Platelet-activating factor (PAF) has been implicated as a potential mediator in renal immune injury, including hyperacute kidney allograft rejection, but little is known 'of' or 'about' the mechanisms by which this endogenous phospholipid could contribute to the development of glomerular proteinuria which occurs during immunologically mediated inflammatory reactions. We examined the effect of Dexamethasone (Dex) on PAF-induced proteinuria in normal male Sprague-Dawley rat kidney which had been isolated and perfused (IPK) at constant pressure in a closed circuit with a cell-free medium containing 3.5% Ficoll 70 and 1% albumin. After a 10-min baseline period IPK from rats given Dex (1.25 mg/kg s.c., n=8) or vehicle (V, n=8) were exposed to PAF (till 10 nM concentration into the perfusate). No change in glomerular filtration rate (GFR) (Dex: 0.60 ± 0.12 vs. 0.60 ± 0.18; V: 0.48 ± 0.09 vs. 0.53 ± 0.13 ml/min/g kidney), and renal plasma flow RPF (Dex: 26.2 ± 3.36 vs. 27.6 ± 3.69; V: 23.6 ± 3.21 vs. 24.8 ± 2.17 ml/min p <0.05) was found before and after exposure to PAF. Dex prevents PAF-induced proteinuria (V: 7.5 ± 2.64 vs. 59.0 ± 12.45; Dex: 7.6 ± 1.65 vs. 25.3 ± 7.70 mg/min p <0.01). We conclude that in rat IPK (1) Dex almost completely prevented PAF-induced increase in urinary protein secretion, (2) the mechanism of protection is independent of renal hemodynamics, and (3) PAF-induced proteinuria is independent of the action of platelet inflammatory cells.
|Number of pages||6|
|Journal||Polish Journal of Immunology|
|Publication status||Published - 1995|
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