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=1765239215&Signature=owtRqZPYNOBBWQ~jNdpje4gK2SFpSJpX9rFp1Rgz152G2xYZ4ZgmKIpf6ZBPNhaJBMNve027wDnwfWiumSKJHxwlX1r54RfpYi317rmXbK13~5aWQ3m75FGqI6myBaiMbyfad9C-4LkPkiTHgxRg6Po04mrtAeNyIfahtequW3ppihzEFWtwN2WDK3npL2H4-tzC15zjEfQ9YbOzOPFFWMkllW72~cNp-lDpj51WG1HOgq2q5bHpvmR3ywEiXM8~hrYP-Fn0xao5bjHdtBm8FfLCGBv2cLCtXVHSGYxn0QbAVqmIrA5IYOIrl1BuoS4m09gNwPlw-qE57x8GxtuoCQ__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
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