A 75-year-old man with history of hypertension presented with worsening renal function (creatinine, 3 mg/dL; proteinuria, 146 mg/dL [1.46 g/L], and microscopic hematuria). He was asymptomatic. Physical examination was unremarkable. Extensive laboratory evaluation revealed mild pancytopenia (leukocytes, 2 × 109/L; hemoglobin, 9 g/dL [90 g/L]; and platelets, 100 × 109/L) with normal peripheral smear morphology. Serum immunoglobulins were normal whereas λ light chain was elevated with a κ-to-λ ratio of 0.18. Serum and urine immunofixation showed monoclonal λ light-chain protein. Computed tomography imaging and skeletal survey were normal. Bone marrow aspirate (panels A-B; Wright stain, 100× objective) and core biopsy (panel C; hematoxylin and eosin stain, 60× objective) demonstrated acute myeloid leukemia (AML) with minimal differentiation and 42% myeloblasts (arrowhead), and multiple myeloma (MM) with 15% to 20% monoclonal plasma cells containing prominent Dutcher bodies (arrow). Karyotype was 45,X,−Y and AML/MM fluorescence in situ hybridization panel was unremarkable. Renal biopsy showed extensive basement membrane mesangial protein deposition (panel D; periodic acid–Schiff stain, 40× objective) and λ light chain on immunofluorescence. Congo red stain was positive for amyloid.
To our knowledge, simultaneous de novo AML, MM, and light-chain amyloidosis has not been previously reported. The patient developed end-stage renal failure despite bortezomib-dexamethasone therapy. He decided to pursue comfort-focused care and died within 2 months of diagnosis.
A 75-year-old man with history of hypertension presented with worsening renal function (creatinine, 3 mg/dL; proteinuria, 146 mg/dL [1.46 g/L], and microscopic hematuria). He was asymptomatic. Physical examination was unremarkable. Extensive laboratory evaluation revealed mild pancytopenia (leukocytes, 2 × 109/L; hemoglobin, 9 g/dL [90 g/L]; and platelets, 100 × 109/L) with normal peripheral smear morphology. Serum immunoglobulins were normal whereas λ light chain was elevated with a κ-to-λ ratio of 0.18. Serum and urine immunofixation showed monoclonal λ light-chain protein. Computed tomography imaging and skeletal survey were normal. Bone marrow aspirate (panels A-B; Wright stain, 100× objective) and core biopsy (panel C; hematoxylin and eosin stain, 60× objective) demonstrated acute myeloid leukemia (AML) with minimal differentiation and 42% myeloblasts (arrowhead), and multiple myeloma (MM) with 15% to 20% monoclonal plasma cells containing prominent Dutcher bodies (arrow). Karyotype was 45,X,−Y and AML/MM fluorescence in situ hybridization panel was unremarkable. Renal biopsy showed extensive basement membrane mesangial protein deposition (panel D; periodic acid–Schiff stain, 40× objective) and λ light chain on immunofluorescence. Congo red stain was positive for amyloid.
To our knowledge, simultaneous de novo AML, MM, and light-chain amyloidosis has not been previously reported. The patient developed end-stage renal failure despite bortezomib-dexamethasone therapy. He decided to pursue comfort-focused care and died within 2 months of diagnosis.
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![A 75-year-old man with history of hypertension presented with worsening renal function (creatinine, 3 mg/dL; proteinuria, 146 mg/dL [1.46 g/L], and microscopic hematuria). He was asymptomatic. Physical examination was unremarkable. Extensive laboratory evaluation revealed mild pancytopenia (leukocytes, 2 × 109/L; hemoglobin, 9 g/dL [90 g/L]; and platelets, 100 × 109/L) with normal peripheral smear morphology. Serum immunoglobulins were normal whereas λ light chain was elevated with a κ-to-λ ratio of 0.18. Serum and urine immunofixation showed monoclonal λ light-chain protein. Computed tomography imaging and skeletal survey were normal. Bone marrow aspirate (panels A-B; Wright stain, 100× objective) and core biopsy (panel C; hematoxylin and eosin stain, 60× objective) demonstrated acute myeloid leukemia (AML) with minimal differentiation and 42% myeloblasts (arrowhead), and multiple myeloma (MM) with 15% to 20% monoclonal plasma cells containing prominent Dutcher bodies (arrow). Karyotype was 45,X,−Y and AML/MM fluorescence in situ hybridization panel was unremarkable. Renal biopsy showed extensive basement membrane mesangial protein deposition (panel D; periodic acid–Schiff stain, 40× objective) and λ light chain on immunofluorescence. Congo red stain was positive for amyloid.](https://ash.silverchair-cdn.com/ash/content_public/journal/blood/134/15/10.1182_blood.2019001832/4/m_bloodbld2019001832f1.png?Expires=1765044415&Signature=gxR1ut9TzUDGAW-ArWQoD6oDi5qBq9JYgO8EiUxRUVn6qzm~zRveFSTI~HSoo9yDCx3LlmdYdFdIMLHtKbLCMYWe8jzYRS9FSi8IdK-SqGUZLZ2V3oTyN9L0wJjcl6GmdbDGNtFpKc1G-EM-4QtUk9o~gbrcNMb0NAQB1MtmcY6f8Rb~sWIyIqIVX8~lu-NHKm5TLn69i5OtzvQs822ABOGXUYRzrKTqxUKzVCPmXqi-XEMYuqKs-oB2mE~7Wzq-5AIwGMFC4LPW11UZRT-15e1pkOHEra3JDl5jbp0Sr72tv44-UkKEPYTu--O2gFLFQjKLg~F8y69ZmLdI0DNuHg__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)