Rare Dual Leukaemia Case Reveals Hidden Plasma Cell Disorder Behind Kidney Failure

A 79-year-old man already living with two unrelated blood cancers—chronic lymphocytic leukaemia and chronic myeloid leukaemia—developed nephrotic syndrome and acute kidney injury, and a renal biopsy revealed the unexpected culprit: AL amyloidosis, with amyloid fibrils depositing in the kidney. The case, published in BMC Nephrology, illustrates how a third, previously undetected blood disorder can drive organ damage in patients whose medical histories already look bewilderingly complex.

AL amyloidosis occurs when abnormal light-chain proteins, produced by a clonal population of cells, misfold into amyloid fibrils that infiltrate the glomeruli, tubulointerstitium or vessels of organs, commonly causing nephrotic syndrome and progressive renal dysfunction. The pathogenic clone usually arises from a plasma cell dyscrasia and only rarely from lymphoproliferative B-cell disorders. Pinpointing which clone is responsible matters enormously, because it determines which chemotherapy regimen is likely to work.

In this patient, the renal biopsy showed amyloid deposition with lambda light chain restriction. A bone marrow biopsy then confirmed a monoclonal plasma cell population expressing lambda light chains, alongside his pre-existing haematological malignancies. In other words, the amyloid was not a complication of his CLL or CML but stemmed from a de novo plasma cell disorder that had emerged independently.

The disease was not confined to the kidneys. Cardiac markers and a transthoracic echocardiogram indicated an infiltrative cardiomyopathy, leading the team to diagnose AL amyloidosis with cardiorenal involvement. The patient was started on clone-directed chemoimmunotherapy, and although a complete haematological response was achieved, his nephrotic syndrome and cardiac dysfunction persisted. He progressed to refractory fluid overload that ultimately necessitated renal replacement therapy.

The authors argue the case underscores the necessity of robust clonal subtyping—using mass spectrometry or immunohistochemistry—to direct therapy appropriately in patients with concurrent haematological malignancies. It also highlights the clinical challenge of managing delayed organ response and balancing therapeutic efficacy against complication risks in elderly, comorbid populations, where even a successful attack on the clone may not rescue organs already burdened by amyloid.

Subject of Research: A case report of renal AL amyloidosis arising from a de novo plasma cell dyscrasia in a patient with concurrent CLL and CML.

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

Article References: Nim, J., Viswanathan, S., Kwok, F., & Vucak-Dzumhur, M. (2026). De novo plasma cell dyscrasia causing renal AL amyloidosis in a patient with synchronous chronic lymphocytic leukaemia and chronic myeloid leukaemia; a case report. BMC Nephrology. https://doi.org/10.1186/s12882-026-05366-2

Image Credits: AI Generated

DOI: 10.1186/s12882-026-05366-2

Keywords: AL amyloidosis, plasma cell dyscrasia, chronic lymphocytic leukaemia, chronic myeloid leukaemia, nephrotic syndrome, renal biopsy, lambda light chain, cardiorenal involvement, clonal subtyping, case report, novo, plasma