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What is IgA nephropathy?

  What is IgA nephropathy?

  IgA nephropathy

  Since Iger's first report of IgA nephropathy 40 years ago (IgAN1, IgAN has been increasing year by year, and IgAN is now recognized as a group of clinical syndromes rather than a single disease. Clinical manifestations can be seen from asymptomatic hematuria (or ) Proteinuria to typical nephrotic syndrome, or rapid progressive nephritis with crescent formation, about 20% to 25% after 20-25 years of slow development to end-stage renal disease (ESRD). In the exact mechanism of IgAN Clearly before the active intervention to increase the risk of renal disease progression, different clinical types of different treatment strategies are the basic principles of the current treatment of IgAN.However, how to implement the type of treatment? Which treatment is more protection of long-term renal function also requires a large number of clinical The test.

  Risk factors for progression of IgAN

  Clinical observation found that epidemiological, clinical manifestations and histology in a variety of risk factors and IgAN progress is closely related. Men with obesity or smokers have poor prognosis. Persistent proteinuria (even if only 0.5-1.0g / d), high blood pressure, early treatment of renal insufficiency, especially blood (Scr)> 176.8mmol / L poor prognosis. Recent reports of serum uric acid levels are also associated with progression of IgAN. Renal biopsy showed a high proportion of glomerular sclerosis, crescent formation, renal tubular atrophy and interstitial fibrosis were poor prognosis. Therefore, but in the treatment should pay special attention to the intervention of these risk factors, in particular, should actively control the high blood pressure and proteinuria. Hypertension treatment target ≤ 120 / 75-130 / 80 mm Hg. A small amount of proteinuria (20% of IgAN 4 years of renal survival rate of less than 50% .Once studies have found that even if the crescent ratio is only 10% .3 years later 40% of patients into ESRD. If the crescent> 5O% 5-year survival was significantly lower than that of anti-neutrophil cytoplasmic antibody (ANCA) vasculitis due to crescentic nephritis.Therefore, it is generally considered necessary to strengthen immunosuppressive therapy in this type, but the current ratio of crescent The standard has not yet unified (foreign studies have crescent ratio as "10%).

  A large number of proteinuria IgAN treatment

  A small number of IgAN showed a large number of proteinuria or typical nephrotic syndrome, no or only a small amount of microscopic hematuria, may have high blood pressure, renal insufficiency and renal tubular dysfunction. Renal biopsy pathology mainly podocyte lesions, glomerular mesangial disease is very light, light similar to "small lesions", severe cases may have segmental sclerosis and sclerosis, with tubulointerstitial lesions. The glomerular podocyte marker Wilms tumor gene (WT1) expression may be attenuated or fragmented. This type of IgAN treatment is very difficult, the current lack of effective treatment, the prognosis is poor. Renal biopsy showed glomerular and tubulointerstitial lesions, no cell shedding or WT1 expression in patients with missing segments, you can try glucocorticoid induction therapy. Sensitive can continue to use hormone maintenance therapy. But the glomerular or renal tubulointerstitial lesions, or have been renal insufficiency, hormone or cytotoxic drug treatment is poor, the main choice of symptomatic treatment and protection of renal function strategies, such as low salt and low protein diet, ACEI And (or) ARB, lipid-lowering treatment and correction of electrolyte balance disorders, such as anemia or renal tubular damage can be applied to erythropoietin and Cordyceps preparations. Should avoid excessive immunosuppressive therapy to bring infection and other comorbidities, such patients we do not advocate the use of MMF or CTX.