Spontaneous immunoglomerulonephritis in Wistar rats.
A strain of rats bred at the Nuclear Study Center of Mol (C.E.N.) develops a nephropathy characterized by granular deposition of immunoglobulin and complement in the renal glomeruli and tubules. We have attempted to specify the complement activation pathways (classical or alternate) in this disease by looking for their initial components (C1q, C3 and C4) in tissue lesions. The immunohistologic and histologic course of the disease has been followed in male and female rats. Immunohistologic results show that glomerular and tubular injury in CEN Wistar rats may be mediated by the classical pathway of complement activation. Histologic data demonstrate that the tubular, glomerular, and interstitial lesions appear in both sexes, but are more extensive and develop earlier in male rats. The lipopigments found in tubular cells suggest a lysosomal dysfunction which might contribute to the progress of the disease.
D000818:Animals; D003165:Complement System Proteins / Q000032:analysis; D005260:Female; D005921:Glomerulonephritis / Q000473:pathology*; D007154:Immune System Diseases / Q000473:pathology*; D007136:Immunoglobulins / Q000032:analysis; D007678:Kidney Glomerulus / Q000032:analysis; D007684:Kidney Tubules / Q000032:analysis; D008297:Male; D051381:Rats; D012737:Sex Factors
D007136:Immunoglobulins; D003165:Complement System Proteins