Unveiling the Link: Exploring the Association between Cancer and Leukocyte Chemotactic Factor 2 (ALECT2)-Associated Amyloidosis

Introduction: We present a case of a 53-year-old Hispanic male diagnosed with mantle cell lymphoma with subsequent decline in glomerular filtration rate (GFR) found to have LECT2 amyloidosis on renal biopsy. Notably, following treatment of the lymphoma, his GFR stabilized. Given the correlation between his GFR and lymphoma course, we hypothesize that his lymphoma, possibly via dysregulated Wnt/β-catenin signaling, served as a trigger for ALECT2 amyloidosis. Case Description: The patient was diagnosed with mantle cell lymphoma in June 2022 and underwent alternating R-CHOP and R-DHAP until December 2022. In May 2023, he had an autologous stem cell transplant with BEAM induction, followed by rituximab maintenance. Despite a normal baseline creatinine, his creatinine worsened to 1.5 mg/dL by May 2023. Post-transplant, creatinine continued to rise to 1.89 mg/dL by the time of initial nephrology consultation in December 2023. Urinalysis, urinary microalbumin and protein-to-creatinine ratio, monoclonal gammopathy screening, and renal sonogram were all unremarkable. Due to the unclear cause of worsening renal function, he had a renal biopsy in January 2024 showing tubulointerstitial amyloid deposition. Mass spectrometry was consistent with the ALECT2 type. As of March 2024, his creatinine was stable at 1.76 mg/dL Discussion: ALECT2 amyloidosis is characterized by LECT2 protein accumulation, a molecule involved in neutrophil chemotaxis and implicated in multiple inflammatory conditions. Our patient's course and Hispanic origin align with other documented ALECT2 cases in the literature. However, no cases describe an association with lymphoma nor hypothesized treatment. Given the patient’s course and the pathophysiology of ALECT2 amyloidosis, we suggest that a surge in LECT2 possibly occurred due to dysregulated Wnt/β-catenin signaling, a pathway implicated in carcinogenesis. We highlight the potential interplay between cancer and ALECT2 amyloidosis, with treatment addressing the underlying cause of amyloid accumulation.