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Pediatric nephrotic syndrome

  Pediatric nephrotic syndrome is a clinical syndrome caused by renal fibrosis from various causes, in which the increased permeability of the glomerular capillaries leads to massive proteinuria. The main manifestations are massive proteinuria, followed by hypoproteinemia, hyperlipidemia, and varying degrees of edema. The edema of pediatric nephrotic syndrome is palpable edema of the lower extremities. If the urine is checked, proteinuria can be ++ to ++++, and blood > 0.1 grams/kg.

Table of Contents

1. What are the causes of pediatric nephrotic syndrome
2. What complications can pediatric nephrotic syndrome easily lead to
3. What are the typical symptoms of pediatric nephrotic syndrome
4. How to prevent pediatric nephrotic syndrome
5. What laboratory tests are needed for pediatric nephrotic syndrome
6. Diet taboos for patients with pediatric nephrotic syndrome
7. Conventional methods of Western medicine for the treatment of pediatric nephrotic syndrome

1. What are the causes of pediatric nephrotic syndrome

  The age of onset of nephrotic syndrome is most common in children aged 3 to 6 years, and boys are more than girls. The etiology is unknown, and it is prone to recurrence and prolongation, with a long course. Children with nephrotic syndrome can attend kindergarten during the stable phase of the disease, as long as the kindergarten strengthens the care of the children, which is conducive to the comprehensive recovery of the children.

2. What complications can pediatric nephrotic syndrome easily lead to

  1. Infection: Infection is a common complication and cause of death in nephrotic syndrome. Common infections include Streptococcus pneumoniae, Streptococcus, Haemophilus influenzae, Klebsiella, and other bacterial infections; Kaposi's sarcoma infection may occur occasionally, with the peritoneum, lungs, and skin often affected. The reasons for the frequent occurrence of infection in this disease, in addition to fluid, cellular immune deficiency, and complement factors, include the use of ascites as a culture medium, hormones, and immunosuppressants, which can further lower immune function and increase the risk of infection.

  2. Hypovolemic shock and acute renal failure

  3. Hypocoagulability and thromboembolism: When patients with kidney disease suddenly develop lumbago (costovertebral angle tenderness), hematuria, renal function impairment, and hypertension, a high suspicion of RVT should be entertained. Thromboembolic complications can also occur in the veins or arteries, with an incidence of 8.5% to 44%; thrombophlebitis of the femoral vein, pulmonary artery, femoral artery, mesenteric artery, cerebral artery, coronary artery, and thrombophlebitis of the lower leg can also be seen.

  4, Disruption of renal tubular function can lead to various transport disorders of substances, such as glycosuria, aminoaciduria, increased urinary potassium, decreased urine concentration, and so on.

  5, Protein and calorie malnutrition is caused by the loss of a large amount of protein in urine for a long time.

  6, Deficiency of other trace elements, caused by the loss of zinc-binding protein, ceruloplasmin, and transferrin in urine, leading to zinc deficiency, copper deficiency, and iron deficiency; 1,25-(OH)2D3 synthesis disorder and long-term hormone use can lead to renal osteopathy and growth retardation.

3. What are the typical symptoms of pediatric nephrotic syndrome?

  1, The degree of edema in NS varies, with obvious edema in loose tissues and low body positions. Edema moves with gravity and is more prominent in the morning or after a long period of lying down, such as around the eyelids, posterior head, or sacrum. After getting up and moving, edema in the lower limbs is more obvious. Severe cases may have generalized edema, scrotal edema, or pleural effusion and peritoneal effusion, even pericardial effusion. In cases of severe edema, local skin becomes shiny, thin, and even white streaks (commonly seen in the abdomen, buttocks, and thighs) may appear. When the skin is damaged, tissue fluid leakage is continuous. Serous cavity effusion often produces compressive symptoms, such as chest tightness, shortness of breath, or dyspnea. Chest and abdominal effusions are often milky white, containing emulsified lipids, with very low protein content (1~4g/L), and specific gravity below 1.016. The Rivalta test is negative, indicating an exudate. The degree of edema is not related to the severity of the disease or lesions, although it is related to hypoalbuminemia, but not closely related. Minimal change NS often presents with severe generalized edema. Membranous nephropathy and membranous proliferative nephritis may present with moderate lower limb edema when NS occurs. Edema is an outstanding manifestation at a certain stage of the glomerular disease process, and some patients may spontaneously regress after several months or 1~2 years. The degree of edema is often affected by sodium salt intake, and urine output decreases before and during the onset of edema.

