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IgA nephritis

  IgA glomerulonephritis (IgA glomerulonephritis) is a recurrent naked eye or microscopic hematuria, glomerular mesangial cell proliferation, increased matrix, with extensive deposition of IgA characterized by primary glomerular disease. In 1968 Berger first described the disease, it is also known as Berger disease. In addition, also known as IgA-IgG mesangial deposition glomerulonephritis and IgA mesangial nephritis. IgA nephropathy can also be interpreted as renal biopsy immunofluorescence glomerular mesangial area has a large number of granular IgA deposition is characterized by primary glomerular disease.


  The disease must be confirmed by renal biopsy can be diagnosed. However, in the glomerular mesangial area of ​​the more obvious IgA deposition of many diseases, should pay attention to identification. The most common should be included in the identification of: Henoch-Schonlein purpura and purpura nephritis, systemic lupus erythematosus and liver-derived glomerulosclerosis. In addition to ankylosing spondylitis, rheumatoid arthritis, mixed connective tissue disease and post-infection arthritis and other collagen diseases; gluten bowel disease, ulcerative colitis and enteric bowel disease and other limitations; herpes-like dermatitis and silver Cystic disease and other skin diseases; lung cancer, laryngeal cancer, mucinous adenocarcinoma, IgA glomerulonephritis, mycosis fungoides and non-Hodgkin's lymphoma and other neoplastic disease; cyclophilic neutropenia, mixed cryoglobulin Hematological disorders such as idiopathic pulmonary hemosiderosis, sarcoidosis, retroperitoneal fibrosis, amyloidosis, myasthenia gravis, leprosy, HIV infection, and / Thin basement membrane nephropathy should also be included in the identification.

  Treatment measures

  So far, there is no satisfactory treatment of the disease. Of the disease associated with progressive renal dysfunction in patients with adrenal cortex hormones with or without the results of immunosuppressive agents are not consistent. Recent data suggest that proteinuria more than 1g / d, the application of every other day of the adrenal cortex hormones on proteinuria beneficial to improve. For IgA deposition of minimal change nephropathy is likely to ease proteinuria. Combined use of cyclophosphamide, dipyridamole and Hua Linlin can reduce proteinuria and no effect on glomerular filtration rate; combined use of cyclosporine A can also reduce proteinuria, but also reduce the creatinine clearance rate. Phenytoin, anti-platelet drugs, disodium glycoside, diphenylhydantoin drugs such as the efficacy of uncertainty. Although urokinase may be reported to protect the glomerular filtration rate, but far from conclusive. Recurrent tonsillitis, tonsillectomy may be beneficial; antibiotic prophylaxis and treatment of infection on some acute nephritic syndrome and acute renal failure as the performance may be helpful. A smaller series of observations has found that fish oil preparations have the effect of reducing proteinuria and increasing glomerular filtration rate. Severe IgA nephropathy (glomerular filtration rate decreased 2 ~ 4ml / min per month) the use of high-dose intravenous immunoglobulin during the glomerular filtration rate can be reduced to improve hematuria and proteinuria, but after stopping Often relapse. In patients with hypertension and severe proteinuria, the use of converting enzyme inhibitors can slow down the rate of glomerular filtration rate and reduce proteinuria, so in severe IgA nephropathy, conversion enzyme inhibitors is the preferred antihypertensive drugs. It is not clear whether the conversion inhibitor is effective in normotensive subjects.

  IgA nephropathy in renal transplant recipients, the rapid occurrence of renal mesangial IgA deposition; if renal donors have subclinical IgA nephropathy, non-IgA nephrotic uremia implanted, the donor mesangial IgA deposits often Quickly disappear. Transplantation of renal disease with recurrent IgA nephropathy does not necessarily occur with progressive renal failure, however, immunosuppressive therapy after renal transplantation, including cyclosporine A also can not prevent its development. For cadaveric kidney transplantation, the survival rates of renal allografts at 1 year and 3 years were 87% and 77% respectively. However, IgA renal transplant recipients with anti-HLA antigens were 100% It is reasonable to believe that these anti-HLA antigens have a beneficial effect on the survival of transplanted kidneys.

  Auxiliary examination

  Microscopic hematuria, urinary red blood cells to deformed mainly. About 50% of patients with serum IgA increased, but has nothing to do with the disease activity. Serum IgA lambda light chain concentration increased. Urine immunoglobulin determination of no special significance. Blood complement components are mostly normal. Certain complement components or factors may be reduced, mainly in a family of patients with high tendency, but does not have diagnostic value. About half of the patients IgA-fibronectin aggregates may have a transient increase, although it helps to identify with other nephropathy, but it has nothing to do with the disease activity, so there is no diagnostic value. 10% to 15% of patients with IgA circulating immune complexes increased, 32% of patients with elevated levels of IgA rheumatoid factor. Several immunological parameters, including virus and food antigens, antibodies, T cell subsets, HLA loci antigen and other determination of the results may have changed, but no diagnostic value. 50% of the patient's forearm volar skin biopsy can be seen in the capillaries with IgA and C3 deposition.


  The disease may have spontaneous remission, accounting for about 4% to 20%. Each year about 1% to 2% of cases of end-stage renal failure. Life table statistical analysis showed that 10-year survival rate of 80% to 90%. Estimated to eventually develop into uremia were about 35%. The remainder were persistent hematuria or proteinuria. Suggesting that poor prognosis factors are: onset of renal insufficiency, proteinuria more than 1.5g / d, high blood pressure and no gross hematuria; renal biopsy with glomerulosclerosis, interstitial fibrosis, glomerular capillary was Invasion, diffuse proliferation and diffuse crescent formation.

