Non-IgA mesangial proliferative glomerulonephritis

　　The onset of this disease is often insidious, with a history of infection before onset in some patients, mostly upper respiratory tract infection, and the pathogen is unclear. The exact role of infection in this disease is still unclear. The pathogenesis of membranous proliferative glomerulonephritis is unknown, but immunofluorescence examination suggests that the disease is an immune complex disease. The nature of the antigen and antibody is still unclear. Although insoluble and immobile immune complexes are an important cause of mesangial damage, the exact process is not clear. The degree of mesangial proliferation can be affected by many factors, such as the size, number, charge, and shape of immune complexes. When the mesangial function is low or suppressed, immune complexes or macromolecular substances that cannot be processed or transported can remain in the mesangial area, leading to mesangial lesions.

　　It can be complicated with nephrotic syndrome, renal insufficiency, cyst粘连, glomerulosclerosis, tubular atrophy, and interstitial fibrosis, etc.

　　The 'Nephrotic Syndrome' is abbreviated as Nephrotic Syndrome, referring to a group of syndromes caused by various etiologies, mainly characterized by increased permeability of the glomerular basement membrane and decreased glomerular filtration rate due to glomerular lesions. Clinically, it has four major characteristics:

　　1. Large amounts of proteinuria, more than 3.5g/d, with possible lipiduria.

　　2. Hypoalbuminemia, serum albumin less than 30g/L.

　　3. Hyperlipidemia.

　　4. Edema, according to different etiology and pathology, this syndrome is divided into three categories: primary nephrotic syndrome, congenital nephrotic syndrome, and secondary nephrotic syndrome.

　　Membranous proliferative glomerulonephritis can occur at any age, but it is more common in adolescents, with slightly more males than females, and about 30% to 40% of patients have an infection before onset, mostly upper respiratory tract infection. The onset is often insidious, with 20% to 25% presenting with acute nephritis syndrome, and about 25% (up to 37% in children) presenting with nephrotic syndrome. The rest often present with asymptomatic proteinuria and/or hematuria, with a hematuria incidence of about 80%. It can present with recurrent episodes, gross hematuria, or microscopic hematuria. The amount of proteinuria varies, but it is usually non-selective. About 30% of patients have hypertension at the time of consultation, but it is often mild, and there may be renal area pain, which can be unilateral or bilateral, but it is not common. Most renal function tests at the time of consultation are normal, with a few showing mild decline. The serum complement components are generally normal, and the level of blood immunoglobulins is rarely significantly abnormal. The antigen and antibody nature is still unclear. Although insoluble and immobile immune complexes are an important cause of mesangial damage, the exact process is not clear. The degree of mesangial proliferation can be affected by many factors, such as the size, number, charge, and shape of immune complexes. When the mesangial function is low or suppressed, immune complexes or macromolecular substances that cannot be processed or transported can remain in the mesangial area, leading to mesangial lesions.

　　Active prevention of infection, infection is a general term for diseases such as pyelonephritis, cystitis, urethritis caused by bacteria. It belongs to the category of 'Dribbling' and 'Retention' in traditional Chinese medicine. The main clinical characteristics are usually low back pain, frequent urination, urgency, and dysuria. According to traditional Chinese medicine, this disease is often due to downward invasion of damp-heat, affecting the kidney and bladder, and the malfunction of Qi transformation in the lower jiao. Children are more common than adults, and women are more common than men, and it is prone to recurrence.

　　Under light microscopy, diffuse mesangial cell proliferation can be seen, with 4 to 5 cells in each mesangial area, and in severe cases, it may exceed 5. Endothelial cells may also proliferate, usually less severe; the proliferating cells may also contain infiltrating monocytes; mesangial matrix increases; although there may be segmental exacerbation at times, it is usually a diffuse and uniform manifestation; the glomerular capillary wall is intact, without the phenomenon of vascular丛 necrosis; usually not accompanied by adhesion and sclerosis changes, about half of the patients have eosinophilic deposits in the glomeruli, limited to the mesangial area. Occasionally, similar eosinophilic deposits and 'hyaline change' changes can be found in the glomerular capsule basement membrane and small artery wall. Mesangial cells and matrix do not penetrate into the peripheral capillary wall. The findings in immunofluorescence examination are quite diverse. Those dominated by IgA are IgA nephropathy, which is not discussed in this section.

