Infections and Glomerular Diseases

Abstract

There is good evidence that glomerular injury may be related to many infectious agents in both experimental animals and in man, generally through an immune complex mechanism. Whether these infectious agent antigens are ’planted’ or within a deposited, previously circulating, immune complex is not known. The two mechanisms are not mutually exclusive. New concepts of a dynamic and constantly fluctuating involvement of immune reactants in the production of glomerular inflammation have received considerable emphasis.

Ideally, to manage postinfectious glomerulonephritis, one should eradicate the involved antigen(s) or inhibit production of specific antibody. A rapid and complete healing is usually observed in acute postinfectious glomerulonephritis characterized by proliferation and humps. Recovery after treatment is also possible in a few other situations, i.e. glomerulonephritis secondary to infective endocarditis or to infection of a ventriculoatrial shunt and glomerulonephritis associated with congenital and secondary syphilis.

Unfortunately, in most varieties of glomerulonephritis, as yet unexplained immune mechanisms of glomerular injury interfere so that spontaneous recovery of the infection does not always result in clinical improvement and resolution of the immune deposition. Moreover, the treatment of patients by specific therapy as well as with combinations of steroids and immunosuppressive agents does not appear to change the course of the disease. It seems that, once the clinical picture is manifested, mechanisms of glomerular damage are triggered and continue independent of the infective organism. The introduction of appropriate vaccines should reduce the frequency of postinfectious glomerulonephritis.