| Popis: |
Renal glomerular diseases began to be reasonably understood during the first part of this century when the major emphasis for classification shifted from pure clinical grounds to clinicopathological correlations. The popularization of renal biopsies, the refinements of laboratory methods for detection of possible etiological factors, the availability of electron microscopy, the development of experimental models, and the wealth of immunologic information accumulated during the last two or three decades all have contributed greatly to advance our knowledge; yet as of now there is not one generally accepted classification of glomerular diseases. The reason for this is multifactorial. The glomerulus has very limited ways of reacting to injury; therefore, different etiological insults might express indistinguishable structural and functional alterations. Furthermore, the humoral and cellular response may vary from patient to patient and similar etiological challenge may result in different morphological and clinical pictures. Most glomerulonephritides are of unknown etiology and usually present as primary renal disease. Similar glomerular alterations, however, may develop during the course of systemic diseases or may rarely precede them. Whether primary or associated with systemic disease the majority of glomerulonephritides are mediated by humoral immunologic mechanisms, as proven by the presence of glomerular deposits of immunoglobulin and complement demonstrable by immunofluorescence microscopy and rarely by the identification of specific antibody or antigen in the glomerular eluates. |
