Deregulated platelet-activating factor levels and acetylhydrolase activityin patients with idiopathic IgA nephropathy

Background. Platelet-activating factor (PAF) is a phospholipid mediator wit h potent inflammatory activities. PAF stimulates IgA synthesis by B cells w hile IgA aggregates enhance PAF production by neutrophils and mesangial cel ls. These results led us to investigate blood PAF levels and plasma acetylh ydrolase (AHA, the PAF catabolic enzyme) activity in patients with idiopath ic IgA nephropathy (IgAN). Methods. PAF and AHA levels were investigated using the platelet aggregatio n assay and degradation of H-3-labelled PAF, respectively. The genotype of AHA with regard to the G994-->T mutation in exon 9 was assessed by an allel e-specific polymerase chain reaction. Results, Blood PAF levels were significantly (P=0.003, Mann-Whitney U-test) elevated in IgAN patients (50.6 +/- 6.8 pg/ml, n = 33) compared with healt hy controls (18 +/- 5 pg/ml, n = 18). In contrast, plasma AHA levels were s ignificantly (P = 0.0001, Mann-Whitney U-test) reduced in patients with IgA N (61 +/- 2 nmol/ml/min, n = 51) compared with healthy controls (78 +/- 4 n mol/ml/min, n = 53). G994-->T transversion in exon 9 of AHA was not found i n any of the IgAN patients. Conclusion. Elevated circulating levels of PAF in IgAN patients might resul t from an insufficient AHA probably related to environmental factors rather than genetic ones. The mechanism and the precise role of the PAF/AHA dereg ulation in IgAN patients remain to be clarified.