Lupus nephritis is kidney damage in SLE. About more than 50% of SLE patients have clinical manifestations of kidney damage, and kidney biopsy shows almost 100% kidney involvement. Lupus nephritis is one of the important causes of end-stage renal failure in China, which may be closely related to genetic factors, infectious factors, sex hormone abnormalities, and drug factors. Immune complex formation and deposition are the main mechanisms causing lupus nephritis. Circulating autoantibodies such as anti-double-stranded DNA combine with corresponding antigens to form immune complexes, which are deposited in the glomeruli; or circulating anti-double-stranded DNA antibodies directly combine with antigens deposited in the kidneys; or circulating autoantibodies combine with intrinsic glomerular antigens to form in situ immune complexes. The deposited immune complexes activate complement, which can cause inflammatory cell infiltration, activation of coagulation factors and release of inflammatory mediators, thus leading to kidney injury. The renal manifestations of lupus nephritis vary widely, and may be asymptomatic proteinuria and/or hematuria, or manifest as hypertension, nephrotic syndrome, or acute nephritic syndrome. The disease may progress gradually to chronic kidney disease, with uremia occurring in advanced stages. Proteinuria is the most common and varies in severity. Large amounts of proteinuria and even nephrotic syndrome can be seen in diffuse proliferative and/or membranous lupus nephritis. It is recommended that patients with lupus nephritis should seek medical treatment as soon as possible, complete the relevant examinations as prescribed by the doctor, and standardize the treatment under the doctor’s guidance to avoid aggravation of the condition.