Pediatric Nephrotic Syndrome
Introduction
Introduction to Pediatric Nephrotic Syndrome Nephrotic syndrome (NS) is a clinical syndrome in which a large number of albumin is lost from the urine due to increased plasmin permeability of the glomerular filtration membrane and causes a series of pathophysiological changes. The disease is characterized by massive proteinuria, hypoalbuminemia, severe edema, hyperlipidemia and hypercoagulability. A large amount of proteinuria refers to a daily discharge of >100 mg/kg of urine protein or more than 3.5 g/L of urine protein. The disease has a tendency to increase year by year. basic knowledge The proportion of illness: 0.002% Susceptible people: children Mode of infection: non-infectious Complications: hematuria malnutrition
Cause
Causes of Pediatric Nephrotic Syndrome
(1) Causes of the disease
Almost all NS can cause glomerular disease, classification:
Clinical classification
For the current domestic main classification method.
(1) Simple nephropathy: that is, patients with four clinical features of nephrotic syndrome, more men than women, clinically more common.
(2) Nephritic nephropathy: In addition to typical symptoms, it also has one of the following characteristics, including hypertension [preschool children, blood pressure higher than 16/10.7kPa (120/80mmHg), school-age children higher than 17.3/12kPa (130/90mmHg)]; hematuria (up to 10/Hp in uterine microscopy); azotemia (BUN>10.7mmol/L, >30mg/dl) and persistent hypocomplementemia.
(3) Congenital nephropathy: the disease occurs after birth or shortly after birth (<2 months after birth), presenting the above-mentioned typical symptoms, with a family history, the child's birth weight is low (multiple premature infants), intrauterine asphyxia Meconium-contaminated amniotic fluid, breech production and large placenta are helpful in the diagnosis of this disease. The disease has a high incidence in Finland, is rare in China, has no response to hormones or is dysfunctional, and mostly died within 6 months after birth. Infection, kidney failure or other complications.
(4) refractory nephropathy: According to the diagnostic criteria proposed by the Chinese Pediatric Nephrology Research Group:
1 for a sufficient amount of hormones (such as daily prednisone 2mg / kg) for 8 weeks ineffective or partial effect,
2 Repeated or repeated recurrence (2 times within half a year, 3 times within 1 year),
3 hormone dependent.
2. Pathological classification
(1) Mild lesions (including minimal lesions): Children are mainly small lesions.
(2) focal, segmental glomerulosclerosis.
(3) Mesangial proliferative nephritis.
(4) membranous lesions.
3. Classified by clinical practice
(1) primary or idiopathic: that is, the original lesion occurs in the glomerular disease, according to the current domestic clinical classification, primary glomerular disease, acute glomerulonephritis, rapid glomerular Nephritis, chronic glomerulonephritis and glomerular nephropathy can occur NS in the course of the disease, pathologically, minimal lesions, focal segmental glomerulosclerosis, membranous nephropathy, membrane proliferative glomerulus Nephritis and lipoprotein glomerulopathy, collagen III glomerulopathy, fibrotic glomerulopathy and collapse glomerulopathy found in recent years are mainly NS, mesangial proliferative glomerulonephritis can also occur NS.
(2) Secondary nephrotic syndrome: NS secondary to systemic diseases, the causes are extensive and complex, and are summarized as follows:
1 Infectious diseases: Many infections can cause NS, according to their pathogens are as follows:
A. Viral infection: hepatitis B and C viruses, cytomegalovirus, Epstein-Barr virus, HIV type I, herpes zoster virus, Coxsackie virus and adenovirus infection,
B. Bacterial infections: infections such as streptococci, staphylococcus, pneumococci, salmonella, leprosy and syphilis,
C. Protozoal infections: such as Plasmodium (common to Plasmodium malaria) and toxoplasmosis infection,
D. Parasitic infections: various types of schistosomiasis [especially Manson schistosomiasis], trypanosomes and filarials, etc.
2 multiple system and connective tissue diseases: such as systemic lupus erythematosus, systemic vasculitis, rheumatoid arthritis, Sjogren's syndrome, ulcerative colitis, dermatomyositis, allergic purpura, herpes dermatitis, sarcoidosis and Psoriasis, etc.
3 allergens: such as snake bites, bee stings, pollen, serum, vaccines, poison oak, ivy (ivy), D860, penicillamine and probenecid, etc.
4 metabolic diseases: such as diabetic nephropathy, amyloidosis, lipoprotein nephropathy and mucinous edema,
5 nephrotoxic substances: such as mercury, strontium, gold and trimethyl ketone, etc.
