Maryam Dehghani Mobarakeh
1 
, Ahmadreza Maghsoudi
2* 1 Department of Pathology, Isfahan University of Medical Sciences, Isfahan, Iran
2 Department of Internal Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
Abstract
The pathophysiological mechanisms of secondary IgA nephropathy (IgAN) containing IgA-mediated immune complex deposition in the glomeruli. However, the specific triggers can vary widely, including infections, liver disease, and malignancies, in addition to drug-induced factors. IgAN is a rare however is a serious complication of immune checkpoint inhibitor (ICI) therapy that can lead to acute kidney injury. Clinically, the diagnosis of sIgAN typically follows a temporal association between medication administration and the onset of renal symptoms, such as hematuria or proteinuria. A kidney biopsy is often necessary to confirm the diagnosis and rule out other causes of nephropathy
Implication for health policy/practice/research/medical education:
Primary IgAN is a complex interplay of genetic and environmental factors that lead to the production of galactose-deficient IgA1 and formation of immune complexes. However, the pathogenic mechanisms in secondary IgAN are less well-defined but may involve drug-induced immune dysregulation and inflammation. Immune checkpoint inhibitor (ICI)-associated IgAN is uncommon; however, anti-PD-1 inhibitors are the most commonly associated ICIs with IgA nephropathy, although the overall risk remains low and may be influenced by individual patient factors.
Please cite this paper as: Maghsoudi A, Dehghani Mobarakeh M. Immune checkpoint inhibitors and IgA nephropathy; A rare side effect. J Nephropharmacol. 2025;14(2):e12762x. DOI: 10.34172/npj.2025.12762.