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Laboratory diagnosis of autoimmune kidney diseases
Medical expert of the article
Last reviewed: 05.07.2025
Glomerulonephritis is the most common form of primary kidney disease with predominant damage to the renal glomeruli. The concept of immune-inflammatory genesis of this disease is currently generally accepted.
Glomerulonephritis is the result of an inflammatory response to antigens that causes tissue damage. Although the specific antigens responsible for glomerulonephritis are often unknown, they can be classified by their primary origin, that is, whether they originate within the kidney itself (renal antigens) or outside the kidney (nonrenal antigens). To initiate glomerulonephritis, nonrenal antigens (with or without antibodies) must eventually be deposited within the kidney: in the glomerular mesangium, in the basement membrane itself, or on the subendothelial side of the basement membrane. The subsequent histologic damage in glomerulonephritis depends on the location of the antigens and the type of immune response that their deposition elicits.
There are two possible immunopathological variants of glomerulonephritis development. One of them occurs as a result of interaction of autoantibodies with autoantigens - protein components of renal tissue, mainly the basement membrane of the glomerular capillary wall. These complexes are formed and located directly on the basement membrane of the glomeruli, causing its damage (antibody-induced glomerulonephritis caused by autoantibodies to the basement membrane of the glomeruli). In the second variant, formation of immune complexes occurs in the blood due to binding of antibodies to extrarenal and extraglomerular antigens. Initially, these immune complexes circulate in the blood, then settle on the basement membranes of the glomerular capillaries and cause their damage (immune complex 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 glomerular basement membrane.
The same immunological reactions that induce glomerulonephritis can cause damage to tubular cells and vessels. The result of such an impact is mononuclear or neutrophilic infiltration of the renal interstitium and the development of an inflammatory process, which is united by the concept of tubulointerstitial nephritis. The latter can be caused by autoantibodies to the tubular basement membrane, immune complexes antigen-antibody, cell-mediated immune reactions. 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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