6 tumors: such as Hodgkin's disease, lymphoma, chronic lymphocytic leukemia, multiple myeloma, colon cancer, lung cancer, breast cancer, stomach cancer and kidney cancer, etc.
7 other: such as pre-eclampsia, renal artery stenosis, renal vein thrombosis, reflux nephropathy, renal transplant chronic rejection, chronic ileitis, chronic heart failure and constrictive pericarditis.
(3) Congenital and hereditary diseases: such as Alport syndrome, Fabry disease, nail-patella syndrome, congenital (Finnish) nephrotic syndrome and sickle cell disease.
(two) pathogenesis
Pathogenesis
(1) citrate theory: the classic pathogenesis, due to swelling and fusion of glomerular epithelial podocytes, the original citrate glycoprotein structure is destroyed, the negative charge disappears and the negatively charged albumin is formed. Proteinuria.
(2) Immunological pathogenesis:
1 humoral immune participation: including immune complex (IC), immunoglobulin abnormalities (low blood IgG, increased decomposition, reduced synthesis), decreased antibody production and many other factors,
2 Cellular immune abnormalities: a series of abnormal changes occur in the number of circulating T lymphocytes and decreased in function.
3 Complement system: including the bypass pathway B factor deficiency affects the body's ability to regulate the capsules of Escherichia coli, pneumococcal, decreased complement viability, and the appearance of C5b-9 (membrane attack complex).
(3) Other factors: including direct damage to the glomerulus by the antibody, neutral polymorphonuclear granulocytes (PMN) release proteolytic enzymes, produce reactive oxygen species, release cationic proteins, and mononuclear cells aggregate to release various proteases, collagenase, oxygen Free radicals, cytokines, and platelet activating factors are involved in the pathogenesis of nephropathy.
(4) Edema: The mechanism of edema in nephrotic syndrome has been improved in recent years. The proportion of hypovolemia is only 7% to 38%. It can be explained by traditional viewpoints. More research indicates that there are still many Intrarenal factors work.
(5) Hyperlipidemia: refractory nephropathy resistant to hormones is type IV hyperlipidemia, which is an increase in very low density lipoprotein (VLDL) and a decrease in high density lipoprotein (HDL), which affects cholesterol. The removal of hyperlipidemia is not only due to atherosclerosis, but also to NLDL with nephrotoxicity. It can bind to the multivalent anion of GBM and enter the mesangial area to cause kidney damage, reducing the negative charge and transparent membrane. The increase in sex causes macromolecular lipoproteins to deposit in the mesangial area, resulting in glomerular sclerosis. In addition, hyperlipidemia not only increases blood viscosity, but also cholesterol deposition causes the capillary endothelial wall to become rough and the negative charge to change. Thus, the negatively charged platelets are deposited to form a thrombus, and a series of changes in the fibrinolytic system, including plasma fibrinogen, coagulation cofactor (V, VIII), -thromboglobulin elevation, increased platelet count, adhesion And the aggregation function is enhanced, the activity of plasmin and antithrombin III (ATIII) is decreased, and the enzyme cause (II, X, etc.) is decreased.
Prevention
Pediatric nephrotic syndrome prevention
The disease is often associated with various infections and nephrotoxic substances such as mercury, strontium, gold and trimethyl ketone. It should actively prevent and treat various infections, enhance physical fitness, and prevent exposure to various nephrotoxic substances. Keep the air in the living room fresh, not in crowded places, keep the skin clean, prevent skin damage, prevent infection, and promptly diagnose and treat infections. Easy to digest, light diet. Pay attention to the combination of physical and mental work and rest, enhance the body's immunity, pay attention to exercise. Regular review of urine routine and renal function.
Complication
Pediatric nephrotic syndrome complications Complications, hematuria, malnutrition
Infection
Infection is a common complication and cause of death in nephrotic syndrome. Common infections are bacterial infections of pneumococci, streptococci, Haemophilus influenzae, Klebsiella, etc.; occasional infection with Pneumocystis carinii, peritoneum, lung, skin Often involved, the disease is prone to infection in addition to body fluids, cellular immune deficiency and complement factors; ascites can be used as a medium, hormones and immunosuppressive agents, so that immune function is reduced and more susceptible to infection.
