Thrombotic microangiopathy in IgA nephropathy: pathophysiology, histopathology, and treatment perspectives

Abstract

The current narrative review study aims to provide an overview of thrombotic microangiopathy (TMA) in immunoglobulin A nephropathy (IgAN), with a particular emphasis on its pathophysiology, histopathology, and treatment options. The prevalence and clinical significance of TMA in IgAN may vary across different populations. Estimates suggest that TMA events occur in 2-50% of patients with IgAN. Endothelial injury is a key factor in TMA development in IgAN, triggered by immune complex deposition, complement activation, and potentially hypertension. TMA in IgAN correlates with vascular lesions, including arterial intimal sclerosis, arteriolar lumen reduction, and smooth muscle hypertrophy. Notably, patients with TMA show more intense deposition of C4, C3d, and C5b-9 complements. Treatment involves blood pressure management, immunosuppression, and targeted therapies such as eculizumab.

Keywords

• thrombotic microangiopathy
• iga nephropathy
• complement
• histopathology
• pathophysiology
• treatment