　　Common manifestations are granular and diffuse distribution mainly of IgG or IgM, which may be accompanied by C3 deposition in the mesangial area, or with a small amount of IgM or IgG and IgA deposits to varying degrees. The pathogenesis and clinical significance of this IgM deposition as the main mechanism are still unclear. Some mesangial proliferative glomerulonephritis may have no immunoglobulin and complement deposition, and whether it can be classified as a minimal change nephropathy with obvious mesangial proliferation is controversial. Occasionally, it may only have C3 deposition without immunoglobulin deposition. The electron microscopy examination is more typical with fine granular or uniform electron-dense deposits in the mesangial area. Some people believe that when there are large granular electron-dense deposits, IgA nephropathy and systemic disease renal damage should be excluded. In addition, epithelial cells may have foot process swelling and disappearance, and the basement membrane may also have slight changes.

　　First, dietetic recipe for non-IgA mesangial proliferative glomerulonephritis

　　1, Corn and Clam Soup:Take one fresh corn cob, remove the husk, leave the silk, clean and cut into segments; 60g of clam meat cleaned. Put the corn into the pot, add an appropriate amount of water, bring to a boil with high heat, then simmer for 20 minutes with low heat, add clam meat, cook for half an hour, and season to taste. Drink the soup as desired, and eat the corn kernels.

　　2, Winter Melon and Fish Soup:Winter melon (without skin and seeds) 500g, crucian carp 1 piece (about 250g, with the internal organs and scales removed, cleaned), add salt, wine, and other seasonings, and then cook into soup for eating.

　　3, Lotus and Jujube Soup:Lotus seeds with the core removed 60g, 10g of raw licorice, and appropriate amount of rock sugar, the first two ingredients are boiled in water until the lotus seeds are soft, then add rock sugar, eat lotus seeds and drink the soup.

　　4, Astragalus Fish Soup:Raw Astragalus 60g, fresh fish or crucian carp three pieces (weight 250-500g). First decoct Astragalus to get the juice, add fish to cook the soup, drink the juice, and eat the meat.

　　5, Kelp and Mung Bean Sweet Soup:Take kelp 60g soaked, washed and cut into strips, mung bean 80g washed, put all the materials together in a pot, add an appropriate amount of water, boil with high heat, then cook with low heat until the mung bean is soft, add an appropriate amount of sugar to adjust the sweet soup, and then boil again.

　　Second, what is good for the body in non-IgA mesangial proliferative glomerulonephritis

　　1, Eat light and easy-to-digest food.

　　2, In the diet, give quality protein in a moderate amount, mainly referring to lean meat, eggs, and milk.

　　3, You can eat more melon, sweet potato, grape, radish and other things.

　　4, Appropriately supplement trace elements, can eat vegetables, fruits, coarse grains, seafood containing vitamins and trace elements rich in supplements.

　　Third, what food should be avoided in non-IgA mesangial proliferative glomerulonephritis

　　1, Avoid seafood, beef, mutton, spicy and刺激性 food.

　　2, Abstain from alcohol and all kinds of stimulants such as five-spice allspice, coffee, cilantro, etc.

　　3, Avoid high-salt, high-protein, high-fat foods.

　　(The above information is shared by netizens, not reviewed by doctors, for reference only.)

　　First, prevention:

　　Active prevention of infection, Traditional Chinese Medicine treatment for non-IgA mesangial proliferative glomerulonephritis

　　Second, Traditional Chinese Medicine Treatment:

　　According to the patient's symptoms, tongue, pulse, clinical differentiation is mainly divided into Qi deficiency and blood stasis type and Yin deficiency and blood heat type.