2. Hypovolemic shock and acute renal failure
(1) hypovolemic shock: some patients with low blood volume, showing a "fragile" state, once vomiting, diarrhea, insufficient intake, infection and other incentives, prone to hypovolemic shock, if long-term use of larger doses Hormones, once stopped, can show "adrenal crisis."
(2) acute renal failure: due to hypovolemia, renal interstitial edema and (or) tubular obstruction, acute renal vein thrombosis (RVT) and other factors can cause prerenal, renal, post-renal acute renal function Depletion.
3. Hypercoagulable state and thromboembolism
When patients with kidney disease suddenly have low back pain (ridge rib angle tenderness), hematuria, renal dysfunction and hypertension, RVT should be highly suspected, and thromboembolic complications may occur in the vein or artery, the incidence rate is 8.5% to 44%; Veins, pulmonary artery, femoral artery, mesenteric artery, cerebral artery, coronary artery, and calf thrombophlebitis are also seen.
4. Renal tubular dysfunction
There may be a variety of substance transport disorders, such as diabetes, amino aciduria, increased urinary potassium, and decreased urine concentration.
5. Protein, calorie malnutrition
Due to the loss of large amounts of protein in the urine for a long time.
6. Other
The lack of trace elements, due to the loss of zinc-binding protein in the urine, ceruloplasmin, transferrin, zinc deficiency, copper deficiency and iron deficiency; 1,25-(OH)2D3 synthesis disorders and long-term use of hormones, can cause renal Osteopathy and growth retardation.
Symptom
Symptoms of Pediatric Nephrotic Syndrome Common Symptoms Edema Hypercoagulable State Proteinuria Scrotum Edema Hypoproteinemia Venous Thrombosis Weight Loss Hypocalcemia Ascites Chronic Renal Insufficiency
1. Edema: The degree of edema of NS is different. The tissue is loose and the position is low. The edema moves with gravity. For a long time or early morning, the eyelids, the back head or the sacral edema, after getting up. The lower extremity edema is obvious, severe systemic edema, scrotal edema or pleural cavity and peritoneal effusion, and even pericardial effusion, localized skin is bright when the body is highly edematous, skin becomes thinner, and even white lines appear (more common in the abdomen, buttocks and thighs) ), the skin is damaged, the tissue fluid leaks, the serous effusion often produces compression symptoms, such as chest tightness, shortness of breath or difficulty breathing, chest and ascites are often milky white, containing emulsified lipids, protein content is very small (1 ~ 4g / L), the specific gravity is less than 1.016, the Rivalta test is negative, it is leakage, the degree of edema has nothing to do with the severity of the disease and the severity of the disease. Although it is related to hypoalbuminemia, it is not closely related. The small lesion type NS tends to be highly systemic edema. Moderate edema of the lower extremities is common in the presence of NS in membranous nephropathy and membranous proliferative nephritis. Edema is a prominent manifestation of a certain stage of glomerular disease, and some patients are months or 1 2 years may subside on their own, often influenced by the degree of edema sodium intake, decreased urine output when before edema and edema.
2. Hypertension: 20% to 40% of adult NS patients have hypertension, about half of those with obvious edema have hypertension, and hypertension can be renin-dependent or volume-dependent. Persistent hypertension is mainly related to basic renal diseases. For example, membrane proliferative nephritis and focal segmental glomerulosclerosis have about half of the patients with hypertension, membranous nephropathy only about 1/4 have high blood pressure, fewer minor lesions, even if there is high blood pressure, most of them are transient When the edema subsides, the blood pressure returns to normal. It is generally considered that the hypertension caused by glomerular disease, especially in NS, is mainly volume-dependent, but closely related to pathological changes, such as microscopic lesions and membranous nephropathy. Hypertension is mostly volume-dependent; NS caused by proliferative and sclerosing glomerulonephritis, its hypertension is both volume-dependent and renin-dependent, most of which are both. In recent years, some people think that the kidney is small. The plasma renin activity of the ball disease does not necessarily increase, and even some patients have lower plasma renin. At the same time, there is much evidence that sodium excretion disorder is the cause of hypertension caused by glomerular disease. Hypertension is usually moderate and blood pressure is often Between 18.7 ~ 22.7 / 12.7 ~ 14.7kPa (140 ~ 170/95 ~ 110mmHg), therefore, rare hypertensive crisis or hypertensive encephalopathy when NS.
