In China, IgA nephropathy accounts for 30%-40% of primary glomerular diseases and has become one of the most common causes of end-stage renal disease in China. Clinically, IgA nephropathy is characterized by insidious onset, more factors influencing the disease, delayed course, and large individual differences in outcome. Most of the research literature on IgA nephropathy is based on the “Chinese medicine classification scheme for chronic nephritis” adopted at the Fourth National Conference on Chinese Medicine and Nephrology in 1988. With the development of modern medicine, quantitative criteria have been introduced into the identification of IgAN in TCM, and the most important factors of IgAN renal function impairment and prognosis are focal segmental sclerosis, interstitial fibrosis and tubular atrophy, which are graded according to the degree of occurrence and then controlled. The evidence of deficiency of kidney qi and yin (kidney deficiency), stasis and paralysis of kidney ligament (stasis and paralysis), wind and dampness disturbing kidney (wind and dampness), internal movement of liver wind (liver wind), and internal retention of drowning toxin (drowning toxicity) are more consistent with the spectrum of IgAN, the pattern of evidence evolution and pathogenic changes. The most critical basic symptom of IgAN is kidney deficiency, and the deficiency of kidney qi and yin is common to many chronic kidney diseases from the beginning of abnormal urinalysis. The Chinese medicine believes that: the kidney is the foundation of the innate nature, hiding the true yin and the Yang, all kidney diseases are mostly Yang loss and Yin depletion, so the kidney deficiency is extremely common in the clinic. Most patients with chronic kidney disease have a certain degree of deficiency, although each individual patient may differ in the degree of deficiency of Qi and Yin, but on the whole, it is still a deficiency of Qi and Yin, no need to further divide the deficiency of Qi, Yin or even Yang deficiency. The main symptom is only trace foamy urine (urine protein quantification <1.0g/24h). The pathological changes in these patients are mostly thylakoid proliferative lesions, and interstitial and vascular lesions are not obvious; microscopic polymorphic erythrocyturia and small amount of proteinuria.