Glomerulonephritis is thought to be caused by
immune complexes trapped or formed in the glomeruli. But
immune complexes are found in the glomeruli of many normal mammals and of patients with non-renal diseases, and
immune complexes trapped or formed experimentally in the glomeruli induce mild
proteinuria at most suggesting that additional factors must be responsible. An induction of serious renal damage in experimental
glomerulonephritis demands a chronic supply of
antigen, rarely seen in human
glomerulonephritis; or the use of
heterologous antibodies, a design with questionable clinical relevance; or immuno- and nephrotoxic chemicals; or
Freund's adjuvant which is also nephrotoxic. It is therefore suggested that the pathogenesis of human non- systemic
glomerulonephritis includes exposure to nephro- and immunotoxic chemicals, the deposition of glomerular
immune complexes being secondary. The hypothesis has clinical support: a majority of patients have been exposed to such chemicals, mainly
hydrocarbons; and the tubulointerstitial changes in
glomerulonephritis are better correlated to renal function and
clinical course than are the glomerular changes. The chemicals enhance or derange immunizations and sensitize the kidneys to immunological reactions.