Renal Biopsies in Children

It is over 120 years since Richard Bright first described the condition of nephritis, a symptom complex of oedema, haematuria, and proteinuria, following scarlatina. Since then various investigators have suggested that nephritis and the nephrotic syndrome may be immunologically determined. The possibility of 'hypersensitivity' as the pathogenic mechanism was suggested by Schick (1907) and the experimental production of heteroimmune nephritis by Masugi (1934). At present the evidence for the immunopathogenesis of nephritis and the nephrotic syndrome can be summarized as follows. (i) Antecedent infection, especially by P-haemolytic streptococci Group A, type 12, or others, and the latent period before the onset of glomerulonephritis. (ii) Decrease in the serum complement level during the active phase of glomerulonephritis and the nephrotic syndrome (McCrory, 1960). (iii) Demonstration of circulating anti-kidney antibody in the serum in these diseases (Lange, Gold, Weiner, and Simon, 1949; Liu and McCrory, 1958). (iv) Immunohistochemical demonstration of y-globulin and complement bound to the glomeruli in these diseases. (v) Various renal disorders associated with conditions such as the Schonlein-Henoch syndrome, polyarteritis nodosa, systemic lupus erythematosus, rheumatoid arthritis, and serum sickness. (vi) Experimental production of these diseases by immunological methods. Among this evidence, the immunohistochemical demonstration ofglomerular-bound globulin appears to be of practical and theoretical importance. This was first shown in human tissue by Mellors and Ortega (1956), by means of Coons' fluorescent antibody method. Since then the same method has been applied to various types of renal disease, and