Autoimmune glomerulonephritis - a mechanism of development and treatment

  • Autoimmune glomerulonephritis - a mechanism of development and treatment

    Glomerulonephritis is based on autoimmune processes or otherwise called auto-allergic ones. These lesions are mainly manifested with the capillary network of renal glomeruli. Subsequently, they develop inflammatory processes, and they, as a rule, are bilateral. The most characteristic signs of glomerulonephritis are general renal symptoms - edema and hypertension, as well as manifestations from the urine - micro- or macrohematuria, proteinuria, cylindruria. The prolonged existence of glomerulonephritis leads to hypertrophy of the heart, chronic renal failure and uremia.

    Mechanism of development and causative factors

    Among glomerulonephritis, many forms are distinguished, they differ, both during the disease and in external manifestations. In addition, this disease can occur in an acute, subacute, latent( latent) and chronic form. Belonging to one or another kind depends on the duration of the disease and to a certain extent on the severity of the symptoms. As for the mechanisms of glomerulonephritis development, in some cases autoimmune processes play an important role, in others these processes can have insignificant influence on the pathogenesis of the disease.

    Different types of microorganisms can contribute to the onset of glomerulonephritis. The most important is cocci flora, viruses, some types of vaccines and serums. In some cases, alcohol abuse, severe hypothermia in combination with high humidity, trauma and surgery in the lumbar region can lead to damage to the renal apparatus.

    And yet, the leading role is given to re-infection with β-hemolytic streptococcus, especially group A. At its first penetration, the body developed an increased sensitivity to this type of pathogen, however, it did not appear in outward appearance. But with its re-entry, a violent immune reaction develops. In the case of such a mechanism of development of the process, the main emphasis is on re-penetration of streptococcus or exacerbation of the existing focus of infection.

    Usually the mechanism of the development of the disease looks approximately as follows:

    • The first infection of the pathogen in the body with the development of, for example, tonsillitis, tonsillitis, influenza, acute respiratory infections, herpes, hepatitis B, the person is subsequently cured of the disease, but the organism "remembered" the infectious agent and developedon it antibodies.
    • When repeated infection in the body, especially streptococci, begins to develop antibodies. As a result, antigen-antibody complexes are formed, they combine with blood plasma proteins and settle on membranes of renal tubules.
    • In response to this, autoantigens are released from the kidney tissue, which are designed to protect tissues from the effects of agents of different nature, but at the same time, autoantigens exert a stimulating effect to support immune processes and further development of the disease.
    • In addition, under the influence of infectious and other provoking factors, anti-kidney antibodies are formed in the blood, they are called cytokines, which further aggravate the situation. They dramatically change the immune responses of the body, as a result, the body stops correctly recognizing its own antibodies and perceives them as foreign agents. So the autoimmune reaction develops.

    What happens in the kidney with autoimmune glomerulonephritis

    Autoimmune glomerulonephritis has the above-described developmental mechanism. Damage to the glomerular apparatus of the kidney leads to a violation of the inverse absorption of sodium and water, both in the blood and in the tissues, edema develops.

    Due to circulatory disorders in the glomerulus of the kidneys, the blood is redistributed and ceases to flow into the cortical substance of the kidneys. This is how ischemia develops( the lack of blood supply) of the kidney and a temporary dysfunction of the cortical substance occurs, and with the prolonged existence of ischemia. In response to anemia of the kidney bark, the renin substance is released. The worse the blood supply of the kidney and the less sodium salts in the blood, the more renin is produced. Thanks to this mechanism, hypertension of renal origin develops.

    Glomerulonephritis at the initial stages is manifested by immune reactions at the level of the glomeruli of the kidney, but later the inflammation of the glomerular apparatus develops, and as a result, the spasm of the vascular bed is replaced by a sharp weakening of its tone. In the future, inflammation can develop in different directions - towards proliferation or exudation. With proliferative inflammation, the epithelium of the kidneys multiplies and slushes, this is typical for extracapillary glomerulonephritis. Also, proliferation within the capillaries-intracapillary glomerulonephritis-can occur. If the exudative process prevails, the liquid part of the blood - plasma - is swilled into the cavity of the renal capsule. Then in the urine appear the uniform elements of blood.

    Hypersensitivity of the delayed type is characteristic for the development of mesangioproliferative and membranous( mesangiocapillary) glomerulonephritis.

    Treatment of autoimmune glomerulonephritis

    The main method of treatment without exacerbation is nephroprotection, i.e.measures aimed at maintaining the efficiency of the kidneys and inhibiting the development of pathological processes that reduce the functional activity of the glomerular apparatus. An important area is preventing or slowing the development of chronic kidney failure.

    For inhibition of renin-angiotensin activity, which leads to the progression of renal dysfunction and renal hypertension, inhibitors of the renin-angiotensin-aldosterone system( ACE inhibitors) -captopril, zofenopril, enalapril, benazepril, are used. It is also necessary to take AT1-angiotensin receptor blockers - valsartan, irbesartan, candesartran, losartan, telmisartan. This group of drugs protects the glomerular apparatus of the kidney from the effects of hypertension and nephrosclerosis. These drugs are usually prescribed on a long-term or even permanent basis.

    In addition to drug therapy, it is necessary to prescribe a therapeutic diet with a reduced amount of salt and protein. It is recommended that smoking cessation and lifestyle changes be directed towards increasing physical activity with a deliberate reduction in weight to normal levels. All patients with autoimmune glomerulonephritis should, if possible, refuse to take non-steroidal anti-inflammatory drugs, due to their negative impact on the kidney function.

    Like the article? Share with friends and acquaintances: