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Abstract titles should be brief and reflect the content of the abstract.
Monoclonal gammopathy of renal significance (MGRS) is defined by renal injury caused by the deposition of a monoclonal immunoglobulin. In IgG-type MGRS, diagnosis is often straightforward using immunofluorescence staining for IgG subclasses (IgG1–4) and κ/λ light chains. In contrast, IgA-type MGRS poses greater diagnostic challenges because most glomerular IgA deposits belong to the IgA1 subclass, and light chain predominance (κ or λ) is also frequently observed in polyclonal diseases such as IgA nephropathy (IgAN). The KM55 monoclonal antibody, which recognizes galactose-deficient IgA1, is typically positive in IgAN but may be weak or negative in IgA-type MGRS. Recent reports have described IgA-PGNMID and IgA-MIDD as rare manifestations of IgA-type MGRS, occasionally showing negative KM55 staining and restricted IgA subclass expression. We evaluated the diagnostic value of light chain and IgA subclass staining in IgA-dominant glomerular deposits.
We retrospectively reviewed cases diagnosed between January 2015 and August 2024 that demonstrated IgA-dominant glomerular deposition in native kidney biopsies. We analyzed κ/λ light chain restriction, IgA subclass predominance, KM55 intensity, pathological diagnosis, presence of serum M-protein, and renal outcomes, and assessed their association with the final clinical diagnosis.
Among 328 cases with IgA-dominant glomerular deposits, 302 were diagnosed as IgAN, 19 as IgA vasculitis, and 7 as other diseases. Light chain predominance (≥ 1+) was observed in 14 κ-dominant and 36 λ-dominant cases (15.3%), and ≥ 1.5+ in 10 κ and 16 λ cases (8.0%). The IgA2 subclass was comparable to IgA1 (difference −0.5 to +0.5) in 26 cases and only one case showed IgA2 predominance.Among 48 cases with ≥ 1+ light chain predominance and subclass imbalance (14 κ, 34 λ), the pathological diagnoses were 45 IgAN, 1 IgA vasculitis, 1 IgA2-κ MIDD, and 1 suspected IgA1-λ PGNMID.Of 23 cases with available follow-up (mean age 42.8 ± 14.6 years, mean eGFR 73.1 ± 27.6 mL/min/1.73 m², proteinuria 1.6 ± 2.0 g/gCr), all were negative for serum M-protein. Fifteen patients received steroid pulse therapy, and 13 achieved proteinuria < 1 g/gCr; one improved after an additional steroid pulse, and one was refractory to treatment and was diagnosed as IgA1-κ PGNMID on repeat biopsy, in which weak KM55 staining provided a diagnostic clue. The other patient with suspected IgA1-λ PGNMID responded to repeated steroid pulses plus cyclosporine, achieving partial remission (< 1 g/gCr).
Light chain restriction in IgA-dominant glomerular deposition is not uncommon but often reflects polyclonal IgA nephropathy rather than MGRS. While KM55 staining for galactose-deficient IgA1 is useful for differentiating IgAN from monoclonal IgA deposition, its negativity or weak reactivity should raise suspicion for IgA-type MGRS. Ultimately, IgA-type MGRS should be diagnosed through an integrated assessment of light chain restriction, IgA subclass predominance, KM55 staining pattern, and clinical course, supported by repeat biopsy and clone-directed evaluation when indicated.
