ArticleArthritis research & therapy2022
Hydroxychloroquine administration exacerbates acute kidney injury complicated by lupus nephritis.
Article in Arthritis research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 23 citations in OpenAlex.
- A single-center, open label, randomized, controlled study of hydroxychloroquine sulfate in the treatment of low risk PLABMC nephrology · 2024Trial
- ATF6 ameliorates renal warm ischemia-reperfusion injury through FHL2-mediated NF-κB signaling pathway.iScience · 2026Article
- Hydroxychloroquine Associated With Lower Glomerular Filtration Rate Decline in Lupus Nephritis.Arthritis care & research · 2026Article
- Comparative risks of mortality, cardiovascular events, and dementia with methotrexate versus hydroxychloroquine in rheumatoid arthritis: a retrospective cohort study.Annals of medicine and surgery (2012) · 2025Article
- Uncovering latent biological function associations through gene set embeddings.BMC bioinformatics · 2025Article
- Macrophage autophagy protects against acute kidney injury by inhibiting renal inflammation through the degradation of TARM1.Autophagy · 2025Article
- Potential role of host autophagy in Clonorchis sinensis infection.Parasitology research · 2024Article
- Sex differences in mortality among patients with lupus nephritis.European journal of medical research · 2024Article
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Authors and funding
12 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundHydroxychloroquine (HCQ) has been recommended as a basic treatment for lupus nephritis (LN) during this decade based on its ability to improve LN-related renal immune-mediated inflammatory lesions. As a classical lysosomal inhibitor, HCQ may inhibit lysosomal degradation and disrupt protective autophagy in proximal tubular epithelial cells (PTECs). Therefore, the final renal effects of HCQ on LN need to be clarified.
methodHCQ was administered on spontaneous female MRL/lpr LN mice with severe proteinuria daily for 4 weeks. Moreover, the MRL/lpr mice with proteinuric LN were subjected to cisplatin-induced or unilateral ischemia/reperfusion (I/R)-induced acute kidney injury (AKI) after 2 weeks of HCQ preadministration.
resultsAs expected, HCQ treatment increased the survival ratio and downregulated the levels of serum creatinine in the mice with LN, ameliorated renal lesions, and inhibited renal interstitial inflammation. Unexpectedly, HCQ preadministration significantly increased susceptibility to and delayed the recovery of AKI complicated by LN, as demonstrated by an increase in PTEC apoptosis and expression of the tubular injury marker KIM-1 as well as the retardation of PTEC replenishment. HCQ preadministration suppressed the proliferation of PTECs by arresting cells in G1/S phase and upregulated the expression of cell cycle inhibitors. Furthermore, HCQ preadministration disrupted the PTEC autophagy-lysosomal pathway and accelerated PTEC senescence.
conclusionHCQ treatment may increase susceptibility and delay the recovery of AKI complicated by LN despite its ability to improve LN-related renal immune-mediated inflammatory lesions. The probable mechanism involves accelerated apoptosis and inhibited proliferation of PTECs via autophagy-lysosomal pathway disruption and senescence promotion.
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