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Dioscin Mediated IgA Nephropathy Alleviation by Inhibiting B Cell Activation In Vivo and Decreasing Galactose-Deficient IgA1 Production In Vitro

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Deciphering the Underlying Mechanisms Linking Psoriasis and IgA Nephropathy.

Zijie Tang^1,2, Jintong Wu^1,2, Meihan Dong^1,3

¹Medical School of Chinese People's Liberation Army (PLA), Beijing, China.

Journal of Immunology Research

|May 27, 2026

Summary

Psoriasis patients, especially those with severe or joint involvement, have an increased risk of developing Immunoglobulin A nephropathy (IgAN). Shared genetics and inflammation link these autoimmune conditions, but more research and screening are needed.

Keywords:

IgA nephropathy chronic kidney disease interleukin mechanism psoriasis signaling tonsillitis tumor necrosis factor

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Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase (G6PI)-Induced RA Mice

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Published on: January 31, 2020

Area of Science:

Immunodermatology
Nephrology
Autoimmune Diseases

Background:

Psoriasis is a chronic inflammatory disease with systemic effects, including kidney complications.
Immunoglobulin A nephropathy (IgAN) is the most common autoimmune glomerular disease globally.
Evidence suggests a link between psoriasis and IgAN, particularly in moderate-to-severe or psoriatic arthritis cases.

Purpose of the Study:

To review and synthesize current evidence connecting psoriasis and IgAN.
To identify shared genetic and immune pathways.
To propose a framework for clinical screening and future research.

Main Methods:

Review of epidemiological, genetic, and transcriptomic studies.
Analysis of inflammatory pathways involved in IgA1 production and deposition.
Synthesis of evidence linking psoriatic inflammation to aberrant IgA1 glycosylation.

Main Results:

Mendelian randomization studies indicate a shared genetic basis between psoriasis and IgAN.
Transcriptomic analyses reveal overlapping immune signatures.
Psoriatic inflammation may drive galactose-deficient IgA1 (Gd-IgA1) production and glomerular deposition, connecting skin and kidney disease.

Conclusions:

Aberrant IgA1 glycosylation and tonsillar immune activation are proposed as key links between psoriasis and IgAN.
Knowledge gaps exist due to limited renal screening in psoriasis trials and population-specific data.
Establishing dedicated registries and integrating urinary tests into trials are crucial for personalized management.