De novo plasma cell dyscrasia causing renal AL amyloidosis in a patient with synchronous chronic lymphocytic leukaemia and chronic myeloid leukaemia; a case report

Amyloid light-chain (AL) amyloidosis involves glomerular, tubulointerstitial and/or vascular infiltration with amyloid fibril deposition commonly manifesting in nephrotic syndrome and progressive renal dysfunction. The abnormal light chain clonal population originates predominantly from plasma cell dyscrasias and rarely from lymphoproliferative B-cell disorders. Accurately identifying this underlying pathogenic clone is critical for guiding targeted chemotherapeutic interventions. We describe a 79-year-old male with preexisting chronic lymphocytic leukemia (CLL) and chronic myeloid leukemia (CML) who presented with nephrotic syndrome and acute kidney injury. Renal biopsy demonstrated AL amyloid deposition with lambda light chain restriction. Bone marrow biopsy confirmed a monoclonal plasma cell population expressing lambda light chains, in addition to pre-existing haematological malignancies. Cardiac markers and transthoracic echocardiogram indicated an infiltrative cardiomyopathy. A diagnosis of AL amyloidosis with cardiorenal involvement from a de novo monoclonal plasma cell disorder was made. The patient was initiated on clone-directed chemoimmunotherapy and although a complete hematological response was achieved, ongoing nephrotic syndrome and cardiac dysfunction persisted, progressing to refractory fluid overload that necessitated renal replacement therapy. This case underscores the necessity of robust clonal subtyping (via mass spectrometry or immunohistochemistry (IHC)) to appropriately direct therapy in patients with concurrent hematological malignancies. Furthermore, it highlights the clinical challenge of managing delayed organ response and balancing therapeutic efficacy against complication risks in elderly, comorbid populations.