Purpose: Dendritic cells, Toll-like receptor (TLR), interleukin-6 (IFN-α), interferon-alpha (IFN-α) and tumor necrosis factor-alpha (TNF-α) play an important role in the pathogenesis of IgA nephropathy (IgAN). Hydroxychloroquine (HCQ) is an antimalarial agent and had a notable impact on immune activation by the reduction of circulating activated immune cells that including decreased TLR-expressing cells, reduced IFN-secreting DCs, reduced production of cytokines including IFN-α,IL-6 and TNF-α. We evaluated the efficacy of HCQ in reducing proteinuria in patients with IgAN.
Methods: Twenty-eight IgAN patients with persistent proteinuria (0.5-2.0 g/24 h) despite treatment with losartan for 3 months were matched to receive HCQ and losartan (group 1) or continue losartan therapy (group 2) for 24 weeks. The primary end point of this prospective, paired case-control study was reduction of proteinuria by 50% or more over entry level.
Results: Six patients (42.9%) in group one versus two patients (14.3%) in group 2 reach the primary end point (P = 0.004). By 24 weeks, the mean urinary protein excretion was 65.9 ± 25.5% (P = 0.002) and 95.3 ± 30.0% (P = 0.791) that of the corresponding baseline value in group 1 and group 2, respectively. Baseline proteinuria and histologic grades, blood pressure control and changes in serum creatinine and eGFR were not different between the two groups.
Conclusions: In selected patients with IgAN, HCQ is effective in ameliorating proteinuria.
Keywords: Hydroxychloroquine; IgA nephropathy; Proteinuria; Remission.