Introduction of experimental glomerulonephritis by anti-kidney mitochondrial antiserum in the rabbit.

THE SIGNIFICANCE of auto-antibodies in the initiation and progression of certain types of kidney diseases in man and in experimental animals has often been considered to be of little or of no importance. It is often suggested that antibodies, which can be detected by various in vitro techniques, are the consequence of the immuno-pathological processes rather than the cause of the kidney disease (Boss, Silber and Nelken, 1968; Mathur et al., 1968). In spite of controversy it is well established that glomerulonephritis in man and in experimental animals can be produced either by anti-glomerular basement membrane antibodies or by antigen antibody complex depositions in the glomeruli (Dixon, 1968). An experimental model produced by Heymann and his co-workers (1959) facilitated the understanding of one type of disease process involved in the socalled auto-immune nephrosis of rats. Since morphological and clinical features of the experimentally induced autologous immune complex nephritis (Lannigan et al., 1969) show remarkable resemblance to membranous nephropathy in man, further studies which might shed light on the initiation of this disease would be desirable. In one experiment (Barabas and Lannigan, 1969) it was observed that