3. Hypoproteinemia and malnutrition: Long-term persistent large amounts of proteinuria are known to cause malnutrition. The patient has sparse hair, crisp and yellowish skin, pale skin, muscle wasting and white lines of nails (Muchreke line). The manifestations of malnutrition, when the albuminemia is obvious, the concentration of other proteins in the plasma also changes, the protein with a small molecular weight and the charge similar to albumin tends to decrease, which is mainly lost from the urine, such as the thyroid-binding sphere. Protein (molecular weight 36,500), vitamin D binding protein (molecular weight 59,000), antithrombin III (molecular weight 65,000), transferrin (molecular weight 80,000) and complement system B factor (molecular weight 80,000) from urine The increase in the discharge is accompanied by a corresponding symptom in the clinic.
(1) Hypothyroidism: NS patients are mostly in a low-metabolism state, and the decrease in oxygen consumption may be related to systemic edema and decreased blood flow to the skin. 30 years ago, it was found that plasma protein-binding iodine decreased, and urinary protein-bound iodine increased. The patient's high-dose thyroxine does not undergo high metabolic status, and the thyroid iodine uptake rate is normal or increased. These data indicate that triiodothyronine (T3) and thyroxine (T4) are excreted from the urine, resulting in a decrease in plasma concentration. The patient has a low metabolic state, but plasma free T3 and T4 tend to be normal.
(2) Hypocalcemia: due to the loss of vitamin D-binding protein from the urine, the concentration of plasma 25-OHD3 and 1,25-(OH)2D3 is lowered, causing intestinal calcium absorption disorder and bone-to-parathyroid hormone reaction destruction. The patient has hypocalcemia and secondary hyperparathyroidism, leading to osteomalacia and cystic fibrosis, serum calcium reduction and serum albumin reduction are balanced, it is generally considered that serum albumin is reduced by 10g / L, then Serum calcium decreased by 0.25mmol/L, serum free calcium decreased by 0.050.07mmoL/L, which is the decrease of albumin-binding calcium, serum albumin decreased by 10g/L, HCO3- increased by 3.7mmol/L, and anion gap decreased. 3mmoL / L, so there may be metabolic alkalemia when severe hypoalbuminemia.
(3) Iron deficiency anemia: Due to the continuous loss of transferrin from the urine, patients may develop iron deficiency anemia, which is often ineffective for iron therapy.
4. Secondary infection: due to immune dysfunction (B factor, opsonin and IgG reduction), a large number of protein loss, malnutrition and other factors make the patient extremely susceptible to secondary infection, lack of factor B in the complement system, loss of serum conditioning activity, Intrarenal immunoglobulin catabolism increased and lost from the urine, resulting in decreased anti-infective capacity of the body, so it is easy to secondary infection, NS is common for respiratory infections, urinary tract infections, skin infections and peritonitis, etc. These infections often make NS Further worsening, when antibiotics are not widely used, infection is the main cause of NS death. Routine corticosteroids and anti-cytotoxic drugs are used to treat NS, so that the secondary infection rate is increased, and antibacterial drugs are used to control and prevent bacterial infection. The incidence of viral infections and fungal infections has increased, so the current infection is still an important complication of NS.
5. Hypercoagulable state: Most patients with NS are hypercoagulable and have a tendency to form thrombosis. Addis (1948) first reported NS patients with leg vein thrombosis, followed by pulmonary artery, hernia, subclavian, and external jugular vein. Coronary artery, tendon and mesenteric artery and other thrombosis, renal vein thrombosis was first discovered by Raver (1840), more common in patients with lupus nephritis, amyloid nephropathy, membranous nephropathy and membrane proliferative nephritis, but focal segment Glomerulosclerosis, rare lesions and diabetic nephropathy are rare. The cause of hypercoagulable state of NS is multifaceted. Many scholars have confirmed that platelet dysfunction plays an important role in glomerular damage of chronic immune complex nephritis. Intravascular coagulation is a decisive factor leading to irreversible glomerular damage. Cochrene et al., 1972, pointed out that immune complex-induced platelet aggregation is the first step in the deposition of chronic fibrin in the glomerulus. C432, C3b and C6, IgG2 and IgG4 in immune complexes can aggregate platelets and release platelet factor 3, glomerular capillaries Vascular endothelial injury, collagen exposure and platelet aggregation (release of ADP) can promote the activation of coagulation factor XII, leading to intravascular coagulation, which is one of the factors that cause an increase in plasma viscosity.
