IgA nephropathy, also known as Berger’s disease, is a specific type of glomerulonephritis that occurs mostly in children and young adults, often preceded by upper respiratory tract infections, and is characterized by glomerular thylakoid hyperplasia with IgA deposits in the thylakoid region as seen by immunofluorescence. IgA nephropathy is a group of chronic glomerular diseases with the same immunopathological features caused by multiple etiologies. Its clinical manifestations are diverse, mainly presenting as hematuria, which may be accompanied by varying degrees of proteinuria, hypertension and impaired renal function, and is one of the common primary glomerular diseases leading to end-stage renal disease. Approximately 40% to 45% of patients present with carnal or microscopic hematuria, 35% to 40% present with microscopic hematuria with proteinuria, and the rest present with nephrotic syndrome and renal failure. IgA nephropathy is a common glomerular disease worldwide. In Asia and the Pacific, IgA nephropathy is the most common primary glomerular disease, accounting for 30-40% of patients with renal biopsies. In China, IgA nephropathy accounts for 40-47.2% of primary glomerular diseases. And the data show that in the past 10 years and the trend is clearly increasing. To date, the exact pathogenesis of IgA nephropathy has not been elucidated, and multiple factors are involved in the development and progression of the disease; the synthesis and release of IgA1 molecules (i.e., immunoglobulins deposited in the glomerular thylakoid region) and their persistence in peripheral blood, binding to thylakoid cells and deposition, and the triggered inflammatory response are the pathogenic processes specific to IgA nephropathy, and the subsequent inflammatory response results in Glomerular cell proliferation, glomerulosclerosis, tubular atrophy, and interstitial fibrosis are common pathways for the progression of all glomerular diseases. Patients with IgA nephropathy may present with the following clinical manifestations: 1. Episodic granulomatous hematuria: Most often seen in children. Their granulomatous hematuria mostly occurs after upper respiratory tract infections (tonsillitis, etc.), with an interval of 24 to 72 hours. Sarcopenic hematuria can last for a few hours to a few days, then it turns into persistent microscopic hematuria, and some patients’ hematuria can disappear. 2. Microscopic hematuria and asymptomatic proteinuria: This is the main clinical manifestation of IgA nephropathy in children and adolescents and is often detected during physical examination, which can be manifested as simple microscopic hematuria or microscopic hematuria with a small amount of proteinuria. 3.Proteinuria: Mild proteinuria, urine protein quantification is generally <1g/24h, a small number of patients may have a large amount of proteinuria or even nephrotic syndrome. 4.Other: Some patients with IgA nephropathy may develop nephrotic syndrome, acute nephritis syndrome, renal failure, and a few may develop severe back and/or abdominal pain with hematuria. The diagnosis of IgA nephropathy can be considered if the following conditions are met: 1. carnal hematuria or microscopic hematuria (glomerular origin, predominantly aberrant red blood cells) or asymptomatic proteinuria after upper respiratory tract infection; 2. serum IgA may be elevated; 3. immunofluorescence of granular IgA predominantly seen in the glomerular thylakoid region on immunopathological examination of renal biopsy; 4. except acute glomerulonephritis after streptococcal infection, non IgA thylakoid proliferative nephritis, thin basement membrane nephropathy, lupus nephritis, purpura nephritis, liver cirrhosis and renal damage of alcoholic liver disease, etc. Treatment principles: 1. deter the invasion of pathogens and various antigens; 2. alleviate the abnormal immune response, such as through the use of hormones and other immunosuppressive drugs; 3. clear immune complexes; 4. repair glomerular damage; 5. Chinese medicine evidence-based treatment; 6. B-cell monotherapy to reduce IgA production; 7. general treatment: control blood pressure; avoid strain, high-quality protein diet, etc.