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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
An 84-year-old man was admitted to our hospital for surgical treatment of a lumbar burst fracture. Eight years earlier, he had been diagnosed with asymptomatic, subclinical multiple myeloma (MM) based on urinary M-protein excretion (IgG λ). Since his renal function had remained normal (serum creatinine [sCr] 0.7 mg/dL), no treatment, including chemotherapy, had been initiated. On hospital day 3, posterior lumbar fixation was performed. Twelve hours after surgery, his systolic blood pressure dropped to 60 mmHg due to local surgical-site bleeding, and his sCr level increased to 1.96 mg/dL. Although his blood pressure promptly recovered after red blood cell transfusion, renal dysfunction persisted, with sCr further rising to 6.12 mg/dL.
To investigate the cause of sustained acute kidney injury (AKI), a renal biopsy was performed on hospital day 17. On light microscopy, periodic acid–Schiff (PAS) staining showed global glomerulosclerosis in 8% of glomeruli, while the remaining glomeruli were unremarkable. Prominent hypereosinophilic casts were present within the tubules, with inflammatory cell accumulation surrounding the casts. Notably, there was marked plasma cell infiltration occupying more than 70% of the renal cortical tissue, and several veins were occluded by infiltrating plasma cells. Congo red staining was negative in all kidney sections. Immunofluorescence staining for immunoglobulins and complements was negative in glomeruli. Both κ and λ light chains were negative in glomeruli; however, strong λ positivity was observed in the infiltrating plasma cells. Electron microscopy revealed no electron-dense deposits in glomeruli but showed endothelial edema and swelling. Electron-dense bodies were identified within tubular lumina, and plasmablast infiltration was observed in the interstitium. Based on these findings, the cause of AKI was diagnosed as cast nephropathy with massive plasma cell infiltration. Following adequate hydration, his renal function gradually improved, with sCr decreasing to 3.3 mg/dL.
It has been reported that a decrease in urine output can lead to elevated urinary free light chain (FLC) concentrations, which may trigger cast nephropathy. In this case, the presence of abundant tubular casts suggests that marked perioperative hypotension caused a reduction in renal perfusion and urine output, promoting tubular cast formation and subsequent AKI. In addition, plasma cell infiltration into the renal interstitium likely contributed to renal impairment through interstitial edema and compression of the microvasculature. Although previous autopsy reports have described direct invasion of tumor plasma cells into renal parenchyma, renal biopsy findings demonstrating such extensive plasma cell infiltration in MM patients with renal dysfunction are exceedingly rare. Therefore, this case represents a valuable addition to the limited existing literature on MM-associated renal injury.