　　Treatment formula:

　　1, Qi deficiency and blood stasis type:Treatment with Qi tonifying, spleen and kidney nourishing, activating blood and removing blood stasis. The prescription is modified 'Qi Nourishing Kidney Soup': Ginseng, Astragalus, White Atractylodes, White Poria,山药, Cornus, Prepared Licorice, Peach kernel, Safflower, Panax notoginseng powder.

　　2, Yin deficiency and blood heat type:Treatment with nourishing yin and clearing heat, cooling blood and stopping bleeding. The prescription is modified 'Zhibai Dihuang Decoction': Anemarrhena, Phellodendron, Rehmannia,山药, Poria, Alisma, Salvia miltiorrhiza, Polygonum multiflorum, White茅根, Eclipta, Dandelion, Small Dandelion, 半夏. It is not IgA mesangial proliferative glomerulonephritis in Western medicine treatment, when the renal biopsy shows mild mesangial proliferation, no immunoglobulin deposition, or no focal segmental glomerulosclerosis, there is often a benign prognosis. Most of these patients have a good response to sugar adrenal cortex hormone, but the course of treatment should be appropriately prolonged; for patients who are ineffective, or only partially relieved, or recurrent, cytotoxic drugs can be added, such as cyclophosphamide or benzyl mustard nitrogen mustard or azathioprine, etc., which can be effective or increase the rate of remission and reduce recurrence. When adult cases are accompanied by nephrotic syndrome, and renal biopsy shows moderate to severe diffuse mesangial proliferation with focal segmental glomerulosclerosis, they often have a poor response to sugar corticosteroids, tend to persistent proteinuria, and slowly progress to renal insufficiency. These patients are worse if they have cyst粘连, glomerular sclerosis damage, tubular atrophy, and interstitial fibrosis. For these diseases, after trying prednisone standard dose for 8 weeks, if ineffective, it should be changed to alternate-day treatment and reduced dose, the course of treatment should be determined according to the condition, and attention should be paid to prevent and reduce the adverse reactions of hormone treatment.

　　The results of the International Children's Kidney Disease Cooperative Research show that for patients with significant mesangial cell proliferation, extending the hormone treatment course to more than 1 year can achieve a relatively satisfactory effect. This regimen should still be used with caution in adults. For typical mesangial proliferative glomerulonephritis with IgM as the main deposited substance, the response to hormone therapy is also poor, and it is prone to progress into focal segmental glomerulosclerosis.

　　In summary, patients with good response to hormone therapy usually have a better prognosis, although proteinuria may exacerbate and then relieve, and only a few develop into end-stage kidney disease; while patients with no response to hormone therapy, manifested by persistent nephrotic syndrome, have a poorer prognosis, although the speed of renal failure is not consistent. It is not clear whether cytotoxic drugs can slow the progression speed. Some estimates suggest that patients with focal segmental glomerulosclerosis at onset and no response to hormone therapy often develop renal failure 5 to 10 years later. For patients with severe mesangial proliferative glomerulonephritis complicated with focal segmental glomerulosclerosis and nephrotic syndrome, who develop renal failure within 3 years after renal transplantation, there are reports that the incidence of recurrent glomerulonephritis in the transplanted kidney is very high.

　　3. Western Medicine Treatment:

　　1. Dexamethasone 1mg/(kg/d) (not exceeding 60mg) + 10% glucose 150 to 250mL, intravenous infusion, once a day,

　　2. Nitrogen mustard 0, 1mg/(kg/d) (not exceeding 5mg), intravenous injection, once a day. A course of treatment consists of 4 days. During the course, symptomatic treatment such as antiemetic and leukocyte elevation is administered. The second course is given at an interval of 7 to 14 days. If the condition does not improve, the patient may be readmitted for repeated treatment as above every 4 to 12 weeks, depending on the patient's condition; if the condition improves, the patient is readmitted sequentially every 1, 3, 6, and 12 months for consolidation treatment, 4 times each, with each treatment consisting of a course of treatment. The interval between treatments is maintained with prednisone, 14mg/(kg/d) in the first week, and then reduced by 1.1mg/(kg/d) per week, stopping after 4 weeks.