1. what is lupus nephritis?

1. what is lupus nephritis?

Lupus Nephritis refers to the kidney pathological change caused by SLE (Systemic Lupus Erythematosus). During the progression of the disease, various symptoms will appear. Not only kidney, but also other organs will be involved. Some patients may have serious symptoms on other organs but with slight symptoms related to kidney, while some other patients may have severe kidney damaged but have slight symptoms related to other organs. Clinically, Lupus Nephritic is one of the most common secondary kidney diseases, especially for female patients. Sociodemographic factors such as sex, race, and ethnicity play an important role in the incidence of the disease, frequency of its manifestations, and therapeutic response.Apart from the kidneys, SLE can also damage the skin, joints, nervous system and virtually any organ or system in the body.

2. what causes lupus nephritis?

On the one hand, it is not yet known what causes lupus. Some possibilities under investigation are infections and viruses or environmental causes. There are some indications that there may be an inherited factor to lupus. Lupus affects more women than men.

On the other hand, systemic lupus erythematosus (SLE, or lupus) is an autoimmune disease. This means there is a problem with the body's immune system.

Normally, the immune system helps protect the body from infection or harmful substances. But in patients with an autoimmune disease, the immune system cannot tell the difference between harmful substances and healthy ones. As a result, the immune system attacks otherwise healthy cells and tissue.

Autoimmunity plays a major role in the pathogenesis of lupus nephritis. The immunologic mechanisms include production of autoantibodies directed against nuclear elements. The characteristics of the nephritogenic autoantibodies associated with lupus nephritis are as follows :
1.Antigen specificity directed against nucleosome or double-stranded DNA (dsDNA) - Some anti-dsDNA antibodies cross-react with the glomerular basement membrane

2.Higher-affinity autoantibodies may form intravascular immune complexes, which are deposited in glomeruli

3.Cationic autoantibodies have a higher affinity for the anionic glomerular basement membrane

4.Autoantibodies of certain isotypes (immunoglobulin [Ig] G1 and IgG3) readily activate complement

These autoantibodies form pathogenic immune complexes intravascularly, which are deposited in glomeruli. Alternatively, autoantibodies may bind to antigens already located in the glomerular basement membrane, forming immune complexes in situ. Immune complexes promote an inflammatory response by activating complement and attracting inflammatory cells, including lymphocytes, macrophages, and neutrophils.

The histologic type of lupus nephritis that develops depends on numerous factors, including the antigen specificity and other properties of the autoantibodies and the type of inflammatory response that is determined by other host factors. In more severe forms of lupus nephritis, proliferation of endothelial, mesangial, and epithelial cells and the production of matrix proteins lead to fibrosis.

Glomerular thrombosis is another mechanism that may play a role in pathogenesis of lupus nephritis, mainly in patients with antiphospholipid antibody syndrome, and is believed to be the result of antibodies directed against negatively charged phospholipid-protein complexes.