It is generally accepted that most immunologically mediated renal diseases fall into several categories (Box 1).

Box1. Categories of Immunologic Renal Disorders

 Renal Disease Associated With Circulating Immune Complexes

 Renal diseases associated with circulating immune complexes are caused by nonrenal antigens and their corresponding anti bodies. These complexes are deposited in one or more of several loci in the glomerulus. Deposition may depend on the size and other characteristics of the complex. Studies have suggested that potentially damaging immune complexes may be formed in situ and involve antigens already present or fixed in the glomerulus. In addition, immune complex activation of complement in the glomerular basement membrane may be augmented by the presence of cells with receptors for C3 located in that area. Activation probably releases biologically active products such as chemotactic substances and causes an inflammatory type of tissue injury. A renal complication of this type can be manifested in SLE.

Membranoproliferative Glomerulonephritis

Another type of glomerular disease, membranoproliferative glomerulonephritis, is believed to be caused by nonimmunologically activated complement. Activation is thought to be analogous to the alternate pathway activation of C3 by certain bacterial products and polysaccharides.

Renal Disease Associated With Anti–Glomerular Basement Membrane Antibody

Anti–glomerular basement membrane (GBM) antibodies are directed against GBM of the glomerulus of the kidney (Fig. 1). These antibodies are induced in vivo against the basement membrane of the glomerulus and possibly that of the renal tubule or lung. The factors that stimulate antibody production are not well defined, but it appears likely that binding of drugs (e.g., methicillin), certain infectious agents, or renal dam age caused by other immune mechanisms may lead to an immune antibody response. The end result may be direct dam age to the bone marrow, with or without complement activation. Production of anti–bone marrow antibodies, however, appears to be self-limited and lasts for several weeks to months after removal of the inciting agent (i.e., by the kidney).

Fig1. Electron photomicrograph demonstrating an immunoglobulin deposit in the basement membrane of a patient with systemic  lupus erythematosus (SLE). (From Barrett JT: Textbook of immunology, ed 5, St Louis, 1988, Mosby.)

High antibody titers of anti-GMB are suggestive of Good pasture’s disease, early SLE, or anti-GBM nephritis. The absence of antibodies, however, does not rule out Goodpasture’s disease. This type of renal disease represents less than 5% of glomerular disorders.

 Tubulointerstitial Nephritis

 Tubulointerstitial nephritis involving the renal tubules has been associated with a variety of causes, including immune complex–mediated disease. Precipitating factors can include drugs and possibly infection, as well as the involvement of transplanted kidneys.

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