Immunological reactions

Immunological mechanisms in nephrotic syndrome

The modern concept of renal injury is based on the immuno-inflammatory theory. In the first immunological phase, an antigen encounters an antibody, the complement system is activated, and immune complexes are formed.

In the glomerular injury phase, these complexes are deposited on the basement membrane. The main mechanism here is the neutralization of the negative charge of the glomerular filter, which triggers cellular reactions of immune inflammation and leads to membrane destruction. The result is massive proteinuria, hypoproteinemia, and hypoalbuminemia, as the liver is unable to compensate for such extensive protein losses.

Types of immune-mediated renal injury in glomerulonephritis

The leading mechanism in the development of primary glomerulonephritis is immune-mediated inflammation. There are two main variants of complex deposition:

• In situ deposition: antibodies react directly within the glomerulus with resident structures, such as type IV collagen, or with planted antigens. Characterized by linear fluorescence on immunofluorescence.
• Circulating complex deposition: antigens and antibodies bind in the bloodstream and are subsequently fixed subendothelially or subepithelially, forming a granular fluorescence pattern.

Rapidly progressive glomerulonephritis is classified into anti-GBM type I with linear fluorescence, immune complex type II with granular fluorescence, and pauci-immune type III with minimal deposits associated with ANCA-associated vasculitis.

Laboratory parameters of immunological reactivity

Assessment of the immune system state includes the analysis of cellular and humoral defense factors. The main resistance parameters and normal ranges are:

• Phagocytic activity: 72.8 ± 1.5%, and the phagocytic index is within 2.5–4.0.
• Serum bactericidal activity (SBA): normally 80–100%, but this parameter is objective exclusively prior to antibiotic administration.
• T-lymphocytes: 50–80% of lymphocytes, absolute count — 700–1920 cells/µL.
• B-lymphocytes: 13–30%, absolute count — 210–810 cells/µL.
• Immunoglobulins: IgG is 14 ± 3.4 g/L, IgA is 2.25 ± 0.5 g/L, IgM is 1.2 ± 0.4 g/L.

A decrease in these parameters is considered a poor prognostic sign, whereas an increase in circulating immune complexes indicates a distortion of the immune response.

Immunological theory of pulmonary fibrosis

When inhaling dust, such as crystalline silicon dioxide, complex processes are triggered, including the immunological theory of fibrosis. Cell and tissue injury under the influence of silicon dioxide leads to their breakdown and the appearance of autoantigens.

The developing autoimmunity is accompanied by the formation of "autoantigen + antibody" complexes, which adversely affect the connective tissue of the lungs. The ultimate morphological result of this process is the formation of the silicotic nodule, although specific antibodies in silicosis have not yet been identified.

Class and exam questions

What else to study on this topic

• Humoral and cellular defense mechanisms in purulent-inflammatory diseases
• Toxic-chemical and physicochemical theories of pulmonary fibrosis development
• Morphological changes of glomeruli: hypercellularity, hyalinosis, and sclerosis
• The role of phagocytosis and dust cells in the primary cellular response
• Clinical and laboratory consequences and the protein-synthetic function of the liver

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.