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Abstract: TH-PO090

Incidence and Risk Factors of AKI and Tumor Lysis Syndrome in Patients with Multiple Myeloma Treated with Bortezomib

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology, Risk Factors, and Prevention

Authors

  • Song, Seungmin, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea (the Republic of)
  • Park, Kyungho, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea (the Republic of)
  • Lee, Kyungho, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea (the Republic of)
  • Jang, Hye Ryoun, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea (the Republic of)
  • Huh, Wooseong, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea (the Republic of)
  • Kim, Yoon-Goo, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea (the Republic of)
  • Kim, Dae joong, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea (the Republic of)
  • Lee, Jung eun, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea (the Republic of)
Background

Nephrotoxicity of bortezomib, a proteasome inhibitor, has not yet been described frequently, while tumor lysis syndrome (TLS) associated with multiple myeloma (MM) has been increased after introduction of the drug. This study compared the incidence and risk factors of acute kidney injury (AKI) and TLS in patients with MM after bortezomib-based chemotherapy to investigate the drug-related nephrotoxicity.

Methods

From 2006 to 2017, 276 patients who underwent first cycle of bortezomib-based chemotherapy for MM were identified in single tertiary hospital. Laboratory TLS was defined according to the Cairo-Bishop definition. Development of AKI was assessed by AKI Network criteria within 7 days after first chemotherapy.

Results

The age was 65 [56-72] years old, and 47% (n=131) of participants were female and baseline estimated glomerular filtration rate (eGFR) was 61.3 [34.1-89.1] mL/min/1.73m2. The incidences of AKI and laboratory TLS were 17% (n=47) and 13% (n=36), respectively. Ten (3.6%) subjects corresponded to the both AKI and TLS criteria.
Multivariate analyses showed that lower eGFR category (30~59, odds ratio [OR]=3.063 [1.278-7.339]; 15~29, OR=3.417 [1.088-10.726]; <15, OR=10.080 [2.677-37.951] vs ≥ 60), lower serum albumin level (OR=0.491 [0.278-0.868], P=0.0144) and renal amyloidosis (OR=11.174 [3.974-31.420], P<0.0001) were predictors of development of AKI. MM stages and β2-microglobulin were not associated with AKI occurrence.
Regarding laboratory TLS, MM stage and β2-microglobulin were higher in those with TLS. In multivariate analyses, β2-microglobulin levels (OR=1.194 [1.066-1.337], P=0.0021) and any chromosomes abnormalities at high risk (OR=0.115 [0.026-0.503], P=0.0041) were associated with higher risk of TLS.

Conclusion

Development of AKI was often observed without being accompanied by TLS in patients with MM after treatment of bortezomib. In addition, risk factors of AKI and TLS were widely different. These findings implicated the potential nephrotoxicity of bortezomib besides TLS in patients with decreased kidney function. The efforts to prevent the developments of AKI are needed in patients with risk factors, when initiating bortezomib treatment.