Relevance of experimental models for human nephropathology

The relationship of experimentally produced renal lesions to Bright's disease is still a major concern of present day pathology even though the problem has for many years held the attention and interest of numerous investigators.Horn, 1937 [1] Since Bright in 1827 [2] associated renal pathophysiology with structural alterations in the kidney, many investigators have been concerned with the study of kidney diseases, in particular their natural history. Because biopsy techniques were not available at that time, most cases of glomerulonephritis could not be studied before they had reached an end stage. In order to study the acute and early changes of glomerulonephritis and to understand their pathogenesis, experimental models were developed in laboratory animals. Logically the experiments performed in this era were characterized by the prevailing thoughts on pathogenesis, and since glomerulonephritis was often associated with bacterial infections, investigators tried to induce such a disease in animals with bacterial toxins [3] or chemical compounds [1]. At the turn of the century it was realized that glomerulonephritis was caused by immunologic or rather allergic reactions against bacterial products [4–6] and this precipitated a series of experiments in which glomerulonephritis was induced by administration of bacteria or bacterial products [7–9], serum [10–13] or purified serum proteins [14–17].