IgA nephropathy is the most common primary glomerular disease in clinical practice and a common cause of end-stage renal failure. the clinical manifestations of IgA nephropathy are complex and varied, the disease progresses at different rates, the diagnosis must rely on renal biopsy pathology, and the treatment varies from person to person, which should be highly valued in clinical practice. I. What are the clinical manifestations of IgA nephropathy? The clinical manifestations of IgA nephropathy are complex and variable, ranging from asymptomatic to very serious clinical manifestations, and the situation varies from person to person. The most common clinical manifestations are: hematuria, proteinuria, back pain, swelling, hypertension, and renal function impairment. Some patients present only with simple carnal hematuria, while others present with simple mild proteinuria (urinary routine protein +~++). Some patients may present with nephrotic syndrome, while others present with acute kidney injury. Different clinical manifestations often indicate different degrees of disease severity. For example, a large amount of proteinuria, hypertension and renal impairment often indicate a more severe disease. The disease often starts after colds, diarrhea and exertion. In particular, those who exhibit carnitic hematuria often show hematuria immediately after upper respiratory tract infection within 72 hours. Second, how to diagnose IgA nephropathy? The diagnosis of IgA nephropathy depends on renal biopsy. The most common manifestation is thylakoid hyperplasia with IgA-based immune deposits. Some patients may also present with glomerulosclerosis, tubular atrophy, tubulointerstitial inflammatory cell infiltration and fibrosis, and vascular sclerosis. Some patients even exhibit crescent formation and vasculitis changes. The type of pathological changes has a very important impact on the prognosis of the disease. Glomerulosclerosis, tubulointerstitial fibrosis and vascular sclerosis suggest a chronic tendency of the disease, indicating that the disease is irreversible. What are the factors that affect the prognosis of IgA nephropathy? Factors affecting the prognosis of IgA nephropathy are: (1) clinical manifestations: persistent massive proteinuria, hypertension, renal function impairment at the beginning of the disease, poor prognosis for those with recurrent disease; prognosis is generally better for those with simple microscopic hematuria or mild proteinuria and normal renal function; (2) pathological manifestations: obvious chronic tendency (such as glomerulosclerosis, tubular atrophy and interstitial fibrosis, vascular sclerosis), massive glomerulosclerosis, tubular atrophy and interstitial fibrosis, and vascular sclerosis. (2) pathological manifestations: pathology with a clear tendency to chronicity (such as glomerulosclerosis, tubular atrophy and interstitial fibrosis), vascular sclerosis), a large number of crescent formation, and significant tubular interstitial inflammation suggest a poor prognosis and easy progression to chronic renal failure. (3) Whether the treatment is timely and appropriate. How to properly treat IgA nephropathy? The treatment of IgA nephropathy varies from person to person and from condition to condition. First of all, patients should pay attention to rest, avoid exertion, enhance resistance and avoid infection. Infection and exertion are the main triggers for recurrent attacks and accelerated progression of the disease. Secondly, high priority should be given to the treatment of hypertension. Many clinical studies have proved that the progression of renal function is significantly accelerated in those with combined hypertension if the blood pressure is not controlled in a timely manner. The most commonly used antihypertensive drugs are ACEI and ARB drugs Those with significant proteinuria (24-hour urine protein quantification of 1 gram or more) should promptly take comprehensive measures to reduce proteinuria, including RAS blockers and immunosuppressants. In recent years, many studies have shown that early and rational use of immunosuppressants can significantly shorten the course of the disease, significantly reduce proteinuria and improve the long-term prognosis of patients. However, the use of immunosuppressive agents has not been standardized and should be selected clinically on an individual basis by an experienced specialist, taking into account the patient’s clinical presentation and pathological features. The general principle is to avoid unnecessary side effects caused by excessive drug doses, but also to effectively control disease progression. The most commonly used immunosuppressive drugs are: glucocorticoids, cyclophosphamide, tacrolimus, cyclosporine A, and ralston. Those with renal insufficiency or progressive deterioration should take measures to protect renal function as soon as possible, and if necessary, they should be hospitalized by a specialist for a comprehensive examination as soon as possible.