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Laboratory Diagnosis of Autoimmune Kidney Disease
Last reviewed: 23.04.2024
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Glomerulonephritis is the most common form of primary kidney disease with a predominant lesion of the renal glomeruli. Currently, the concept of the immunoinflammatory genesis of this disease is generally recognized.
Glomerulonephritis is the result of an inflammatory response to antigens, leading to tissue damage. Although the specific antigens responsible for the development of glomerulonephritis are often unknown, they can be classified according to their primary origin, that is, whether the kidney itself (kidney antigens) serves as their source or the source is outside the kidney (non-targeted antigens). To trigger the development of glomerulonephritis, the non-targeted antigens (with or without antibodies) should eventually end up inside the kidney: in the mesangium of the glomerulus, in the basal membrane or on the subendothelial side of the basal membrane. The further nature of histological damage in glomerulonephritis depends on the location of antigens and the type of immune response that causes its deposition.
Two immunopathological variants of glomerulonephritis development are possible. One of them arises as a result of the interaction of autoantibodies with autoantigens - the protein components of the renal tissue, mainly the basal membrane of the wall of the glomerular capillaries. These complexes are formed and located directly on the basal membrane of the glomerulus, causing it to damage (antibody, caused by autoantibodies to the basal membrane of the glomerulonephritis glomerulus). In the second variant, the formation of immune complexes occurs in the blood due to binding of antibodies to extrarenal and extra-lute antigens. Initially, these immune complexes circulate in the blood, then precipitate on the basal membranes of the glomerular capillaries and cause their damage (immunocomplex glomerulonephritis).
It has been established that up to 75-80% of glomerulonephritis is caused by immune complexes, less than 10% is associated with antibodies to the basal membrane of the glomeruli.
The same immunological reactions that induce glomerulonephritis can cause damage to the tubular cells, vessels. The result of such an impact is a monocular or neutrophil infiltration of the interstitial kidney and the development of the inflammatory process, which is united by the concept of tubulointerstitial nephritis. The latter can be caused by autoantibodies to the tubular basement membrane, immune antigen-antibody complexes, cell-mediated immune responses. In some cases, tubulointerstitial nephritis accompanies glomerulonephritis, in other cases there are no changes in the glomeruli and tubulointerstitial nephritis exists as an independent disease.
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