Edema: Part of the reason is that due to the decrease in the osmotic pressure of the glue, the hydrostatic pressure of the surrounding capillaries exceeds the osmotic pressure of the glue so that the liquid enters the tissue, and the secondary effective blood volume decreases; the latter increases the sodium and water retention through a compensatory mechanism, but the actual 50 % of patients with normal or increased blood volume, plasma renin at low levels, suggesting that nephrotic syndrome may be related to primary renal sodium retention. The edema mechanism of this disease may be multi-factorial. In different types of lesions, different stages, or different degrees of nephrotic syndrome, there may be different mechanisms or several mechanisms involved, and the sodium-water regulation dysfunction of nephropathy itself may be edema's main reason.

(2) Massive proteinuria: proteinuria within a fixed range generally indicates diffuse glomerular disease.

(3) Hyperlipidemia: Hyperlipidemia in nephrotic syndrome is inversely proportional to the amount of plasma albumin. Blood total cholesterol, free cholesterol, and cholesterol lipids were all increased; triglycerides were generally increased in marked hypoproteinemia; plasma very low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and lipoproteins could be increased in the early stage, but in severe lesions, the increase in VLDL is more obvious. Therefore, chyle in nephrotic syndrome often indicates severe hypoproteinemia. In most nephrotic syndromes, HDL is mostly low. Age, nutritional status, obesity, and comorbidities such as diabetes can affect blood lipids. Hyperlipidemia and hyperlipoproteinemia in nephrotic syndrome are mainly due to increased hepatic synthesis of lipids and lipoproteins, slowed catabolism, and increased lipid depot mobilization. Hyperlipidemia in nephrotic syndrome is the combined result of several disorders along the entire lipid metabolism pathway.

The main risk of hyperlipidemia is cardiovascular disease. Whether there is a high-risk state of cardiovascular disease in nephrotic syndrome depends on the persistence of hyperlipidemia and the level of the protective lipoprotein HDL in the blood

⑷Hypoproteinemia: The normal human liver synthesizes about 12~14 grams of albumin (130~200mg/kg) every day, which is equivalent to the amount of decomposition in the body, of which 10% is metabolized in the kidneys. In nephrotic syndrome, intrarenal metabolism can be increased by 16 to 30%, and the amount of compensatory protein synthesis in the liver can be increased by at least 2 to 3 times. But in fact, liver compensation is often limited by various factors, such as age malnutrition, and liver disease. Therefore, dietary protein intake often has an important effect on plasma protein. Because patients with hypoalbuminemia nephrotic syndrome are very sensitive to blood volume loss, shock and prerenal azotemia can be caused by a small amount of fluid loss, such as the application of diuretics, gastrointestinal and minor surgical procedures. Hypoalbuminemia can increase drug toxicity and increase free drug concentration, even at conventional doses, which can produce toxic reactions. In hypoalbuminemia, the binding of arachidonic acid and plasma albumin is reduced, thereby promoting platelet aggregation and thromboxane TXA2 increase, the latter can aggravate proteinuria and renal damage.

(5) Lipiduria: There are three forms of lipids in the urine of nephrotic syndrome: free fat droplets, fat casts, and oval greasy meridian bodies contained in deciduous epithelial cells. Lipiduria formation and urinary protein excretion are parallel regardless of lipid levels.

3. The etiology and classification of nephrotic syndrome.

Answer: According to its pathogenesis, it is divided into primary and secondary.

(1) Primary disease that originates in the glomerulus. Two-thirds of adults and most children fall into this category. Mainly minimal change nephropathy, membranous nephropathy, mesangial capillary proliferative nephritis. Other primary glomerular diseases that often manifest as acute and chronic nephritic syndrome, such as mesangial proliferative nephritis, focal proliferative nephritis, capillary proliferative nephritis, capillary endothelial proliferative nephritis, and crescentic nephritis, can also manifest as Nephrotic syndrome. In patients over the age of 45, care must be taken to exclude possible associated malignancies, such as small-change nephropathy with Hodgkin's disease, and membranous nephritis with solid tumors of the lung, breast, and gastrointestinal tract.

(2) There are many causes of secondary nephrotic syndrome, common in diabetic nephropathy, renal amyloidosis, systemic lupus erythematosus nephritis, a nephrotic syndrome caused by new organisms and drug infections, 1/3 of adults and 10% of children belong to such.

4. What are the TCM categories of nephrotic syndrome and the etiology and pathogenesis of TCM?

Answer: According to the manifestation, course, and outcome of this disease, it belongs to the category of "edema" in traditional Chinese medicine.

Etiology: Internal lung, spleen, and kidney dysfunction. Covering water is the ultimate yin, and its origin is in the kidneys; water is transformed into qi, and its target is in the lungs; water only fears the earth, and its regulation is in the spleen. If the lungs are deficient, the qi will not transform into water, but if the spleen is deficient, the soil will not control water but will attack it. , is an important external cause of the disease.

Pathogenesis: positive and false evil. Positive deficiency mainly includes spleen-kidney qi deficiency, spleen-kidney yang deficiency, liver-kidney yin deficiency, and both qi and yin deficiency; Some physicians believe that although the pathogenesis of the nephrotic syndrome is most closely related to the deficiency of the three viscera of the lung, spleen and kidney, especially yang deficiency of the spleen and kidney is an important link in the formation of the mechanism of the disease. The basic principle.

5. What are the complications of nephrotic syndrome?

Answer: (1) Hypercoagulation and renal vein thrombosis: Hypercoagulation is mainly due to changes in blood coagulation factors. The incidence of renal vein and peripheral pulmonary vein thrombosis is about 10 to 40%. Patients with the acute form may present with sudden onset of low back pain, hematuria, leukocyturia, increased proteinuria, and decreased renal function. Patients with chronic models may be asymptomatic, but renal stasis after thrombosis often aggravates nephrotic syndrome. Due to thrombus shedding, extrarenal embolism symptoms are common, pulmonary embolism may occur, and renal tubular dysfunction may also be accompanied, such as glycosuria, aminoaciduria, and renal tubular acidosis. A clear diagnosis of renal arteriovenous angiography, radiographic chiral nephrogram, and CT are helpful for diagnosis. Increased plasma β-lipoprotein often indicates thrombosis; increased blood α2 fibrin is also considered to be a sign of renal vein thrombosis. Urinary fibrin degradation products (FDP) generally only indicate changes in glomerular permeability and have no significant relationship with renal blood stasis.

The prognosis of renal vein thrombosis depends on the degree of renal damage of the primary disease, recanalization of the blood vessels, and the formation of collateral circulation. After acute thrombosis, surgery is required to remove the thrombus, and anticoagulation therapy needs to be carried out for a long time. Dosage should be carefully controlled. Hormone therapy can exacerbate hypercoagulability

(2) Acute renal failure with nephrotic syndrome

(3) Renal tubular dysfunction (more common in children), is often manifested as glycosuria, aminoaciduria, hyperphosphatemia, renal tubular potassium loss, and hyperchloremic acidosis. The presence of multiple renal tubular defects often indicates a poor prognosis.

⑷ abnormal bone and calcium metabolism: often manifested as low blood calcium, and low urinary calcium.

⑸ Abnormal hormone metabolism and lack of trace elements

⑹ Infection: Common pathogens are pneumococcus, Klebsiella, and Escherichia coli, and the most common sites of infection are the lungs and abdominal cavity.