Models of Glomerulonephritis

Understanding the mechanisms of glomerular injury is critically dependent on the histologic assessment of cellular responses, immune processes, and ultrastructural changes. However, studies of human disease have been limited by a relative lack of tissue sampling. Renal biopsy is often performed only when the diagnosis of glomerular disease cannot be determined based on clinical grounds or in conjunction with indirect markers such as serologies, complement levels, and urine microscopy. Furthermore, a biopsy is typically undertaken upon clinical presentation, thereby providing a mere “snapshot” of the disease. In the absence of serial histologic evaluation, the opportunity to delineate mechanisms of disease progression is limited. However, the use of animal models has overcome a number of these hurdles, thereby advancing our current knowledge and understanding of the pathogenesis of glomerular disease. Animal studies afford the opportunity to study the development, progression, and resolution of disease over time. Furthermore, the host response to injury may be deliberately modified, either generally (as with nonspecific immunosuppressants) or selectively (as with target gene deletions or neutralizing antibodies), thereby providing further insight into pathogenetic mechanisms that cannot be undertaken in man.