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Immune-mediated membranous nephropathy: Long term fluconazole usage caused podocyte autophagy

Lan Huang¹, Ya-Juan Zhao¹, Qiao-Rong Dong¹

¹Division of Nephrology, Affiliated Hospital of Chengde Medical University, Chengde, Hebei, China.

Journal of Biochemical and Molecular Toxicology

|November 2, 2021

Abstract:

The primary consequences of membranous nephropathy (MN) are the development of nephrotic syndrome including hypogammaglobulinemia, the increased infectious risk, the loss of protein-bound vitamin D, and, above all, an elevated thromboembolic incidence of up to 50% in severe proteinuria patients. Membrane nephropathy may be either idiopathic or primary, not recognized (70%-80%) or secondary (20%-30%) to pathological sicknesses such as hepatitis B, systemic lupus erythematosus, malignancies, and side-effects of medicines. The immunological responses in MN involve multiple components: immunoglobulin G (IgG), long-escaped antigens, and the membrane attachment complex, formed by the supplement to form C5b-9. In general, IgG4 is the most significant IgG subclass deposited in idiopathic membranous nephropathic disease but fluctuating IgG1 levels also are linked with immunological deposits. In contrast, IgG1, IgG2, and IgG3 deposition are greater than IgG4 deposition in secondary nephropathy. Fluconazole is a synthetic antifungal triazole that is often used. It is well tolerated in general and has never been identified as a cause of nephropathies. We report on the development of MN caused by fluconazole therapy that could potentiate podocyte autophagy.

Insights

Membranous nephropathy (MN) can lead to serious complications. This study identifies fluconazole, an antifungal drug, as a potential cause of MN, possibly by affecting podocyte autophagy.

Area of Science:

Nephrology
Immunology
Pharmacology

Background:

Membranous nephropathy (MN) is a kidney disease often causing nephrotic syndrome, increased infection risk, and high thromboembolic events.
MN can be idiopathic (primary) or secondary to conditions like hepatitis B, lupus, malignancy, or drug side effects.
Immunological responses in MN involve IgG, antigens, and complement activation (C5b-9). IgG4 is typical in idiopathic MN, while IgG1-3 dominate secondary forms.

Purpose of the Study:

To report a case of membranous nephropathy (MN) potentially induced by fluconazole therapy.
To investigate the possible mechanism of fluconazole-induced MN, focusing on podocyte autophagy.

Main Methods:

Case report detailing the development of MN in a patient undergoing fluconazole treatment.
Review of immunological markers and kidney pathology associated with MN.
Exploration of fluconazole's potential impact on podocyte autophagy.

Main Results:

A patient developed membranous nephropathy (MN) during fluconazole therapy.
Fluconazole, generally considered safe for kidneys, was implicated as the cause of MN.
The findings suggest fluconazole may potentiate podocyte autophagy, contributing to MN development.

Conclusions:

Fluconazole therapy can be a potential cause of membranous nephropathy (MN).
This case highlights a novel association between fluconazole and MN, possibly mediated by podocyte autophagy.
Further research is needed to confirm this link and elucidate the underlying mechanisms.

Read full analysis

Keywords:

MN antibodies deposition complement cascade C5b-9 activation fluconazole

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