lupus nephritis
Introduction
Introduction to lupus nephritis Lupus nephritis refers to a systemic lupus erythematosus (SLE) with immunological damage of different pathological types of the kidneys, accompanied by a clinical manifestation of obvious renal damage. Lupus nephritis (LN) is an important clinical component of SLE. Clinical manifestations of renal involvement include proteinuria, erythrocyte urine, leukocyteuria, tubular urine, and decreased glomerular filtration and tubular dysfunction. The severity of renal damage is closely related to the prognosis of SLE. Renal involvement and progressive renal impairment are one of the major causes of death in SLE and should be given sufficient clinical attention. basic knowledge The proportion of illness: 0.008% Susceptible people: no specific population Mode of infection: non-infectious Complications: femoral head necrosis, cardiovascular disease
Cause
Causes of lupus nephritis
Genetic factors (20%)
The occurrence of SLE is related to genetic factors. The family incidence rate is as high as 3% to 12%, and there is a tendency for family aggregation. After extensive research on the HLA line of SLE patients, it was found that the genes closely related to SLE are mainly at certain loci of HLA, especially in the HLA DR region, and the HLA phenotype is polymorphic. Studies have shown that people with haploid HLA B8/DR2 in the population are more likely to produce hypersensitivity immune responses to cells and body fluids; this may be due to HLA-encoded polymorphism in T and B lymphocytes and antigens. For T inhibition of cell dysfunction, autoantibodies and globulin increased. It is now believed that the SLE susceptibility gene is a gene of a different structure of the T cell antigen receptor. Recent studies have found that some polypeptide structures of the T cell B chain appear simultaneously with HLA DR in the same individual, increasing the likelihood of SLE onset. In addition, SLE also has a variety of complement defects, such as C2, C1q, C1r, C1s, C4, C5, C8 and Bf, TNF, C1 esterase inhibitor deficiency. These complement components or genetic defects can affect the traditional activation pathway of complement, increase the body's sensitivity to excitation factors such as infection and are related to SLE susceptibility.
Endocrine factors (20%)
SLE mainly affects women, and the prevalence of women of childbearing age is 9 to 13 times higher than that of men of the same age, but the prevalence of women before and after menopause is only slightly higher than that of men. Therefore, it is believed that estrogen is involved in the occurrence of SLE. Regardless of male or female SLE patients, the levels of 16-hydroxyated estrone and estriol were significantly increased. Female contraceptives can sometimes induce lupus-like syndrome. Both human and animal studies have shown that estrogen can increase B cells to produce antibodies against DNA, and androgen can inhibit this reaction. Recently, it has been found that serum prolactin in patients with SLE is elevated, leading to secondary changes in sex hormones. Further research confirmed.
Virus infection (20%)
Commonly known as chronic viral infection, it is found under electron microscopy that there are tubular corpuscular inclusions in the tissues of SLE patients, similar to the nuclear structure of the paramyxovirus nucleoprotein and core, but further studies suggest that this is a non-specific cellular damage. which performed. Some people with similar inclusion bodies were found in glomerular endothelial cytoplasm, vascular endothelial cells and lesions of SLE patients. However, the virus has not been isolated from tissues containing inclusion body-like substances, so the relationship between these substances and viral infections remains to be confirmed. In SLE patients, there are a variety of high titer anti-viral antibodies, such as anti-measles, anti-rubella, anti-parainfluenza, anti-EB virus, anti-mumps, anti-mucosa and other antibodies. Antisera antibodies such as ds-DNA, dsRNA and RNA-DNA are also present in the patient's serum. It has also been suggested that the pathogenesis of SLE is closely related to the C-type RNA virus. In general, there are many indications that viral infection may be one of the causes of SLE, but it has not been confirmed that viral infection is associated with abnormal immune regulation and autoimmunity in SLE patients. In addition, it has also been suggested that the onset of SLE is associated with tuberculosis or streptococcal infection.
Drug factor (15%)
A variety of drugs are associated with the pathogenesis of SLE, but the pathogenesis is different.
