Journal of the American Society of Nephrology 235 Detection of Platelet-Activating Factor in Plasma of Patients With Streptococcal Nephritis1 Sergio Mezzano, Marianne Kunick, Fernando Olavarria, Leopoldo Ardiles, Giuseppe Montrucchio, Luigi Silvestro, Luigi Biancone, and Giovanni Camussi2 S. Mezzano. M. Kunick, F. Olavarria. L. Ardiles, Division of Nephrology, School of Medicine, Universidad Aus- tral. Valdivia. Chile G. Morttrucchio, L. Silvestro (Respharma, Pharmaceu- tical Research, Torino), L. Biancone, G. Camussi. La- boratorio di Immunopatologia, Cattedra di Nefrologia. Universit#{224} di Torino. Torino, Italy G. Camussi. Cattedra di Nefrologia. Dipartimento di Biochimica e Biofisica. Seconda Universit#{224} di Napoli. Napoli. Italy (J. Am. Soc. Nephrol. 1993; 4:235-242) ABSTRACT The purpose of this study was to evaluate whether platelet-activating factor (PAF) is released in the plasma of patients with acute poststreptococcal gb- merulonephritis, because previous studies have shown an involvement of platelets in the active phase ofthis disease. The results ofthis study indicate that PAF bioactive material is released in significant amounts in the plasma of 49 out of 50 patients with acute poststreptococcal gbomerubonephritis. The ob- served release of PAF was not a direct consequence of the bacterial infection, because it was minimal or absent in patients with streptococcal infection with- out glomerular involvement. PAF bioactive material extracted and purified from the plasma of patients was shown to be chemically and biologically iden- tical to the synthetic C-16 PAF (1-O-hexadecyl-2- acetyl-sn-glyceryl 3-phosphorylcholine). Key Words: Glomerulonephritis. nephritic syndrome. platelet. immunopathology, acute poststreptococcal glomerulo- nephritis I Received September 17. 1992. Accepted April 14. 1993. 2 Correspondence to Dr. G. Camussi, Laboratorlo di Immunopatologla, Dlvi- sione dl Nefrologla e Dialisi, Ospedale S.G. Battista, Molinette, Corso Dogliotti 14. 10126 Torlno, Italy. 1046-6673/0402-0235$03.00/0 Journal of th American society of Nephrology Copyright C 1993 by the American society of Nephrology P latelet-activating factor (PAF) was initially rec- ognized as the mediator of the reaction involving platelets and immunoglobulin E-sensitized baso- phils called “leukocyte-dependent histamine release” (1 ). It was more recently found that PAF belongs to a new class of lipid chemical mediators, the acetylated alkyl phosphoglycerides (for a review, see reference 2). Besides its effect on platelets, PAF exerts a broad spectrum of diverse and potent biologic activities. PAF promotes aggregation. chemotaxis, granule se- cretion, and adherence of neutrophils, eosinophils, and monocytes to vascular endothelium, and It enhances vascular permeability leading to hemocon- centration with extravasation of plasma proteins, edema, accumulation of leukocytes, vasoconstric- tion, and vasodilation (for a review, see reference 3). On the basis of these biologic activities relevant for the development of the inflammatory reaction, it was suggested that PAF may be involved in glomerular injury. PAF was indeed synthesized in acute serum sickness concomitantly with the deposition of im- mune complexes in glomeruli (4). More recently, it was shown that the blockade of PAF receptors pre- vented proteinuria and glomerular injury in rabbit nephrotoxic nephritis (5) and in an acute exudative tn situ-formed immune complex glomerulonephritis of rats (6). Direct evidence for PAF involvement in human glomerulonephnitis is still lacking. However, the demonstration that platelets actively participate in glomerular injury in human pathology (7.8) makes PAF a potential candidate for their recruitment. The recent finding that, besides activated leuko- cytes, glomerular mesangial cells may synthesize PAF (9) further supports a potential pathogenic role of this mediator. The aim of this study was to investigate whether PAF is released in the plasma of patients with acute poststreptococcal glomerulonephnitis (APSGN). a dis- ease in which the activation of platelets has been shown (10). MATERIALS AND METHODS Patient and Control Groups Four groups of subjects were studied. Group 1 in- cluded well-documented APSGN patients admitted to the Regional Hospital in Valdivia (Chile). Fifty pa-