Monday, November 30, 2015

IgA nephritis, identification, and treatment of complications

iga nephritis is not easily confused with other diseases, and which diseases will be confused, will not cause other diseases, with how to treat iga nephritis? Let us look at the following presentation experts.

IgA nephritis and the diseases easily confused?

Subject to biopsy confirmed the disease before diagnosis. But there are obvious disease IgA deposition in glomerular mesangial area in many, attention should be identified. Should be included in the differential of the most common are: allergic purpura and purpura nephritis, systemic lupus erythematosus, and hepatic endogenous glomerular sclerosis. There are also ankylosing spondylitis, rheumatoid arthritis, mixed connective tissue disease such as arthritis and collagen disease after infection; gluten enteropathy, ulcerative colitis and enteritis and other intestinal diseases; dermatitis herpetiformis and silver psoriasis and other skin diseases; lung cancer, laryngeal cancer, mucinous adenocarcinoma, IgA gammaglobulin disease, mycosis fungoides and non-Hodgkin lymphoma tumor disease; cyclical neutropenia neutropenia, mixed cryoglobulin hyperlipidemia, immune thrombocytopenia and polycythemia psychosis blood diseases; and idiopathic pulmonary hemosiderosis disease, sarcoidosis, retroperitoneal fibrosis, amyloidosis, myasthenia gravis, leprosy, HIV infection and thin basement membrane nephropathy, should also be included in the differential.

IgA nephritis can be complicated by the diseases?

The disease may have spontaneous remission, or about 4% to 20%. Each year, about 1% to 2% of the patients to end stage renal failure. Statistical analysis showed that the life expectancy table for 10 years graft survival was 80% to 90%. Estimation eventually developed into uremia about 35%. Rest for sustained hematuria or proteinuria. Poor prognosis factors: when the onset of renal insufficiency, proteinuria more than 1.5g / d, high blood pressure and no gross hematuria; renal biopsy glomerular sclerosis, interstitial fibrosis, glomerular capillary was violations, diffuse proliferative and diffuse crescent formation.

IgA nephritis should be treated?

So far, the disease is no satisfactory treatment. Use of this disease were associated with adrenal corticosteroids with or without immunosuppressants renal dysfunction results are not consistent. Recent data suggest that proteinuria exceeding 1g / d who impose adrenocorticotropic hormone medication every other day to improve proteinuria helpful. IgA deposition to have minimal change nephrotic proteinuria is likely to ease. The combined use of cyclophosphamide, dipyridamole and warfarin can reduce proteinuria and no influence on the glomerular filtration rate; combined use of cyclosporine A may also reduce proteinuria, then also reduced creatinine clearance. The efficacy of phenytoin, antiplatelet drugs, anthocyanin acid disodium diphenyl hydantoin and other drugs not sure. Although reports of urokinase may have a role in protecting the glomerular filtration rate, but far from conclusive. Recurrent tonsillitis, tonsillectomy may be beneficial; antibiotics to prevent and treat the infection for some acute nephritic syndrome and acute renal failure as a performer may help. A smaller series has observed that the use of fish oil formulations reduce proteinuria and increased glomerular filtration rate effect. Severe IgA nephropathy (glomerular filtration rate monthly 2 ~ 4ml / min) use of large doses of immune globulin intravenous infusion period, you can stop the glomerular filtration rate, improve hematuria and proteinuria, but after stopping often relapse. To have high blood pressure and severe proteinuria cases, the use of converting enzyme inhibitors can slow the rate of decline in glomerular filtration rate and reduce proteinuria, so severe IgA nephropathy, converting enzyme inhibitors are the first choice of antihypertensive drugs. Blood pressure normal conversion inhibitors can effectively unclear.

IgA nephropathy with end-stage kidney transplant, the transplanted kidney mesangial IgA deposition to happen soon; if there are subclinical kidney donors IgA nephropathy, IgA nephropathy after implantation of non-uremia, kidney mesangial IgA deposits often rapidly disappearing. Renal transplant recurrent IgA nephropathy with progressive renal failure is not inevitable, however administered after kidney transplantation immunosuppressive therapy, including cyclosporine A did not stop its development. Cadaveric renal transplantation, the 1-year and 3-year graft survival rate of up to 87% and 77%, but individual anti-HLA antigen IgA antibody IgA kidney transplants, 2-year graft survival rate of up to 100% reason to believe that these anti-HLA antigens to increase graft survival played a useful role.


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