ArticleBMC nephrology2026
A rare case of renal AHL amyloidosis with marked complement deposition: clinicopathologic and proteomic findings.
Article in BMC nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAmyloidosis comprises a heterogeneous group of diseases characterized by extracellular deposition of β-pleated-sheet fibrillar proteins that cause progressive organ dysfunction. Among immunoglobulin-related amyloidosis, combined heavy- and light-chain (AHL) amyloidosis is extremely rare, which accounts for approximately 7%. Several studies have demonstrated that complement components can be detected in renal amyloidosis. We report a rare case of renal AHL amyloidosis with marked complement deposition with clinicopathologic and proteomic insights. CASE PRESENTATION: A 76-year-old woman with a five-year history of microscopic hematuria developed mild renal dysfunction (serum creatinine 1.05 mg/dL) and proteinuria (0.95 g/day). Physical and serologic evaluations showed no evidence of systemic amyloidosis or autoimmune disease. Serum and urine immunofixation detected an IgG-κ M-protein, and bone marrow findings were consistent with monoclonal gammopathy of undetermined significance. Kidney biopsy demonstrated Congo red-positive fibrillar deposits with IgG1, κ, and complement (C3/C1q) staining. Electron microscopy revealed non-branching fibrils measuring 8 to 12 nm in diameter. Because marked complement deposition was observed, fibrillary glomerulonephritis (FGN) was considered in the differential diagnosis. However, negative Dna J heat-shock protein family B member 9 immunostaining raised suspicion for amyloidosis. Mass spectrometry identified IgG1 heavy and κ light chains together with serum amyloid P and apolipoprotein E, confirming IgG1-κ-type AHL amyloidosis.
conclusionsThis case illustrates a presentation of AHL amyloidosis with marked complement deposition. Recent study reveals that complement components can be detected in a subset of amyloidosis cases. These features can complicate the differential diagnosis from FGN and highlight the importance of an integrated diagnostic approach combining histopathology, immunostaining, and proteomic analysis. Furthermore, clone-directed therapy targeting the pathogenic plasma cell clone may represent a rational therapeutic strategy for monoclonal immunoglobulin-associated renal disease.
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