Platelet-activating factor (PAF) belongs to a new class of lipid chemical inflammatory mediators described as acetyl glyceryl ether phosphorylcholine. Although PAF has been implicated in kidney injury, its role in renal immune injury has not been clearly defined yet. We studied the levels of PAF in the plasma and urine and acetylhydrolase (AH) activities in serum and in renal tissue (cortex, C and medulla, M) in patients with primary glomerulonephritis (PGN). PAF levels in the plasma and urine and AH activity in serum of normal volunteers as well as AH activities in normal renal parenchyma (C and M) from nephrectomized patients (served as control) were also measured. Our results demonstrate increased PAF levels in the plasma and urine as well as increased AH activity in serum in patients with PGN in comparison to normal volunteers. AH activity in cortex of those patients was diminished compared to normal kidney tissue. We propose that the enhanced AH activity in serum in patients with PGN could be due to hyperproduction and low degradation of PAF in nephritic tissue which on one hand results in enhanced PAF levels in the plasma and in urine and on the other hand results in enhanced serum AH activity by virtue of substrate (PAF) availability. These data provide new knowledge in the homeostasis of PAF and its degrative enzyme in the setting of PGN.