Secondary IgA Nephropathy and IgA-Associated Nephropathy: A Systematic Review of Case Reports

Abstract

Primary (pIgAN), secondary IgA nephropathy (sIgAN), and IgA-associated nephropathy can be distinguished. While pIgAN has been thoroughly studied, information about the etiology of sIgAN remains scarce. As concerns sIgAN, several studies suggest that different etiologic factors play a role and ultimately lead to a pathophysiologic process similar to that of pIgAN. In this article, we review a vast number of cases in order to determine the novel putative underlying diseases of sIgAN. Moreover, updates on the common pathophysiology of primary disorders and sIgAN are presented. We identified liver, gastrointestinal, oncological, dermatological, autoimmune, and respiratory diseases, as well as infectious, iatrogenic, and environmental factors, as triggers of sIgAN. As novel biological therapies for listed underlying diseases emerge, we suggest implementing drug-induced sIgAN as a new significant category. Clinicians should acknowledge the possibility of sIgAN progression in patients treated with TNF-α inhibitors, IL-12/IL-23-inhibitors, immune checkpoint inhibitors, CTLA-4, oral anticoagulants, thioureylene derivatives, and anti-vascular endothelial growth factor drugs.

Crohn's Disease Associated With IgA Nephropathy Effectively Treated With the Interleukin-23 Inhibitor Risankizumab

“…However, there has been some literature to suggest that IgAN can be precipitated by IL-23 inhibitors. 15 , 16 Further research could help clarify the complicated relationship between IL-23 and IgAN.…”

An unsuspected histopathological finding —concomitant IgA nephropathy in a patient with ANCA-associated vasculitis: a case report and literature review

“…IgA nephropathy (IgAN) is the most common glomerulonephritis worldwide ( 1 ). Numerous disease entities, such as liver, dermatological, gastrointestinal, autoimmune, oncological, and respiratory disorders, as well as infectious, iatrogenic (drugs), and environmental factors, are recognized as triggers for IgAN development ( 2 ). As regards the pathophysiology of IgAN, the four-hit hypothesis is suggested.…”