1 The drugs that induce SLE symptoms include penicillin, sulfonamides, phenylbutazone, and gold preparations. These drugs enter the body, first cause allergic reactions, and then stimulate the quality of lupus or cause the onset of SLE patients, or make patients with SLE worse, stopping the drug can not prevent the disease from developing.
2 The drugs that cause lupus-like syndrome include hydralazine, procainamide, chlorpromazine, phenytoin, isoniazid, propyl and methylthiouracil. After long-term use of these drugs in large doses, patients may have clinical signs and laboratory changes in SLE, but the pathogenesis is not yet clear. Some people think that chlorpromazine binds to soluble nuclear proteins after UV irradiation to enhance its immunity. The combination of hydralazine and soluble protein can enhance the immunogenicity of its own tissue components in vivo. In such patients, the symptoms can resolve spontaneously after withdrawal or a few symptoms remain. With the emergence of new drugs, it has also been suggested that drugs can be used as exogenous carriers to bind to host tissue determinants to induce autoantibody production. Therefore, the clinical use of drugs should pay attention to the occurrence of drug-induced lupus.
Physical factors (10%)
About 1/3 of SLE patients are allergic to sunlight, UV can induce skin lesions or exacerbate the original lesions, and a few cases can induce or aggravate systemic lesions. Double-stranded DNA in normal human skin tissue can undergo dimerization after ultraviolet irradiation to form thymine dimer, which can repair depolymerization after UV irradiation. SLE patients have defects in repairing dimerized DNA, and excessive thymine dimers may become pathogenic antigens. It is also believed that ultraviolet radiation can damage skin cells, and anti-nuclear factors can enter the cells and interact with the nucleus to cause skin damage. In addition, X-ray irradiation, cold, intense electro-optic irradiation can also induce or aggravate SLE conditions.
Dietary factors (5%)
Foods containing psoralen, such as celery, figs, and European windproof, have the potential to enhance light sensitivity in patients with SLE; mushrooms containing hydrazine genes, smoked foods, food dyes, and tobacco can induce drug-induced lupus; Lupus can also be induced by seeds, sprouts and other pods of L-concanin. Limiting calorie and fatty acid intake can reduce the severity of lupus, suggesting that this may be beneficial for patients with SLE.
Other factors (5%)
Asbestos, silica, vinyl chloride and hair dyes containing reactive aromatic amines may be involved in the pathogenesis of SLE. Severe physical and psychological stress can induce a sudden onset of SLE.
Prevention
Lupus nephritis prevention
There are several main measures to prevent lupus nephritis:
First, attach importance to physical factors
The incidence of systemic lupus erythematosus is as high as 5% to 12%, and the incidence of identical twins is as high as 69%. The incidence of other autoimmune diseases such as rheumatoid, dermatomyositis, scleroderma, xerostomia and psoriasis in relatives of lupus patients Also high, the incidence of black and Asian descendants is higher than that of Caucasians, which suggests that lupus is affected by genetic factors, while women are more frequent, and patients with lower testosterone levels indicate endocrine factors, especially the level of estrogen in patients with lupus. It is related to the pathogenesis of lupus nephritis. Therefore, patients with autoimmune disease who have the basis of autoimmune disease, including autoimmune diseases among relatives, should be highly vigilant. Once they are sick, they should think of autoimmune diseases. If you are sick, you should actively treat it to prevent lupus nephritis and cause kidney damage.
Second, actively treat viral infections
In recent years, experimental studies have found that viral infection may be related to the occurrence of systemic lupus erythematosus. Therefore, we should actively treat various viral infections, especially for "small diseases" such as upper respiratory tract infections, and we must not take it lightly because "the wind is "The longevity of a hundred diseases", many major illnesses are caused by colds and colds, which endanger the population.
Third, pay attention to drug toxicity
Drugs related to lupus erythematosus include hydralazine, procainamide, isoniazid, methyldopa, chloropromazine and quinidine, especially in the past, which may be associated with drugs, Amines, guanidine groups are related, so for patients with lupus genetic basis of lupus, you should be aware of the toxicity these drugs may have on patients with lupus erythematosus.
