Deciphering the Underlying Mechanisms Linking Psoriasis and IgA Nephropathy

Psoriasis is a chronic, immune-mediated inflammatory disease with systemic manifestations that include renal complications. Immunoglobulin A nephropathy (IgAN) represents the most common autoimmune glomerular disease worldwide. Growing epidemiological and genetic evidence supports a clinically relevant association between psoriasis and IgAN, particularly in patients with moderate-to-severe or arthropathic psoriasis. However, current knowledge remains limited by heterogeneous observational data and the absence of systematic renal screening in most psoriasis clinical trials. This review synthesizes evidence linking psoriasis and IgAN across multiple levels. Mendelian randomization studies point to a shared genetic basis, and transcriptomic analyses have uncovered overlapping immune signatures. Several inflammatory pathways may drive the production of galactose-deficient IgA1 (Gd-IgA1) and facilitate glomerular immune complex deposition. Aberrant IgA1 glycosylation driven by psoriatic inflammation, together with tonsillar immune activation, is proposed as a key connection between skin and kidney disease. Important knowledge gaps persist. Routine urinalysis is not performed in most psoriasis trials. Tonsillectomy data derive largely from East Asian populations, and no large-scale international registries are currently available. We therefore propose a clinical screening framework and advocate for the establishment of dedicated registries, along with the integration of urinary tests into future trials. Addressing these gaps will enable mechanism-based, personalized management of psoriasis-associated IgAN.