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G Salvidio

Publications and source records attributed to G Salvidio.

22 records · Page 2Linked to original sources

Effects of hemodialysis on guanidinopropionic acid metabolism.

Blood levels of guanidinopropionic acid (GPA), a putative uremic toxin, have been evaluated in 5 uremic patients before a dialytic session, at the end of it and during the following 68 h. GPA levels are markedly higher in uremic patients than in controls and are significantly reduced at the end of dialysis even if still higher than in controls. The clearance of GPA is similar to those of urea and creatinine, even if at the end of the dialysis session the percent decrease of GPA is significantly lower than that of urea. During the first 8 h after the end of dialysis GPA levels increase steeply; subsequently, the rate of accumulation of GPA in blood declines markedly remaining constant until the 68th hour. In conclusion GPA is markedly increased in blood of uremic patients and is significantly removed by dialysis. The evaluation of GPA increase per hour after the end of dialysis may provide an estimation of GPA production in uremic patients.

Adult↗

Receptor antagonists of platelet-activating factor do not influence the development of passive Heymann nephritis.

Heymann nephritis in the rat is a proteinuric condition caused by glomerular lesions similar to those found in human membranous nephritis. In the present study the effect of two different receptor antagonists of platelet-activating factor (PAF) on the course of passive Heymann nephritis was assessed. It was found that rats treated with either antagonist showed the same degree of proteinuria and the same glomerular immunopathological features as untreated rats. Furthermore, at sacrifice, 7 days after the initiation of the disease, the concentration of circulating PAF in treated as well as untreated rats was normal. These results indicate that PAF is not crucial in the pathogenesis of Heymann nephritis.

Animals↗

Immune deposits and immune complex disease.

Presence in tissues of immune deposits containing antigens, antibodies and complement is the hallmark of immune complex disease. In the Review the present concepts concerning the pathogenesis of inflammatory injury associated with immune deposits resulting from a local deposition of circulating immune complexes or formed 'in situ' are discussed.

Animals↗