Fourth, avoid sun exposure
Ultraviolet irradiation aggravates the condition of lupus nephritis, because ultraviolet light can convert DNA into thymine dimer, which enhances antigenicity and promotes systemic lupus erythematosus. Therefore, patients with lupus nephritis should avoid strong in daily life. Long-term exposure to sunlight to reduce kidney damage caused by excessive UV exposure.
Complication
Lupus nephritis complications Complications femoral head necrosis cardiovascular disease
It is prone to complications such as infection, cardiovascular complications, and femoral head necrosis.
Symptom
Lupus nephritis symptoms common symptoms hepatosplenomegaly ascites hypertension tubular urinary lymphadenopathy facial butterfly erythema nephrotic syndrome edema alopecia hematuria
First, medical history and symptoms
More common in young women, light asymptomatic proteinuria (<2.5g / d) or hematuria, no edema, high blood pressure; most cases may have proteinuria, red and white cell urine, tubular urine or nephrotic syndrome With edema, hypertension or renal dysfunction, nocturia is more common; a few cases have a sharp onset, renal function deteriorates rapidly, most kidney involvement occurs after fever, arthritis, rash and other extrarenal manifestations, severe cases often Rapidly involving the serosa, heart, lung, liver, hematopoietic organs and other organ tissues, with the corresponding clinical manifestations, about one-fourth of patients with kidney damage as the first performance, for women of childbearing age should have routine examination of kidney disease The immunological serological indicators related to this disease are mostly diagnosed according to the diagnostic criteria for systemic lupus erythematosus established by the American College of Rheumatology in 1982.
Second, physical examination found
Acute fever is more common; most patients have anemia; facial butterfly erythema is a characteristic change, which may be associated with joint swelling, hair loss, rash, heart murmur or pericardial effusion, hepatosplenomegaly, lymphadenopathy and varying degrees of edema Or chest and ascites, etc.
Examine
Examination of lupus nephritis
(A) urine routine examination can have varying degrees of urinary protein, microscopic hematuria, white blood cells, red blood cells and tubular urine.
(B) Most have moderate anemia, occasionally hemolytic anemia, blood white blood cells decline, platelets are mostly less than 100 × 109 / L, ESR is faster.
(3) Immunological examination: serum autoantibodies are positive, -globulin is significantly increased, blood circulation immune complex is positive, and hypocomplementemia is low, especially in active phase, hemorrhagic lupus cells are positive, and skin lupus test is positive.
(4) Severe active lupus nephritis with reversible Ccr decreased, blood urea nitrogen and creatinine increased, blood albumin decreased or liver function transaminase increased; end stage lupus nephritis Ccr decreased significantly and serum creatinine, urea Nitrogen is significantly elevated.
(5) Image examination: B-ultrasound shows that the enlargement of the kidneys suggests acute lesions; some patients have liver, splenomegaly or pericarditis.
(6) Renal biopsy can understand the pathological type, pathological activity and treatment plan, and systemic lupus erythematosus with kidney damage as the first manifestation. Kidney biopsy can help to confirm the diagnosis.
Diagnosis
Diagnosis and diagnosis of lupus nephritis
For patients with a clear diagnosis of SLE, lupus nephritis can be diagnosed if the above-mentioned renal involvement is present.
Pathological classification
There are 6 types of pathological classification of lupus nephritis in the World Health Organization. From type I to type VI, the prognosis is from good to bad. Type I: normal or minimally pathological; type II: mesangial proliferative lupus nephritis; type III: focal proliferative lupus nephritis; type IV: diffuse proliferative lupus nephritis; type V: membranous lupus nephritis; Type VI: sclerosing lupus nephritis.
2. Lupus nephritis renal pathological activity index
(1) Proliferative changes of glomerular cells;
(2) Cellulose necrosis and nuclear lysis;
(3) a cellular crescent;
(4) Platinum ear phenomenon and glassy thrombus;
(5) glomerular neutrophil infiltration;
(6) Renal interstitial mononuclear cell infiltration.
3. Chronic indicators
(1) glomerular sclerosis;
(2) fibrous crescent;
(3) tubular atrophy;
(4) Renal interstitial fibrosis.