Other macromolecular proteins, such as 2-globulin (molecular weight 8.2×10 5 ), -globulin (molecular weight 3.2×10 5 ) and -pre-lipoprotein (molecular weight 5×106 2×10 7 ) were significantly increased. Among the coagulation factors, fibrinogen (I), variability factor (V), stabilizing factor (VII), anti-hemophilic globulin (VIII) and Staurt factor (X) are increased, while antithrombin III is decreased. These are important signs of increased blood coagulation. Some people think that the decrease in fibrinolytic activity is also closely related, and it is proved that plasminogen inhibitor (2 -antiplasmin) is increased in NS, and corticosteroid is excessively used in the course of disease. And diuretics can make the hypercoagulable state more serious, hypercoagulable state is easy to promote intravascular thrombosis, glomerular extensive fibrin deposition, renal function is further deteriorated, in the NS process, if renal vein thrombosis occurs, the kidney The congestion is more serious, the kidney volume is increased, the renal function is further reduced, and the edema and proteinuria are intensified.
6. Renal insufficiency: renal dysfunction can occur in all pathological types of NS. There are two types of renal insufficiency in NS, namely acute and chronic. In acute clinical onset, acute nephritic syndrome is manifested. And prone to oliguric acute renal failure, minimally pathological NS and mild renal disease occur more acute renal failure, in addition to the basic renal lesions, effective blood volume reduction, cardiac output decreased and electrolyte imbalance It is also a predisposing factor, and its prognosis is closely related to the basic lesions in the kidney. In the period of high edema or significant activity, it often has renal insufficiency, serum urea nitrogen and creatinine increase, and when the edema subsides, it returns to normal, chronic kidney small NS of glomerulonephritis, even if the edema completely subsides, most of the renal function can not return to normal, patients with persistent severe proteinuria, may be associated with tubular atrophy and interstitial fibrosis, manifested as Fanconi syndrome, renal tubular poisoning, rickets or bone Physico-softening, which symbolizes a poor prognosis. In terms of pathological type, the small disease type NS is sensitive to corticosteroids, and the renal function is basically normal. Chronic renal failure does not occur, there is often a focal segmental glomerulosclerosis reduced creatinine clearance rate, about 10% of azotemia early diagnosis of focal segmental glomerular sclerosis patients.
Within 10 years, about 40% of patients progress to renal failure, membranous nephropathy has normal renal function, and then slowly declines, and develops to chronic renal failure in 15 years, accounting for 50% in adulthood and 10% in children~ 15%, NS caused by membrane proliferative nephritis, most of them have renal dysfunction at the time of onset, about half of them develop renal failure within 10 to 15 years, clinical manifestations can be acute and slow, and there may be respiratory tract before onset. Infection or skin infection, etc., without any incentives, systemic severe edema is a prominent symptom of the disease, with decreased urine output, some patients have hematuria (human or microscopic hematuria), some sick children have high blood pressure, some severe Patients with edema nephropathy may have pleural effusion and ascites.
Examine
Examination of pediatric nephrotic syndrome
Urine routine
Urinary protein increased significantly, qualitative examination , urine protein quantitative examination diagnostic criteria are different, the International Pediatric Nephrology Research Organization (ISKDC) is based on >40mg / (h · m2), there are also advocates > 50mg / (kg · d For patients with nephropathy range of proteinuria, in view of the 24h urinary difficulty in children, there is a tendency to measure the urine protein/urinary creatinine ratio in morning urine. When the ratio (in mg/mg) is >3.5, it is the nephropathic proteinuria.
2. Plasma protein
Total plasma protein is lower than normal, albumin is more obvious, often <25 ~ 30g / L, sometimes less than 10g / L, and albumin, globulin ratio inverted, globulin 2, globulin and fibrinogen Increased, gamma-globulin decreased, IgG and IgA levels decreased, IgE and IgM sometimes increased, and erythrocyte sedimentation rate increased.
3. Serum cholesterol
More obvious increase, other lipids such as triglycerides, phospholipids, etc. can also be increased, because the lipids can be milky white.
4. Renal function test
Generally normal, simple urine, there may be temporary azotemia, a small number of nephritis may be associated with azotemia and hypo-complementemia, routine B-ultrasound, X-ray and ECG examination, generally The case does not require renal biopsy, steroid-resistant, recurrent or hormonally dependent cases, or changes in the course of the disease, suspected interstitial nephritis or crescent formation, or slow renal dysfunction A biopsy should be performed to determine the type of pathology and to guide treatment.
Diagnosis
Diagnosis and diagnosis of pediatric nephrotic syndrome
According to typical clinical features, combined with laboratory tests, including 24h urinary protein excretion >100mg / (kg · d), hypercholesterolemia, hypoalbuminemia, can make a diagnosis of nephrotic syndrome.
