Glomerular platelet-activating factor levels and origin in experimental glomerulonephritis

• Published in: Kidney international Vol. 37; no. 2; pp. 736 - 740
• Main Authors: Lianos, Elias A., Zanglis, Anthony
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01-02-1990; Nature Publishing
• Subjects: Animals; Biological and medical sciences; Glomerulonephritis; Glomerulonephritis - metabolism; Glomerulonephritis - physiopathology; Kidney Glomerulus - analysis; Kidney Glomerulus - metabolism; Kidney Glomerulus - physiopathology; Male; Medical sciences; Nephrology. Urinary tract diseases; Nephropathies. Renovascular diseases. Renal failure; Platelet Activating Factor - analysis; Platelet Activating Factor - physiology; Rats; Rats, Inbred Strains; Renal glomerulus; Glomerulonephritis; Vertebrata; Experimental disease; Mammalia; Urinary system disease; Rat; Animal; Rodentia; Etiopathogenesis; Complement; Platelet activating factor
• ISSN: 0085-2538; 1523-1755
• DOI: 10.1038/ki.1990.40

Glomerular platelet-activating factor levels and origin in experimental glomerulonephritis. The content of platelet activating factor (PAF) in glomeruli isolated from rats with nephrotoxic serum glomerulonephritis (NSGN) was quantified at various stages of the disease and the role of complement, platelets and neutrophils in mediating changes in glomerular PAF levels was evaluated. PAF content was assessed following extraction, isolation and quantification of this alkyl ether lipid using a bioassay based on [3H]-serotonin release from labelled rabbit platelets. Following induction of NSGN using proteinuric doses of rabbit immune serum raised against rat glomerular basement membrane, enhanced glomerular PAF levels were observed at 3 hours, 24 hours and on day 15 following induction of the disease. In complement depleted rats and at three hours following induction of NSGN, glomerular PAF levels were significantly lower than in complement replete controls studied in parallel. At the same time point of the disease, platelet depleted rats with NSGN demonstrated significantly lower glomerular PAF levels than parallel controls, whereas in neutrophil depleted rats glomerular PAF levels were no different than controls. These observations indicate that in infiltrative and complement dependent forms of glomerular immune injury, glomerular PAF levels are increased via a complement mediated mechanism. Infiltrating platelets, but not neutrophils, partially account for the enhanced glomerular PAF levels. The observations are of potential importance in the pathophysiology of glomerulonephritis.