  2, About 20% to 40% of adult NS patients with hypertension, and about half of those with obvious edema have hypertension. Hypertension can be renin-dependent or volume-dependent, and persistent hypertension is mainly related to renal underlying lesions, such as membranous proliferative nephritis and focal segmental glomerulosclerosis. About half of the patients have hypertension, membranous nephropathy only about 1/4 has hypertension, and minimal change disease is even less. Even if hypertension occurs, most of it is transient, and blood pressure returns to normal when edema subsides. It is generally believed that hypertension caused by glomerular disease, especially in NS, is mainly volume-dependent, but closely related to pathological changes, such as hypertension caused by minimal change and membranous nephropathy, which is mostly volume-dependent; NS caused by proliferative and sclerotic glomerulonephritis has hypertension that is both volume-dependent and renin-dependent, and most cases have both. In recent years, some people believe that plasma renin activity in glomerular disease may not increase, and even some patients may have decreased plasma renin. At the same time, many evidence suggests that sodium excretion disorder is a cause of hypertension in glomerular disease. Hypertension is usually moderate, and blood pressure is often between 18.7~22.7/12.7~14.7 kPa (140~170/95~110 mmHg). Therefore, hypertension crisis or hypertensive encephalopathy is rarely occurred in NS.

  3. Hypoproteinemia and malnutrition. The well-known massive proteinuria leading to malnutrition is well known. Patients may show signs of malnutrition such as sparse, dry, and yellow hair, pale skin, muscle wasting, and white transverse bands on the nails (Muchreke lines). When there is a significant decrease in serum albumin, the concentration of other proteins in the plasma also changes. Proteins with a smaller molecular weight and a charge similar to albumin tend to decrease, and they are mainly lost in urine. These include thyroid-binding globulin (molecular weight 36,500), vitamin D-binding protein (molecular weight 59,000), antithrombin III (molecular weight 65,000), transferrin (molecular weight 80,000), and the B factor of the complement system (molecular weight 80,000), etc., which are excreted in increased amounts in urine. Clinically, corresponding symptoms may appear.

  4. Secondary infection due to immune dysfunction (reduction of B factor, opsonin, and IgG), massive protein loss, malnutrition, and other factors make patients prone to secondary infections. The lack of complement system B factor, the loss of serum opsonic activity, and the increased catabolism of intrarenal immunoglobulins and their loss in urine lead to a decrease in the body's ability to resist infection, making secondary infection more likely. NS patients are prone to respiratory infections, urinary tract infections, skin infections, and peritonitis. These infections often worsen NS. In the past, before the widespread use of antibiotics, infection was the main cause of death in NS. The routine use of corticosteroids and anticytotoxic drugs for NS has not reduced the incidence of secondary infection. The use of antimicrobial agents to control and prevent bacterial infections has led to an increasing trend in viral and fungal infections, so infection is still an important complication of NS.

  5. The patients with nephrotic syndrome (NS) are mostly in a hypercoagulable state, with a tendency to thrombosis. Addis (1948) was the first to report venous thrombosis in the legs of NS patients, followed by pulmonary artery, axillary, subclavicular, external jugular, coronary artery, humeral, and mesenteric artery thrombosis, etc. Renal vein thrombosis was first discovered by Raver (1840). It is more common in patients with lupus nephritis, amyloid nephropathy, membranous nephropathy, and membranoproliferative glomerulonephritis, but it is rare in focal segmental glomerulosclerosis, minimal change disease, and diabetic nephropathy. The causes of hypercoagulability in NS are multifaceted. Many scholars confirm that platelet dysfunction plays an important role in glomerular damage in chronic immune complex nephritis. Intra-vascular coagulation is a decisive factor leading to irreversible glomerular damage. In 1972, Cochrene et al. pointed out that the induction of platelet aggregation by immune complexes is the first step in the chronic fibrin deposition within the glomerulus. It is now known that complement components such as C432, C3b, and C6, and immune complexes such as IgG2 and IgG4 can cause platelet aggregation and release platelet factor 3. Glomerular capillary endothelial damage, collagen exposure, and platelet aggregation (release ADP) can promote the activation of coagulation factor XII, leading to intravascular coagulation. Hyperlipidemia is one of the factors that cause an increase in plasma viscosity.

