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.
For additional images, visit the ASH Image Bank, a reference and teaching tool that is continually updated with new atlas and case study images. For more information, visit http://imagebank.hematology.org.
![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=1769303885&Signature=Yt8mmaYpqZihu~XEm4P31XMW3aaR5~etMF-zXRGJlS~jTxbdEd8yyRt4lX5-loyy6IedAn4rRkzUTVgJ1znvj8fwsJDNAeV-VSRd7RmicUVUI03pCT29REHlfedYn9pfZkL6oQiQKDb20EwiVV1XmPZ9oy0gAfoKlDVmBfb8LWzXIA8K-zWfjGTv5cugZhyTrGoQpHIuhrkvyYPAL9bHpmN64E1NWkoxi6RUz-esjyEgLt7hXIxepVH8fZAgpkZ16E1h4NYz9-LUd2v1tZEpfGHovuIMOz9gN4fDWE29ytoGbTQzkOMSSj1K7CvCWNK3z8izwTor3LJhoGIv7AwqPg__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)