Ravnskov U
Med Hypotheses. 1989 Oct;30(2):115-22. doi: 10.1016/0306-9877(89)90096-0.
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.
肾小球肾炎被认为是由被困在肾小球或在肾小球中形成的免疫复合物引起的。但是在许多正常哺乳动物以及非肾脏疾病患者的肾小球中都发现了免疫复合物，而且实验性地在肾小球中被困或形成的免疫复合物最多只会引起轻度蛋白尿，这表明一定还有其他因素在起作用。在实验性肾小球肾炎中引发严重肾损伤需要长期供应抗原，这在人类肾小球肾炎中很少见；或者使用异源抗体，这种设计的临床相关性存疑；或者使用免疫毒性和肾毒性化学物质；或者使用同样具有肾毒性的弗氏佐剂。因此有人提出，人类非全身性肾小球肾炎的发病机制包括接触肾毒性和免疫毒性化学物质，肾小球免疫复合物的沉积是次要的。这一假说得到了临床支持：大多数患者都接触过此类化学物质，主要是碳氢化合物；而且肾小球肾炎中的肾小管间质变化与肾功能和临床病程的相关性比肾小球变化更好。这些化学物质会增强或扰乱免疫反应，并使肾脏对免疫反应敏感。