  6. Renal insufficiency can occur in various pathological types of nephrotic syndrome (NS). Renal insufficiency associated with NS has two types, namely acute and chronic. Clinically, those with acute onset present with acute nephritic syndrome and are prone to oliguric acute renal failure. Microscopic polyserositis NS and mild renal lesions are more likely to develop acute renal failure. In addition to renal intrinsic lesions, factors such as decreased effective blood volume, decreased cardiac output, and electrolyte disorders are also precipitating factors. The prognosis is closely related to renal intrinsic lesions. During the period of marked edema or active stage of lesions, renal insufficiency often occurs, with increased serum urea nitrogen and creatinine. After edema subsides, it returns to normal. In chronic glomerulonephritis, even if the edema completely subsides, renal function in most cases cannot return to normal. Patients with persistent severe proteinuria may have renal tubular atrophy and interstitial fibrosis, presenting with Fanconi syndrome, tubular toxicity, rickets, or osteomalacia, which symbolize poor prognosis. In terms of pathological type, patients with microscopic polyserositis who are sensitive to corticosteroids generally have normal renal function and are unlikely to develop chronic renal insufficiency. Focal segmental glomerulosclerosis often has decreased creatinine clearance, with about 10% having azotemia. Patients diagnosed early with focal segmental glomerulosclerosis.

4. How to prevent pediatric nephrotic syndrome?

  1. During the epidemic of infectious diseases, parents should avoid taking their children to public places and crowded areas to prevent exacerbation of pediatric nephrotic syndrome.

  2. Cultivate good habits through simple labor. Increase the amount of exercise and engage in moderate physical exercise consistently.

  3. Repeated colds can lead to recurrence of the condition, with persistent positive urinary protein, or a shift from negative to positive, or an increase of two plus signs or more, which can worsen the patient's suffering or medical expenses. Timely immunization can effectively improve children's immune levels, and to prevent pediatric nephrotic syndrome, it is important to avoid infectious diseases.

  4. To prevent pediatric nephrotic syndrome, it is important to ensure adequate nutrition, especially to consume more protein, iron, calcium, and vitamins A, C, D, and E in the diet.

5. What laboratory tests are needed for pediatric nephrotic syndrome?

  Items to be examined for pediatric nephrotic syndrome:

  1. The routine urine test shows a significant increase in urinary protein, with qualitative examination ≥. The diagnostic criteria for urinary protein quantification vary, with the International Society of Pediatric Nephrology (ISKDC) using >40mg/(h·m2) as the standard, while some advocate using >50mg/(kg·d) as the threshold for nephrotic range proteinuria. Considering the difficulty of collecting 24-hour urine from children, some propose measuring the ratio of urinary protein to urinary creatinine in morning urine. When this ratio (measured in mg/mg) is >3.5, it indicates nephrotic level proteinuria.

  2. Plasma protein The total protein in plasma is lower than normal, and the decrease in albumin is more obvious, usually less than 25-30g/L, and sometimes less than 10g/L. There is an inversion of the ratio of albumin to globulin, an increase in α2, β globulin, and fibrinogen in globulin, a decrease in γ-globulin, a decrease in IgG and IgA levels, an increase in IgE and IgM at times, and an accelerated erythrocyte sedimentation rate.

  3. Serum cholesterol is significantly increased, and other lipids such as triglycerides, phospholipids, etc., can also be increased. Due to the increase in lipids, the serum may appear milky.

  4. Renal function tests are generally normal. In simple cases, when urine output is extremely low, there may be transient azotemia. A few patients with nephritis may have azotemia and low complement levels. Routine ultrasound, X-ray, and electrocardiogram examinations are performed. Generally, needle biopsy of the kidney is not needed for initial cases. For cases that are resistant to hormones, frequently relapse, or depend on hormones, or whose condition changes during the course of the disease and there is a suspicion of interstitial nephritis or crescent formation, or when there is a slow decline in renal function, biopsy should be performed to clarify the pathological type and guide treatment.

6. Dietary taboos for children with nephrotic syndrome

  1. Low-salt diet:The daily salt intake should not exceed 2-3g (the sodium content of 1g of salt is 400mg), and no other salt-containing foods should be eaten.

