SLE is an atopic autoimmune disease involving multiple factors including genetics, sex hormones, environment, infection, drugs, and immune response. Patients mainly present with multiple autoantibodies involved and cause multisystem damage through immune complexes and other pathways, and almost every system and organ in the body may be involved. Infection, renal failure and central nervous system damage are the main causes of death in patients. 1. SLE and infection SLE patients are prone to co-infection, and infection is also an important cause of death in SLE patients. Risk factors for infection include glucocorticoids, immunosuppressants, kidney involvement, and immune disorders. Types of infection include bacterial infection, fungal infection, viral infection, and parasitic infection, and the sites of infection involve the skin, bladder, joints, brain, and lung. Clinically, the infection is often insidious, and it is difficult to identify with the primary disease. In some patients, the infection and the primary disease activity exist simultaneously, which brings great contradiction and difficulty to the treatment. 2. Lupus nephritis Renal manifestations are one of the most important clinical manifestations of SLE, and almost all SLE patients can develop renal involvement during the course of the disease. Uremia is a serious complication in SLE patients and an important cause of death in SLE patients. Many studies have shown that renal lesions may be quite serious even if patients do not have obvious clinical manifestations, so renal biopsy should be one of the routine examinations for SLE. According to the classification criteria of renal pathology established by WHO in 1982, lupus nephritis can be divided into 6 types. Membranous lupus nephritis is type V. The clinical manifestations of membranous nephropathy are mainly nephrotic syndrome with massive proteinuria, but the deterioration of renal function is slower than that of value-added nephropathy, and some patients with membranous nephropathy also have combined value-added changes. Membranous nephropathy is less responsive to glucocorticoid and immunosuppressive therapy, and its condition improves more slowly. The neurological manifestations of SLE are quite common, and all parts of the nervous system can be involved, with a variety of clinical manifestations, including headache, dizziness, decreased attention span, various movement disorders, increased intracranial pressure, epilepsy, stroke, and even coma states. Psychiatric manifestations in SLE patients include psychosis, affective disorders, organic encephalopathy syndromes, cognitive impairment, drug reactions (especially glucocorticoids), biorhythm disturbances, and autonomic nervous system disorders. Depressive symptoms, mania, schizophrenia or paranoid psychosis are seen clinically, and some patients present with acute delirium. Inflammatory myopathies (dermatomyositis/polymyositis/dermatomyositis without myositis) The most serious complication of inflammatory myopathies is acute progressive alveolitis, manifested by fever, shortness of breath, severe cough, rapidly progressive dyspnea, and in severe cases, adult respiratory distress syndrome. The first report of myositis associated with malignancy was seen in 1916. There are reports that patients with dermatomyositis are more likely to develop tumors than patients with polymyositis, but some reports do not distinguish between the two. Special attention should be paid to searching for tumors that are predisposed in the appropriate gender and age group in such patients. Systemic vasculitis Vasculitis is a group of diseases that differ in their pathological features, mainly due to inflammation and destruction of blood vessels. The classification of vasculitis is mostly based on the size, type, distribution, extravascular manifestations, clinical features, and primary or secondary characteristics of the involved vessels. Wegener’s granulomatosis is a necrotizing granulomatous vasculitis, an autoimmune disease, involving small arteries, veins and capillaries, and occasionally large arteries, whose pathology is characterized by inflammation of the vascular wall, mainly invading the upper and lower respiratory tract and the kidneys. Clinical manifestations often include nasal and paranasal sinusitis, pulmonary lesions, and progressive renal failure. It may also involve joints, eyes, ears and skin, as well as the heart and nervous system. Common critical complications include hemoptysis, acute respiratory failure, acute/chronic set failure, deafness, blindness, and neurological lesions.