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The aim of this study was to examine whether the frequent short-time hemodiafiltration (FSHDF) could remove beta2-microglobulin (beta2m), an amyloidogenic factor, more effectively compared with the conventional hemodiafiltration (CHDF). A uremic patient underwent FSHDF (each 90 min, 6 times/week) for 6 weeks after CHDF (each 4 h, 3 times/week) for 6 months. Pretherapeutic plasma concentrations of beta2m, small molecules, electrolytes and bicarbonate were measured every Monday for 4 weeks during CHDF and for 6 weeks during FSHDF. The body weight gain during these weeks was also determined. The time average concentrations in beta2m and blood urea nitrogen (TACbeta2m and TACBUN) were evaluated based on their concentrations in pre-, post- and intertherapeutic plasmas frequently collected for 1 week each during CHDF and FSHDF. The quantities of total protein, albumin and beta2m in the removed fluids for the same week were determined. The pretherapeutic concentration in beta2m was significantly lower (18.7 +/- 1.3 mg/l) during FSHDF than CHDF (32.4 +/- 2.8 mg/l). The TACbeta2m was decreased during FSHDF (from 23.5 to 13.7 mg/l), while the TACBUN did not change. The pretherapeutic bicarbonate concentration was higher and the gain of body weight per week was lower during FSHDF although the other parameters were not different. It is concluded that FSHDF therapy is more effective to decrease beta2m concentration and correct acidosis together with an adequate urea removal and clinical safety.

To investigate the pathogenetic mechanisms of mesangial interposition (MI) in IgA nephropathy, we examined renal biopsy samples from 20 patients with IgA nephropathy. Electron microscopic morphometric analysis showed that cytoplasmic protrusion of mesangial cells (MCs) into endothelial cells (ECs) or capillary lumina, and widening of the lamina rara interna (LRI) were significantly more prominent in glomeruli with MI than in those without. Immunoelectron microscopy revealed that the ratio of positive endothelial staining with a polyclonal antibody against human platelet-derived growth factor (PDGF) BB was significantly higher in capillary loops with MI than in those without. Enhanced capillary staining of fibronectin related to MI was not recognized. These results suggest that MI in IgA nephropathy is caused by factors such as enhancement of cytoplasmic extensibility of the MCs, widening of the LRI and chemotactic influence of PDGF-BB located in the glomerular ECs.