  2. No-salt diet:Do not add salt or use other salt-containing foods during cooking in daily meals. Sugar and vinegar are usually added to enhance flavor, but the sodium content in food should not exceed 1000mg.

  3. Low-sodium diet:In addition to not adding salt or other salt-containing foods during cooking, the sodium content in food should not exceed 250-500mg per day.

7. Conventional methods of Western medicine for treating children with nephrotic syndrome

  One, treatment is more convenient

  1. The micro-powdered Chinese medicine permeation therapy is an innovative model of integrated traditional Chinese and Western medicine in treating kidney diseases. Treating kidney diseases with this method not only avoids the toxic effects of a large amount of oral Chinese medicine on the whole body but also effectively solves the弊端 of Western medicine that对症不对病. As long as under the action of the micro-powdered Chinese medicine permeation instrument, by using the permeability and selective targeting of micro-powdered Chinese medicine, the active components of micro-powdered Chinese medicine can be delivered to the kidney area in the body through the skin of the kidney area on the patient's lumbar and back.

  2. This kidney treatment method outside the body allows patients to receive treatment comfortably while lying in bed, without taking medicine or receiving injections. Even patients who go home to consolidate treatment can fully master the operation, only needing to lie in bed for a few hours, which does not hinder daily work and study at all.

  Two, treatment

  1. The fast-acting micro-powdered Chinese medicine is finely divided, with extremely small drug molecule volume, which can effectively penetrate the basement membrane pores of the glomerular capillaries to directly reach the lesion, exerting anti-inflammatory, anticoagulant, and degrading effects. It can quickly counteract the body's inflammatory response and immune complexes, repair kidney damaged cells, restore glomerular filtration function, and solve problems such as proteinuria and hematuria in a short period of time. Generally, patients with kidney disease treated by the micro-powdered Chinese medicine permeation therapy can show some changes in body symptoms within about a week, such as darker urine, gradual disappearance of edema, redness on the palms and face, sweating, and precipitates in the urine.

  2. It can be seen that the permeation therapy of microcosmic traditional Chinese medicine has exerted a powerful pharmacological effect during the treatment of kidney disease, with the strong advantage of quick effect.

  Three, Treatment

  1. More thorough traditional treatment methods for kidney disease, whether it is pure traditional Chinese medicine or pure Western medicine, the primary cause is often that kidney disease patients have some abnormal symptoms before seeking medical treatment, such as a large amount of foam in urine, hematuria, and high creatinine levels. Due to these obvious abnormalities, both patients and doctors often focus on these symptoms and indicators, and the treatment of kidney disease is also more focused on the treatment of these abnormal conditions. However, the disadvantages of this traditional treatment often recur due to minor ailments such as colds or fatigue, which can exacerbate the condition. The permeation therapy of microcosmic traditional Chinese medicine avoids this disadvantage and treats the root cause of abnormal conditions such as proteinuria and hematuria.

  2. That is, treating the injury of renal innate cells and the course of renal fibrosis, removing the root, completely solving the problem of proteinuria and hematuria, and to the greatest extent avoiding the recurrence of kidney disease, thus enabling patients to achieve the ultimate effect of 'more thorough treatment.'

  Four, Treatment

  1. More accurate treatment for kidney disease, although traditional treatment methods can exert the effects of anti-inflammatory, anticoagulant, and vasodilation, these effects all require the joint use of multiple drugs. Whether considering the economic burden of patients or the繁琐的服药情况, there are many disadvantages. The permeation therapy of microcosmic traditional Chinese medicine for kidney disease can achieve the function of 'multiple effects with a single drug.' And this therapy is far from just that! The treatment of the root cause of kidney injury requires the repair of the damaged innate cells as a primary treatment measure.

  2. At this time, the degradative function of microcosmic traditional Chinese medicine has become a key treatment measure. It is based on the comprehensive therapeutic effects of anti-inflammatory, anticoagulant, vasodilation, and degradation exerted by the permeation therapy of microcosmic traditional Chinese medicine that many disadvantages of traditional treatment are avoided, and a fundamental treatment for kidney disease is achieved, realizing the ultimate effect of 'treating the disease first and treating the symptoms, and the symptoms disappear when the disease is cured,' and solving the problem of the recurrence of kidney disease to the greatest extent, making the treatment of kidney disease by microcosmic traditional Chinese medicine more accurate.

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