The influence of selective thrombocytopenia on immune complex glomerulonephritis.
Anticoagulation in experimental GN has not uniformly reduced inflammation and prevented functional impairment. The observation that platelet thrombi are occasionally present in nephritic kidneys prompted the suggestions that platelet aggregation may play a fundamental role and that inhibition of aggregation may be of therapeutic value. To test this hypothesis, the effect of selective platelet depletion on acute IC GN in the rabbit was evaluated. IC GN was induced with bovine albumin, and platelet depletion with APS. Platelet depletion preceded proteinuria by more than 36 hr and was sustained for 5 days. Platelet accumulation within the nephritic kidney was quantitated with chromium-labeled platelets. The hemodynamic effect of parenteral administration of APS on the evolution of IC GN was assessed by comparing IV with IP administration. Thrombocytopenia in the absence of hypotension had no inhibitory effect on IC GN, nor was there platelet accumulation within the nephritic kidneys of the platelet-depleted animals. These results indicate that platelet aggregation is not essential in the pathogenesis of IC GN and that inhibition of platelet aggregation may be of little value.
D000818:Animals; D001791:Blood Platelet Disorders / Q000150:complications / Q000503:physiopathology*; D001794:Blood Pressure; D001806:Blood Urea Nitrogen; D004195:Disease Models, Animal; D005260:Female; D005921:Glomerulonephritis / Q000150:complications / Q000503:physiopathology*; D007105:Immune Complex Diseases / Q000150:complications / Q000503:physiopathology*; D007678:Kidney Glomerulus / Q000473:pathology; D008297:Male; D010974:Platelet Aggregation; D011507:Proteinuria; D011817:Rabbits