Recurrent dense deposit disease after renal transplantation: an emerging role for complementary therapies.

Dense deposit disease is a rare glomerulonephritis caused by uncontrolled stimulation of the alternative complement pathway. Allograft survival after kidney transplantation is significantly reduced by the high rate of disease recurrence. No therapeutic interventions have consistently improved outcomes for patients with primary or recurrent disease. This is the first reported case of recurrent dense deposit disease being managed with eculizumab. Within 4 weeks of renal transplantation, deteriorating graft function and increasing proteinuria were evident. A transplant biopsy confirmed the diagnosis of recurrent dense deposit disease. Eculizumab was considered after the failure of corticosteroid, rituximab and plasmapheresis to attenuate the rate of decline in allograft function. There was a marked clinical and biochemical response following the administration of eculizumab. This case provides the first evidence that eculizumab may have a place in the management of crescentic dense deposit disease. More information is necessary to clarify the effectiveness and role of eculizumab in dense deposit disease but the response in this patient was encouraging. The results of clinical trials of eculizumab in this condition are eagerly awaited.

Effect of Colquhoumia root on the expression of transforming growth factor-beta in mesangial proliferation glomerulonephritis model.

To study the efficacy and the mechanism of Colquhoumia root (Tripterygium hypoglaucum (Le,vL) Hutch) in the treatment of mesangial proliferation glomerulonephritis (MsPGN), SD rats were injected with anti-thymocyte serum (ATS) to make MsPGN model (anti-Thyl model). The rats were then divided into 3 groups: normal control group, anti-Thyl model group and treatment group. Histopathological (HE, PAS), immunohistochemical, RT-PCR technique and computer imaging analysis system were used to evaluate mesangial matrix production, the expression of TGF-beta1 protein and mRNA in the tissues of kidney. Our result showed that proteinuria and the ratio of extracellular matrix/glomerular capillaries area (ECM/CA) were increased significantly in model group. The expression of both TGF-beta1 protein and mRNA in glomeruli was much higher in model group than in control group (P < 0.01). After the treatment with Colquhoumia root, proteinuria, ECM/CA and the expression of both TGF-beta1 protein and mRNA in glomeruli were significantly decreased in treatment group as compared with those in model group. It is concluded that Colquhoumia root is effective in reducing proteinuria and mesangial matrix proliferation in MsPGN and it may achieve these effects by inhibiting the expressions of TGF-beta1 protein and mRNA of mesangial cells.

[Effects of Onpi-to (TJ-8117) on mesangial injury induced by anti Thy-1 antibody].

We investigated the effect of Onpi-to (TJ-8117) on the mesangial injury induced by anti-Thy-1 antibody. TJ-8117 (400 mg/kg/day, p.o.) given from the 1st day (from the day of injection of the anti-thymocyte serum) or 4th day (after mesangial proliferation), markedly inhibited the mesangial proliferation and hypercellularity in glomeruli. TJ-8117 prevented the increase in the number of PCNA or ED-1 positive cells in glomeruli. These results suggest that TJ-8117 is effective against glomerular disease with mesangial injury.