rheumatoid arthritis kidney damage
Introduction
Introduction to rheumatoid arthritis kidney damage Renal damage caused by rheumatoid arthritis is a group of diseases caused by rheumatoid arthritis, chronic interstitial nephritis, renal amyloidosis, renal necrotizing vasculitis and immune complex nephritis, accompanied by corresponding clinical manifestations. . This disease often leads to multiple organ involvement, the main complications are joint destruction and deformation, subcutaneous nodules of varying sizes in the joint kyphosis, acute or chronic cerebral infarction or hemiplegia caused by central nervous system involvement. Therefore, the disease must be Early detection and early treatment to prevent serious complications. basic knowledge The proportion of sickness: 0.003%-0.007% Susceptible people: no specific population Mode of infection: non-infectious Complications: chronic nephritis
Cause
Causes of renal damage in rheumatoid arthritis
Bacterial infection (15%)
Experimental studies have shown that group A streptococci and peptidoglycan may be a persistent stimulator of RA. Group A streptococci have long-lasting antigens in the body, stimulating the body to produce antibodies and immunopathological damage. The animal model of arthritis produced by mycoplasma is similar to human RA, but does not produce rheumatoid factor (RF) specific to human RA. No bacteria have been found in synovial fluid and synovial tissue of RA patients. Or bacterial antigenic material, suggesting that bacteria may be involved in the onset of RA.
Virus infection (15%)
The relationship between RA and viruses, especially EB virus, is one of the problems that scholars at home and abroad pay attention to. Studies have shown that arthritis caused by EB virus infection is different from RA, and RA patients have strong reactivity with EB virus than normal people. There is a persistently high level of anti-EBV-membrane antigen antibody in serum and synovial fluid of RA patients, but so far no Epstein-Barr virus nuclear antigen or capsid antigen antibody has been found in the serum of RA patients.
Genetic factors (18%)
The disease has a high incidence in some families. In the population survey, human leukocyte antigen (HLA)-DR4 was found to be associated with RF-positive patients. HLA studies found that DW4 is associated with the onset of RA, and 70% of patients are HLA-DW4-positive. The patient has a susceptibility gene at that point, so heredity may play an important role in the pathogenesis.
Sex hormones (10%)
Studies have shown that the incidence of RA is between 1:2 and 4, the condition of pregnancy is reduced, and the incidence of contraceptives is reduced. Animal models show that LEW/n females have high sensitivity to arthritis, and males have low incidence. After castration or treatment with -estradiol, the arthritis of the rats is the same as that of the female mice, indicating that sex hormones play a role in the pathogenesis of RA.
Other factors (8%)
Cold, damp, fatigue, malnutrition, trauma, mental factors such as cold, dampness, fatigue, malnutrition, trauma, mental factors, etc., often lead to the disease, but most patients often have no obvious incentives.
Prevention
Rheumatoid arthritis prevention of kidney damage
1. Prevent cold and dampness, avoid mental stimulation, combine work and rest, and enhance resistance.
2, diet, do not eat fish and shrimp and other diseases that cause disease.
3, drug-induced rheumatoid arthritis kidney damage, should pay attention to avoid the re-use of the relevant treatment drugs.
4, rheumatoid activity period, to rest in bed; remission period, to appropriate activities, on the one hand to enhance physical fitness, on the one hand to prevent the use of disposable diseases in sports organs.
Complication
Rheumatoid arthritis kidney damage complications Complications Chronic nephritis hemiplegia
Complications: Rheumatoid arthritis can be associated with chronic kidney damage, or combined with renal immune damage.
Symptom
Rheumatoid arthritis, renal damage symptoms, common symptoms, joint stiffness, proteinuria, nodular extremity, hypertension, hematuria, nocturia
Chronic, multiple joint synovitis history, manifested as fever, hand, foot and limb joint stiffness, redness, swelling, deformation and dysfunction, some patients with non-steroidal anti-inflammatory drugs or gold preparations, kidney damage soon Aggravation, nephrotic syndrome, chronic nephritic syndrome, and even acute renal failure, if timely withdrawal, early treatment, can be restored to a better degree, some patients with long-term application of the above drugs cause direct chronic kidney damage, or Combined with renal immune damage, there may be different degrees of proteinuria and microscopic hematuria. Some patients may have edema, hypertension and renal dysfunction. Nocturia often indicates chronic interstitial nephritis, secondary renal amyloidosis or Necrotic vasculitis is severely damaged by kidney and often develops into chronic renal failure.
Examine
Examination of renal damage in rheumatoid arthritis
(1) Urine routine examination has different degrees of proteinuria or hematuria.
(2) Normal or abnormal renal function; chronic interstitial nephritis is mainly characterized by urinary concentrating dysfunction.
(3) The blood sedimentation is fast, the rheumatoid factor is positive, and the serum complement C3 of a few patients is decreased.
(D) Kidney biopsy can determine the nature and extent of the lesion.
2. Blood test
(1) Serum rheumatoid factor (RF): There are three kinds of RF such as IgG, IgM and IgA. At present, the latex agglutination method is used to detect IgMRF, and the active period is 50% to 80% positive, and the positive rate in the remission period is low.
(2) C-reactive protein-positive ESR increased during the active period.
(3) Serum ANCA: Some RV patients may have P-ANCA positive, and the target antigen is MPO or other antigen.
(4) joint fluid examination: the number of cells 2000 ~ 75000 / mm3 is mainly neutrophils, low viscosity.
Diagnosis
Diagnosis and diagnosis of renal damage in rheumatoid arthritis
diagnosis
Diagnosis can be based on medical history, clinical symptoms, and laboratory findings.
Differential diagnosis
The disease should be differentiated from other kidney damage caused by connective tissue disease:
1. Primary vasculitis (nodular polyarteritis, micro-polyarteritis, Wegener's granulomatosis): Clinical manifestations and renal pathology are similar to RV but negative for renal pathology immunofluorescence. The positive rate of ANCA was high. Wegener's granuloma was CANCA, positive for PR3, and micro-polyarteritis was P-ANCA, which was positive for MPO.
2. Systemic lupus erythematosus: In addition to multiple systemic damage, there are also serum immunological abnormalities: C3 decline, antinuclear antibody positive, anti-ds-DNA, anti-smith antibody positive identification is not difficult.
3. Gout: There may be joint swelling and pain, and more invasion of the metatarsophalangeal joint, easy to attack after high protein diet, self-limiting. Invasion of the early stage of the kidney is interstitial nephritis, and late stage of renal sclerosis can represent proteinuria, hematuria, and uremia. Can be associated with tophi, kidney stones. But no more system damage.
