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Comparative Study
. 2021 Dec;43(1):1520-1527.
doi: 10.1080/0886022X.2021.2000875.

Hydroxychloroquine in IgA nephropathy: a systematic review

Gabriel Stefan  1   2 , Gabriel Mircescu  1   2
Affiliations
Comparative Study

Hydroxychloroquine in IgA nephropathy: a systematic review

Gabriel Stefan et al. Ren Fail. 2021 Dec.

Abstract

Background: Hydroxychloroquine (HCQ) has recently been reported to be a promising and safe anti-proteinuric agent for IgA nephropathy (IgAN) patients. In the present systematic review, we aimed to summarize the evidence concerning the benefits and risks of HCQ therapy in IgAN.

Methods: Electronic databases were searched for randomized, cohort, or case-control studies with IgAN biopsy-proven patients comparing the effects of HCQ with angiotensin-converting enzyme inhibitors/angiotensin receptor blockers or immunosuppression on proteinuria reduction.

Results: Five studies, one randomized and three observational, involving a total of 504 patients, were eligible for inclusion. Overall, there was a tendency of HCQ treatment to reduce proteinuria. In the studies where the control arm was supportive therapy, HCQ significantly reduced proteinuria at 6 months. However, in the studies that compared HCQ to immunosuppressive therapy, we found no difference in proteinuria reduction. HCQ had no impact on eGFR.

Conclusion: HCQ seems to be an efficient alternative therapy for patients with IgAN who insufficiently respond to conventional therapy. However, ethnically diverse randomized controlled studies with long-term follow-up are needed.

Keywords: IgA nephropathy; eGFR; hydroxychloroquine; meta-analysis; proteinuria; systematic review.

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Conflict of interest statement

The authors declare no conflict of interest or competing interests.

Figures

Figure 1.
Figure 1.
Study selection process of the systematic review (PRISMA diagram, Preferred Reporting Items for Systematic Reviews and Meta-Analyses).
Figure 2.
Figure 2.
Potential mechanisms for hydroxychloroquine (HCQ) action in IgA nephropathy (IgAN). HCQ can interfere with immune activation at various cellular levels by inhibiting the innate and adaptive immune systems. In IgAN, mucosal Toll like receptor-9 (TLR-9) activation induces B-cell activating factor (BAFF) overexpression in dendritic cells, stimulates the generation of proliferation-inducing ligand (APRIL) and interleukin-6 (IL-6), which act concurrently to stimulate the production of galactose deficient IgA1. HCQ interferes with TLR9 ligand binding and TLR signaling (through lysosomal inhibition), which inhibits TLR-mediated cell activation and cytokine production. Moreover, in antigen presenting cells, such as dendritic cells and B cells, HCQ inhibits antigen processing and subsequent MHC class II presentation to T cells, preventing T cell activation, differentiation and expression of co-stimulatory molecules.
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