Textbooks often treat IgA-N as an independent disease, but in fact, the pathogenesis and clinical manifestations are too variable, and the treatment and prognosis are too different to be treated as a single disease, but must be typed. The pathological typing of IgA-N currently mentioned in the literature is too old, such as Lee’sHaans, etc. The fundamental problem is that the substance of the disease has not been touched, and at most there is only a certain prognostic significance. The clinical manifestations of IgA-N have shown certain clustering features. Therefore, clinicopathologic typing based on clinical manifestations has the potential to advance our understanding of IgA-N. Certain clinical manifestations have recognized prognostic significance Isolated microscopic hematuria; recurrent carnituria; massive proteinuria; persistent hypertension 2. Guiding significance Recurrent carnitic hematuria that appears rapidly after infection II. New clinical classification (I) Simple microscopic hematuria type (I-H): 1. Abnormal urinalysis: microscopic hematuria, no proteinuria, no carnitic hematuria 2, normal renal function, no hypertension. Pathology: pathological changes were mild, with only IgA deposition in the thylakoid area, fewer sclerosing spheres, no crescent, mild tubular interstitial lesions, and insignificant vascular lesions. The electron microscopy excluded “thin basement membrane nephropathy”. (B) Abnormal urinalysis (U-ab): 1. The onset of the disease is often insidious, the exact course of the disease is not easily determined, and the clinical symptoms have no obvious features. 2, abnormal urinalysis: single episode of microscopic hematuria or carnal hematuria, urine protein <2.0g/24hr. 3, no hypoproteinemia, normal renal function, no hypertension. 4, Pathology: pathological changes varied in severity from mild thylakoid proliferative lesions, FSGS to glomerulosclerosis. Deposits in the thylakoid region are often IgG in addition to IgA, and vascular collateral deposition can occur. Interstitial lesions are mild to moderate. However, extensive sclerosis is not present. (iii) Recurrent episodes of carnitic hematuria (R-GH): 1. Recurrent episodes of carnitic hematuria, which can be fresh or old, ≥2 times. There is a prodromal infection (upper sensation mostly, but also may be cholecystitis or diarrhea) several hours (not longer than 24 hours) before the attack, and there may be back pain and abdominal pain during the attack. There is no obvious hypoproteinemia, and the renal function is normal or mildly abnormal. 3. Age of onset is mostly in youth. 4.Pathology: within 1 month of the onset of carnivorous hematuria, segmental cellular crescents (<10%) are seen without collaterals necrosis. There is little glomerular sclerosis, mild interstitial lesions, and no severe vascular lesions. (iv) Crescentic type (Cres. IgA-N): 1. It is often associated with meatus hematuria can last for a long time, or microscopic hematuria more than 500,000/ml. 2. It can be combined with hypertension, and Scr can be mildly elevated. ANCA may be positive in some patients. 3, Pathology: often with collaterals necrosis, crescent > 15%, blood vessels may show fibrin-like degeneration or necrosis, positive Fibrin stain. (E) Massive proteinuria (MP): 1, urine protein and swelling as the main manifestation, usually without carnal hematuria. Urine protein > 3.5g/24h, hypoproteinemia is obvious, Alb <30g/l, with hyperlipidemia. There is obvious swelling. 2. Blood pressure is normal or mildly elevated, and renal function can be abnormal. The disease duration is long. 3, Pathology: glomerulosclerosis is more common, often with basement membrane lesions and mild-moderate tubulointerstitial lesions. (F) Hypertensive type (HT): The prominent manifestation is persistent elevation of blood pressure, which is often controlled by antihypertensive drugs, and there may be different degrees of renal insufficiency, which may also be combined with a certain degree of abnormal urinalysis. 1. Isolated hematuria or persistent microscopic hematuria, urine protein <3.5g/24h. 2. Elevated blood pressure at the beginning of the disease, blood pressure >140/85mmHg at the time of enrollment, with or without other target organ damage. 3, Scr normal or elevated, but <5mg/dl. 4, Pathology: more chronic lesions, more spherical sclerosis, moderate to severe interstitial lesions. Vascular lesions are prominent, with more vascular hyaline lesions. (G) End-stage renal failure type (ESRD): 1. blood creatinine greater than 5.0 mg/dl; 2. pathology more spherical sclerosis and severe tubular interstitial lesions. III. Treatment recommendations for each type of IgA nephropathy Clinical typing percentage treatment principle Simple microscopic hematuria 2.8% Chinese medicine evidence-based treatment, immunosuppressant is ineffective, follow up for mild cases Abnormal urinalysis 42.9% Chinese medicine evidence-based treatment + Reglan + ACEI + ARB, can try MMF Crescentic type 7.2% MMF + Chinese medicine evidence-based treatment, hormone + Reglan 13.2% Recurrent botrythematous hematuria Chinese herbal treatment, can try Lei Gong Teng + tonsil debridement 10.9% of the type of massive proteinuria Chinese herbal treatment, symptomatic support, can try immunosuppressive drugs 18.9% of the type of hypertension Chinese herbal treatment, symptomatic support, can try immunosuppressive drugs End-stage renal failure Chinese herbal treatment, delay renal failure, if necessary, replacement therapy