Table 1. Secondary Causes and Associations in IgA Nephropathy.

IgA: Immunoglobulin A

System/Trigger	Associated Conditions	Mechanism and Clinical Notes
Chronic Liver Disease	• Alcoholic cirrhosis • Autoimmune hepatitis • Wilson’s disease • Hemochromatosis	The most common cause of secondary IgAN. Impaired clearance of IgA immune complexes by the diseased liver leads to mesangial deposition. IgAN in these patients may improve with better liver function [13]
Gastrointestinal	• Celiac disease (HLA-DQ2/DQ8 linked) • Inflammatory Bowel Disease (Crohn’s, UC) • Gut dysbiosis	Mucosal immune activation increases aberrant IgA production. Gluten-free diet in celiac disease may induce remission. Altered microbiomes reduce barrier function and increases systemic immune activation [14]
Autoimmune Disorders	• Sjögren’s syndrome • Systemic Lupus Erythematosus (SLE) • Ankylosing spondylitis • Behçet’s disease	Chronic immune stimulation leads to aberrant IgA overproduction and immune complex formation. Histologic findings are often similar to primary IgAN [15]
Dermatologic Disorders	• Henoch–Schönlein Purpura (IgA vasculitis) • Psoriasis • Severe eczema, dermatomyositis, blistering disorders	Henoch–Schönlein purpura represents systemic IgA-mediated vasculitis. Psoriasis is the most common dermatologic condition associated with IgAN [16]
Infections	• Upper respiratory infections (synpharyngitic hematuria) • Chronic tonsillitis • HIV, Hepatitis B, COVID-19	Mucosal infections are common triggers of IgAN flares. Chronic tonsillitis increases IgAN risk (2.7-fold). Viral infections stimulate polyclonal IgA responses [17]
Drug Induced	• TNF-α inhibitors (infliximab, adalimumab) • Immune checkpoint inhibitors (PD-1/PD-L1, CTLA-4) • IL-12/23 inhibitors • Warfarin, DOACs, thiourylene drugs	Rare but recognized. Mechanism involves anti-glycan antibodies forming immune complexes with Gd-IgA1. Consider discontinuation if suspected [18]