Glomerulonephritis

Glomerulonephritis

Etiology

Chronic glomerulonephritis can occur at any age, but young, middle-aged men. There is a mode of onset and clinical manifestation related to this. Most of insidious onset, slow, hematuria, proteinuria, hypertension, edema, its basic clinical manifestations. In general, where there is abnormal urine (hematuria, proteinuria, urinary tube), edema, hypertension and a history of prolonged course, with or without renal dysfunction should be considered disease, renal biopsy pathology can be diagnosed and help guide treatment and prognosis. Chronic nephritis early should be given the appropriate treatment, the pathological type inhibition of immune-mediated inflammation, inhibit cell proliferation and reduce kidney sclerosis.

Glomerular etiology and pathogenesis of the disease is very complex, there are many factors involved, such as infection, autoimmune, drugs, genetic, environmental, immune injury is a common link in most glomerular diseases, almost all of the kidney immunological mechanisms involved in the process has mostly small ball diseases. Kidney highly sensitive to immune-mediated injury, the body of pathogenic microorganisms, planted in glomerular foreign antigen, normal tissue components generate excessive, or inappropriate immune response will lead to immune injury of the kidney tissue. May be due to immune complexes in the glomerular basement membrane endothelial and mesangial area, epithelial side deposition, activation of complement, leading to immune injury, also may be some planting in kidney tissue antigens in situ formation of immune complexes with antibodies.

The renal tissue of the immune response to effect, on the one hand, will lead to the T cells, monocytes and other inflammatory cell infiltration in the renal tissue. These cells can secrete many cytokines; can also be mediated renal tissue damage. On the other hand, these inflammatory cells and their secretion of cytokines can stimulate and activate kidney inherent cells to express a variety of chemokines, cytokines, growth factors, adhesion molecules, and extracellular matrix components, to aggravate kidney tissue damage directly or indirectly.

Chronic glomerulonephritis can occur at any age, but young, middle-aged men. This can be considered as a mode of onset and clinical manifestation. Majority of insidious onset, slow its basic clinical manifestations of hematuria, proteinuria, hypertension, edema, may have varying degrees of renal dysfunction, protracted illness, repeatedly, progressive development of chronic renal failure.

Pathogenesis

Development of glomerulonephritis is always associated with acute or chronic infection localized in different organs and generally having strep nature. The most common glomerulonephritis develops in the Staphylococcus aureus, Neisseria meningitidis, Streptococcus pneumoniae, Toxoplasma gondii, Plasmodium malaria infection and infestation of some viruses. In some cases, glomerulonephritis is caused by vaccination, chemical poisoning or eating foods containing preservatives. Leading immunopathological process in glomerulonephritis is education in the blood or kidneys, the so-called immune complexes. With that, the main antigen is usually endostreptolizin nephritogenic, which is a streptococcus. At the very beginning of the disease in the blood a typical pattern is formed which raises and lowers immune complexes, complement the NW, and the C1, C2 and C4 are normal.

Kidney biopsy in the first stage of the disease, with about 28 days and the 42nd day, is found in the material damage of glomeruli from ...