Minimal Change Disease With Mesangial IgA Deposition: A Clinicopathological Case Series From a Tunisian Referral...

Minimal change disease (MCD) associated with mesangial immunoglobulin A (IgA) deposition, historically referred to as "IgA Nephrosis," is a rare and nosologically controversial entity. Whether it represents MCD with incidental mesangial IgA deposition, a dual glomerulopathy combining MCD and subclinical IgA nephropathy (IgAN), or a distinct clinicopathological phenotype remains uncertain. Only isolated case reports and small series have been published to date.

We retrospectively identified six consecutive patients (three children/adolescents and three adults; four males and two females) evaluated at the Kidney Pathology Laboratory of the Department of Nephrology, Charles Nicolle Hospital, Tunis, between 1995 and 2025. All patients presented with nephrotic syndrome, minimal or absent glomerular abnormalities on light microscopy, and dominant mesangial IgA deposits on direct immunofluorescence.

Microscopic hematuria was present in three patients, while one patient reported a remote episode of macroscopic hematuria during childhood. Light microscopy revealed essentially normal glomeruli in three cases and only mild mesangial hypercellularity and/or matrix expansion in the remaining cases, without endocapillary proliferation, crescents, necrotizing lesions, or significant chronic damage. Immunofluorescence consistently demonstrated dominant or exclusive mesangial IgA deposits, variably associated with IgM, IgG, C3, C1q, fibrinogen, or light-chain co-deposition. Electron microscopy was unavailable. Most patients exhibited steroid-sensitive disease, although relapsing courses were frequent.

MCD with mesangial IgA deposition represents an uncommon clinicopathological entity situated at the interface between MCD and IgAN. The marked discrepancy between severe nephrotic syndrome and minimal histological lesions despite mesangial IgA deposition strongly suggests a predominant podocytopathy rather than classical proliferative IgAN. Recognition of this phenotype is important to avoid diagnostic misclassification and inappropriate therapeutic strategies. Further studies integrating ultrastructural and molecular analyses are required to clarify its pathogenesis and nosological position.