SELENIUM STATUS AND PLASMA GLUTATHIONE-PEROXIDASE IN PATIENTS WITH IGA NEPHROPATHY

The abnormal proliferation of mesangial cells with IgA deposition in t he glomeruli characterizes primitive mesangial glomerulonephritis (IgA nephropathy, IgAN); this disease reduces the normal renal parenchyma while renal function becomes progressively impaired. The possible role of selenium has never been considered in evaluating factors involved in the pathogenesis of IgAN. In this work we compared the Se status of 14 IgAN patients (8 with normal renal function, IgAN NRF; 6 with impa ired renal function, IgAN TRF) to that of 14 normal individuals (CG NR F) before and after an oral supplementation with selenite (0.13 mol Se /kg b.w./day for 60 days). The following indices of Se status were mea sured: Se in plasma and urine samples by PIXE; glutathione peroxidase activity in the cytosol of platelets (PLTs-GSH-Px) and of erythrocytes (RBCs-GSH-Px). Both concentrations and activities of plasma glutathio ne peroxidase (pl-GPx), a selenoenzyme mainly synthesized in and secre ted by the kidney, were measured in plasma samples and results compare d among groups. IgAN patients showed lower pl-Se and lower activities of selenoenzymes than normal controls before Se supplementation (p<0.0 01). These findings suggest that an impaired Se status coexisted with the proliferation of mesangial cells in patients. Selenite induced PLT s-GSH-Px activity in all individuals (p<0.001), but no variation was o bserved in RBCs-GSH-Px activity or in the concentration of pl-GPx in t he plasma. On the other hand, selenium induced pl-GPx activity in CG N RF (p<0.001) and in IgAN NRF (p<0.01), but poorly stimulated pl-GPx ac tivity in IgAN IRF (p = n.s.). However, only 17% and 25% of the pl-GPx activity of normal controls was measured in the plasma of IgAN IRF an d IgAN NRF patients, respectively (p<0.001). In conclusion, selenite o nly partially restored a normal Se status in patients whose low pl-GPx activity probably reflects an impaired synthesis of this protein as a consequence of reduced normal functioning of the parenchyma in kidney s affected by IgA nephropathy.