  Diet therapy

  1. Protein supply. Chronic nephritis diet should be based on the extent of renal damage to determine the protein intake, if the long course of disease, renal damage is not serious, the food protein is not strictly limited, but not more than 1 gram per kilogram of body weight per day, Quality protein to reach more than 50%.

  2. Because some patients limit the protein, the heat supply to carbohydrates and fat as the main source of energy supply depending on the labor intensity may be. Rest, adults can supply 126 kilojoules to 147 kilojoules per day (30 kcal to 35 kcal) / kg body weight. And to meet the needs of patient activities.

  3. Control of sodium intake. Severe edema and high blood pressure, the amount of sodium salt to be controlled at 2 g / day, or even given no salt diet, generally low salt is appropriate.

  Chinese tea therapy

  For thousands of years, through a variety of tea therapy practice, people gradually learned that tea with 27 kinds of medicinal effects: kidney, diuretic, sedative Chufan, less sleep sound, eyesight, clear head, gas, digestion, Anti-aging, anti-aging, anti-aging, anti-aging, anti-aging, anti-aging, anti-fatigue, anti-aging, anti-aging Cancer, anti-radiation.

  In addition to the daily life of tea as a drink in addition to prevention and treatment of nephritis can adjust the balance of human body mechanism, anti-inflammatory anti-bacterial, and enhance human resistance, greatly reduced by the nephritis caused by a series of complications. Such herbal tea are mainly Astragalus, honeysuckle, Cordyceps and so on.

  health care

  Chronic nephritis food choices: 1. To give adequate vitamins, in particular, to add vitamin c, because patients with chronic nephritis may have anemia, vitamin c can increase the absorption of iron, it should be eating tomatoes, green leafy vegetables, fresh jujube , Watermelon, heart beauty radish, cucumber, watermelon, citrus, kiwi fruit and natural fruit juice and other food.

  2. Poor appetite can be added vitamin c preparations; at the same time should be more vitamin B and folic acid-rich foods such as animal offal, green leafy vegetables and other foods, help to correct anemia. High potassium when not to eat high potassium foods, to be careful selection of vegetables and fruits. Chronic nephritis patients to avoid carbohydrate drinks and spicy food.

  3, eat more food diuretic swelling of food are: carp, crucian carp, goat's milk, watermelon, melon, mung bean, red bean and so on. Watermelon skin boiled water, its diuretic effect is better.

  IgA nephritis incidence

  The incidence rates reported vary widely across the world, with the highest incidence in the Western Pacific region. Japan reports 50% of biopsy-proven glomerular diseases, compared with about 10% to 30% in Europe and less than 2% in the United States. Reported around the country are not the same, about 20% to 30%. This difference is clearly also affected by indications of renal biopsy and urine censuses across the country, for example in the UK at around 5%, whereas in the Scottish area, 37% of a group of asymptomatic hematuria biopsies. The disease is more common in men, male to female ratio of about 2: 1. There are differences between races, such as the United States New Mexico Indian Indians accounted for 35%, blacks are very rare. Although it was found that black IgA2m (1) was significantly lower than whites, but failed to prove that there is a positive relationship with the low incidence. Since 1978, some reports suggest that the disease has a high tendency of the family, suggesting that at least some IgA nephropathy in the presence of genetic susceptibility. HLA analysis was found to be associated with Bw35 and DR4. A recent analysis of IgA-induced end-stage renal failure suggested an increase in the frequency of B27 and DR1 and a decrease in DR2.

  Related research

  Subpopulations of macrophages in children with IgA nephritis and their

  Satoshi Hisano, MD, Department of Pathology, Second Hospital of Fukuoka Medical College, Fukuoka, Japan To clarify the clinical and pathological differences between acute glomerulonephritis (PSAGN) and IgA nephritis (IgAGN) after streptococcal infection, PSAGN children and 20 children with histologically similar IgA nephritis with PSAGN, the number of infiltrating cells in the glomeruli was observed.

  (CD20), neutrophil marker (CD15), macrophage marker (CD68), four macrophage subsets (early, acute and chronic phase) And mature inflammatory macrophage markers) and proliferating cell nuclear antigen (PCNA) monoclonal antibody, the patient's kidney tissue immunohistochemistry study.

  Thirty-four patients were divided into three groups according to the time from detection of urinary protein to renal biopsy. Glomerular immunopositive cells are expressed as the number of cells in each glomerulus.

  The number of positive cells of CD15, CD68 and macrophages in glomeruli of PSAGN patients was higher than that of IgAGN patients. In PSAGN tissue, infiltration of macrophages in the glomeruli gradually decreased over time, while the number of macrophages in IgAGN remained constant throughout the period. In IgAGN, macrophage infiltration in the macrophage is evident in the acute phase of acute inflammation. The number of proliferating macrophages (PCNA + CD68-positive) and the ratio of proliferating macrophages / total macrophages in IgAGN patients were greater than those in PSAGN patients.

  All patients with PSAGN were followed up for normal urinalysis, whereas 18 of 18 patients with IgAGN had persistent urinary abnormalities.

  He concluded that the difference in the number of mature and proliferating macrophages in infiltrating macrophages was related to the differential clinical and pathological features of PSAGN and IgAGN.


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