IgA nephropathy is an immune complex glomerulonephritis characterized by IgA deposition in the glomerular thylakoid region, which is the most common primary glomerular disease worldwide and the main type of chronic kidney disease in China, and accounts for about 40% of primary glomerular disease in China due to less popular renal biopsy. In the past, IgA nephropathy was considered to be a disease with good prognosis, but it is now clear that IgA nephropathy is a progressive disease, with about 20% of patients progressing to chronic renal failure every 10 years after the onset, and IgA nephropathy is still the first primary cause of chronic maintenance hemodialysis in China (mostly diabetic nephropathy abroad). Therefore, importance should be attached to the early diagnosis and treatment of patients with IgA nephropathy, to delay the deterioration of renal function and reduce the occurrence of uremia in patients with IgA nephropathy as much as possible. Diagnosis of IgA nephropathy IgA nephropathy mainly manifests clinically as hematuria and varying degrees of proteinuria, which are not essentially different from the clinical manifestations of other nephritis; therefore, it is difficult to make an exact diagnosis based on clinical manifestations alone.The diagnosis of IgA nephropathy must rely on the pathological diagnosis of kidney biopsy. Many of the occult nephritis we used to think, in fact, were confirmed to be mostly IGA nephropathy after a kidney puncture biopsy. 1, how to choose kidney biopsy cases Most nephrologists in Europe and America advocate kidney biopsy only for patients with persistent urine protein greater than 1 g/24 h. Some scholars in China found that after summarizing and analyzing the clinicopathological data of more than 1000 cases of IgA nephropathy, some patients who need active treatment may be missed if this criterion is followed. This is because there are many patients with urine protein around 0.5 g/24 h who already have moderate (Lee’s classification grade III) pathological damage. Therefore, it is advocated that in hospitals with more mature renal biopsy techniques, renal biopsy can be considered whenever persistent urine protein >0.5 g/24 h is accompanied by microscopic hematuria. In order to make early diagnosis, early treatment and maintain normal and stable renal function. (Microscopic hematuria alone is not necessary for renal biopsy). Although the clinical manifestation of IgA nephropathy lacks specificity, the recurrent occurrence of carnal hematuria after cold or tonsillitis episodes, as well as an increased serum IgA/C3 ratio (>3) should be highly suspected of IgA nephropathy. 2, the hallmark pathological changes of IgA nephropathy The hallmark pathological changes of IgA nephropathy are the deposition of IgA in the glomerular thylakoid region. The light microscopic changes of IgA nephropathy are diverse, the most common being proliferation of the thylakoid membranes, which can also appear as almost normal “mild lesions” or different sites (inside and outside the capillaries) with different degrees of proliferation and sclerosis. Crescent formation is often seen in renal biopsy specimens of carnaroscopic hematuria with acute renal insufficiency, and the majority of crescent bodies in IgA nephropathy are small crescent bodies of less than half a week. Interstitial tubular lesions are not significantly different from other progressive glomerulonephritis. Our study showed that the incidence of intrarenal arteriopathy in IgA nephropathy is higher than that in non-IgA thylakoid proliferative glomerulonephritis and idiopathic membranous nephropathy, and the incidence of heavy small renal arteriopathy and vitreous lesions is high. electron microscopy in IgA nephropathy mainly shows electron-dense material deposition in the thylakoid and paraganglial areas. 3, the treatment of IgA nephropathy IgA nephropathy pathogenesis is complex, involving more factors, so far, there is no special measures for the treatment of IgA nephropathy. Since the prognosis of IgA nephropathy is mainly related to hypertension, massive proteinuria, impaired renal function, glomerulosclerosis, interstitial fibrosis and small renal artery sclerosis, the treatment of IgA nephropathy should be treated differently according to the presence or absence of these indicators and the degree of severity, and individualized graded treatment should be adopted. Treatment principles: ① Prevent and control infection; ② Control blood pressure within a reasonable range, i.e. control blood pressure according to the level of proteinuria; ③ Apply Chinese and Western medicine to control proteinuria; ④ Protect kidney function; ⑤ Avoid exertion, dehydration and use of nephrotoxic drugs; ⑥ Regular review, etc. Commonly used treatments include: angiotensin-converting enzyme inhibitors (ACEI, such as Lodinexin, Monox) and angiotensin receptor antagonists (ARB, such as Cozoa, Devon) and other antihypertensive drugs, glucocorticoids and other immunosuppressants, anticoagulation, antiplatelet aggregation and pro-fibrinolytic drugs, as well as traditional Chinese medicine and tonsil removal. 1. For patients who develop meatus hematuria or abnormal aggravation of urinalysis after tonsillar infection, actively control the infection and perform tonsil removal early. Retrospective studies have shown that tonsil removal is effective in mild to moderate IgA nephropathy and can reduce the incidence of proteinuria, hematuria and end-stage renal failure. 2. For patients with normal blood pressure, normal renal function and urinary protein <1 g/24 h, most foreign scholars believe that no special treatment is needed and only regular review is required. However, we found that these patients should be combined with the pathological manifestation of renal biopsy and the corresponding treatment plan should be formulated to actively treat the patients, which is conducive to their complete remission. 3. For patients with urine protein >1 g/24 h, ACEI or (and) ARB are preferred, striving to reduce urine protein to less than 0.5 g/24 h. If the blood pressure has been reduced to 125/75 mmHg with adequate ACEI and ARB and the urine protein is still >1 g/24 h, additional glucocorticoid therapy is recommended. The application of hormones and other immunosuppressive agents should be considered in addition to the amount of urine protein and the pathological changes on renal biopsy. Significant inflammatory cell infiltration, cell proliferation, and especially cell crescent formation are indications for the application of hormones and other immunosuppressive agents. For patients with IgA nephropathy combined with microscopic lesion nephrotic syndrome, they are treated as microscopic lesion nephrotic syndrome. If sclerosis or fibrous crescent of the glomerulus has already appeared, the above treatment would be more than worthwhile. For patients with IgA nephropathy combined with hypertension, strive to lower the blood pressure to below 130/80 mmHg or even lower; if urine protein >1.0 g/24 h, try to lower the blood pressure to 125/75 mmHg. Commonly used antihypertensive drugs include ACEI, ARB, long-acting calcium antagonists, diuretics and the therapeutic effect of beta-blockers and alpha-blockers to be supported by further clinical evidence. …… 5. For patients with IgA nephropathy combined with renal insufficiency, it is appropriate to first clarify the cause of renal insufficiency and treat the cause. We gave ACEI combined with urokinase to patients with moderate-to-severe IgA nephropathy with obvious cell proliferation and fibrin deposition, and achieved good results in reducing proteinuria and delaying the deterioration of renal function. We applied combined Chinese and Western medicine therapy to treat IGA nephropathy with certain efficacy, especially in controlling proteinuria, which is more obvious, while the integrated therapy of Chinese and Western medicine can effectively control the progression of IGA nephropathy when chronic renal function impairment occurs, and the specific mechanism is still under study.