Common secondary nephrotic syndrome
(1) purpuric nephritis: in the secondary NS of 3 to 20 years old, the most common cause of allergic purpura, patients with abdominal pain and blood in the stool, such as allergic purpura, hematuria, proteinuria, hypertension And edema and other characteristics of glomerulonephritis, if the skin lesions are light, abdominal pain and joint pain is not obvious, or hematuria, proteinuria and edema, easily misdiagnosed as primary NS, often elevated serum IgA in the early stages of the disease, Skin biopsy was performed at the skin lesions, and IgA deposition was observed in the capillary wall. Most of the renal biopsy was proliferative glomerulonephritis. IgA deposition was common in immunofluorescence, and the formation of crescents was more common. The number of patients after the lesions subsided Nephritic NS symptoms occur only months or longer, so a detailed history must be traced back.
(2) lupus nephritis: lupus nephritis is more common in women aged 20 to 40 years, 20% to 50% of them present clinical manifestations of NS, patients with fever, rash and joint pain, especially the most diagnostic value of facial butterfly erythema Serum antinuclear antibody, anti-double-stranded DNA antibody and anti-Sm antibody are positive, lupus cells can be found in blood, serum protein blood electrophoresis 2 and gamma globulin are increased, immunoglobulin examination is mainly IgG, and skin lupus test is positive.
(3) progressive systemic sclerosis: the disease can be complicated by NS, most patients have Raynaud's phenomenon first, followed by swelling of the face and fingers, thickening of the skin, difficulty in swallowing, increased serum gamma globulin and IgG, antinuclear Antibodies, anti-SCI-70 and AcA antibodies can be positive, so it is not difficult to distinguish from primary NS.
(4) Wegner granuloma: This disease has three major characteristics, namely nasal and paranasal sinus necroinflammation, pneumonia and necrotizing glomerulonephritis. The order of the disease is first nasal lesions, followed by lung lesions, followed by The clinical features of renal damage and renal damage are rapid glomerulonephritis or NS, serum gamma globulin, IgG and IgA increase, serum ANCA positive, and it is not difficult to diagnose the characteristics of the disease.
(5) Diabetic glomerulosclerosis: patients who have developed diabetes for more than 10 years, especially those with diabetes type 1 and have not been satisfactorily controlled. When there is a large amount of proteinuria and NS, there are many microaneurysms in the fundus examination. Kidney volume increases, renal plasma flow and glomerular filtration rate increase or normal, late renal dysfunction, urinary 2 microglobulin, urinary NAG and lysozyme increase, which is helpful for early diagnosis.
(6) multiple myeloma nephropathy: some patients with multiple myeloma first appear proteinuria, nephrotic syndrome and renal insufficiency, then bone pain and bleeding tendency, anemia and bone lesions, early misdiagnosed as primary NS The serum protein electrophoresis gamma globulin and IgG are significantly increased. It is a feature of multiple myeloma. The serum monoclonal immunoglobulin is significantly increased and the urinary lysin is positive for diagnosis. In general, NS patients should be suspected if they encounter the following conditions. The disease:
1 age is over 40 years old;
2 anemia is more obvious, the degree of anemia is not commensurate with the degree of renal dysfunction, often accompanied by neutrophils and thrombocytopenia;
3 hyperuricemia;
4 hypercalcemia.
(7) amyloid nephropathy: amyloid nephropathy has primary and secondary points, the latter secondary to chronic infections (such as tuberculosis, leprosy or chronic lung suppuration, etc.), tumors, multiple myeloma and Rheumatoid arthritis, most patients with cardiac hypertrophy, arrhythmia and heart failure, hepatosplenomegaly, giant tongue, skin with mossy mucus edema, early stage of amyloid nephropathy only proteinuria, generally 3 to 5 years after NS , serum gamma globulin increased, hyperlipidemia is not obvious, combined with heart, liver, splenomegaly diagnosis is not difficult, the diagnosis depends on renal biopsy.
(8) NS caused by malignant tumors: All malignant tumors can cause NS through immune mechanism, and even NS is an early clinical manifestation. For example, lymphoma, leukemia, bronchial cancer and colon cancer can often occur NS, therefore, NS patients should be fully examined. If a systemic lymphadenopathy, chest, and abdominal mass are found, the NS caused by the tumor should be considered, and the diagnosis of the primary tumor should be positively confirmed.
