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Nephrol Dial Transplant (2000) 15: 1344-1347
© 2000 European Renal Association-European Dialysis and Transplant Association

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

Yves Denizot, Corinne Aupetit, Franck Bridoux1, Jean-Claude Alphonse2, Michel Cogné and Jean Claude Aldigier

EP CNRS 118, Faculté de Médecine, 2 rue Dr Marcland, Limoges and Service de Néphrologie, CHU Dupuytren, 2 avenue Luther King, Limoges, 1 Service de Néphrologie, CHU La Milétrie, BP 577, Poitiers and 2 Service de Néphrologie, CHU Gabriel Montpied, 63000 Clermont-Ferrand, France

Background. Platelet-activating factor (PAF) is a phospholipid mediator with potent inflammatory activities. PAF stimulates IgA synthesis by B cells while IgA aggregates enhance PAF production by neutrophils and mesangial cells. These results led us to investigate blood PAF levels and plasma acetylhydrolase (AHA, the PAF catabolic enzyme) activity in patients with idiopathic IgA nephropathy (IgAN).

Methods. PAF and AHA levels were investigated using the platelet aggregation assay and degradation of 3H-labelled PAF, respectively. The genotype of AHA with regard to the G994->T mutation in exon 9 was assessed by an allele-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 healthy controls (18±5 pg/ml, n=18). In contrast, plasma AHA levels were significantly (P=0.0001, Mann–Whitney U-test) reduced in patients with IgAN (61±2 nmol/ml/min, n=51) compared with healthy controls (78±4 nmol/ml/min, n=53). G994->T transversion in exon 9 of AHA was not found in any of the IgAN patients.

Conclusion. Elevated circulating levels of PAF in IgAN patients might result from an insufficient AHA probably related to environmental factors rather than genetic ones. The mechanism and the precise role of the PAF/AHA deregulation in IgAN patients remain to be clarified.

Keywords: acetylhydrolase activity; Berger's disease; IgA nephropathy; platelet-activating factor

Correspondence and offprint requests to: Y. Denizot, EP CNRS 118, Faculté de Médecine, 2 rue Dr Marcland, F-87025 Limoges, France.


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