IgA nephropathy Since Berger first reported IgA nephropathy (IgAN1) 40 years ago, the understanding of IgAN has increased over the years and it is now recognized as a group of clinical syndromes rather than a single disease. The clinical presentation can range from asymptomatic microscopic hematuria with (or without) proteinuria to typical nephrotic syndrome or rapidly progressive nephritis with crescent formation, with approximately 20%-25% slowly progressing to end-stage renal disease (ESRD) after 20-25 years. Until the exact mechanism of IgAN is clarified, active intervention of risk factors that aggravate the progression of renal lesions and different treatment strategies for different clinical types are the basic principles in the treatment of IgAN today. But how to implement staged treatment? Which treatments are more protective of long-term renal function needs to be based on a large number of clinical trials. Risk factors for the progression of IgAN Clinical observations have found that multiple risk factors in epidemiology, clinical presentation and histology are closely related to the progression of IgAN. Men with obesity or smoking have a poor prognosis. Those with persistent proteinuria (even if only >0.5-1.0 g/d), hypertension, and renal insufficiency at the beginning of treatment, especially those with blood muscle (Scr) >176.8 mmol/L, have a poor prognosis. Blood uric acid levels have also been recently reported to be associated with IgAN progression. Renal biopsy shows a high percentage of glomerulosclerosis, crescent formation, tubular atrophy and interstitial fibrosis with a poor prognosis. Therefore, however, special attention should be given to intervene in these risk factors in the treatment, especially to actively control hypertension and proteinuria. The goal of hypertension treatment is ≤120/75-130/80 mm Hg. small amount of proteinuria (20% of IgAN 4-year kidney survival rate is less than 5O%. If the crescent is >5O%, the 5-year kidney survival rate is significantly lower than that of crescentic nephritis due to anti-neutrophil cytoplasmic antibody (ANCA) vasculitis. Therefore . Intensive immunosuppressive therapy is generally considered necessary for this type. However, the criteria for the percentage of crescentic bodies have not been standardized (some foreign studies have defined the percentage of crescentic bodies as >10%). Treatment of IgAN with massive proteinuria A small proportion of IgAN presents with massive proteinuria or typical nephrotic syndrome without or with only a small amount of microscopic hematuria, and may have hypertension, renal insufficiency and abnormal renal tubular function. The pathology of renal biopsy is mainly podocytic lesions, and glomerular thylakoid lesions are very mild, similar to “microscopic lesions” in mild cases, and segmental and globular sclerosis with tubulointerstitial lesions in severe cases. The glomerular podocyte marker Wilms tumor gene (WT1) expression may be diminished or segmentally absent. Treatment of this type of IgAN is difficult, and there is a lack of effective treatment with a poor prognosis. For patients with mild glomerular and tubulointerstitial lesions, no loss of pedunculated cells or segmental loss of WT1 expression on renal biopsy, glucocorticoid induction therapy can be tried. Those who respond sensitively can continue maintenance therapy with hormones. However, in patients with severe glomerular or tubulointerstitial lesions or those who have developed renal insufficiency, hormone or cytotoxic drug therapy is ineffective. The main choice is symptomatic treatment and strategies to protect renal function, such as low salt and low protein diet, ACEI and/or ARB, lipid-lowering therapy and correction of electrolyte balance disorders, etc. In patients with anemia or renal tubular damage, erythropoietin and wormwood preparations can be applied. Comorbidities such as infections brought about by excessive immunosuppressive therapy should be avoided, and we do not advocate the use of MMF or CTX in such patients.