Interplay between Thyroid Autoimmunity and Monoclonal Glomerular Deposits: A Case Report Highlighting Endocrine and Nephrological Dilemmas

A

BSTRACT

Proliferative glomerulonephritis with monoclonal immunoglobulin deposits (PGNMID) is a rare condition marked by glomerular deposition of monotypic immunoglobulin (Ig)G, typically IgG3 with light-chain restriction and limited response to standard immunosuppression. While Graves’ disease (GD) can be rarely associated with glomerular pathology, its overlap with PGNMID is exceptionally uncommon. This case highlights a rare intersection, raising important diagnostic and therapeutic challenges. A 36-year-old woman with newly diagnosed GD presented with nephrotic-range proteinuria, microscopic hematuria, and hypertension. Kidney biopsy revealed diffuse endocapillary and mesangial hypercellularity with monoclonal IgG-λ deposits – consistent with PGNMID. The patient, however, achieved complete remission after 4 weeks of low-dose corticosteroids (0.5 mg/kg/day), contrary to the expected refractoriness of PGNMID. Concurrently, she transitioned from hyperthyroidism to hypothyroidism, suggesting steroid-induced modulation of thyroid autoimmunity. This case underscores two major dilemmas: (1) the atypical responsiveness to steroids challenging the diagnosis of true PGNMID, raising the possibility of pseudo-monotypic immune-complex glomerulonephritis; and (2) the endocrine shift points to immune crosstalk between thyroid and renal axes.