KIM-1 as an Early Predictive Marker for Cyclosporine A Nephrotoxicity in Leukemic Patients Performing Peripheral Stem Cells Transplantation

2020 
Background: Kidney injury molecule-1 (KIM-1) is a transmembrane glycoprotein related to acute kidney injury. Its role in the prediction of cyclosporine A (CSA) nephrotoxicity is unclear and up to our knowledge, this is the first time to investigate its usage after peripheral stem cell transplantation (SCT) as established marker of tubulointerstitial injury. Objective: to explore the usefulness of KIM-1 for early identification of CSA nephrotoxicity in Egyptian leukemic patients performing peripheral SCT. Methods: This study is a cross sectional study that was carried out on 36 leukemic patients performing SCT. Samples were collected from patient before the start of CSA treatment (Just after SCT) and after 14 days of CSA treatment. Serum KIM-1 was measured by ELISA, and CSA was measured by using automated clinical chemistry analyzer. Serum creatinine, blood urea nitrogen, uric acid, serum albumin, ALT & AST, bilirubin, ALP, LDH, sodium, potassium, calcium and magnesium levels were measured by VITROS 5600/XT 7600 Integrated Systems. Complete blood count was measured by fully automated hematology cell counter. After follow up of patients for 32 days, 12 of them developed nephrotoxicity so the patients were further divided according to nephrotoxicity status. Results: Serum level of KIM-1 was significantly higher after CSA treatment than before (p≤0.01). KIM-1 showed significant differences between positive and negative nephrotoxicity groups regarding before, after CSA and ∆Change values (p≤0.01, p≤0.01, p≤0.02) respectively. Whereas the only significant difference obtained regarding traditional kidney markers, was creatinine after CSA treatment (p≤0.02). Conclusion: Serum KIM-1 is superior to other kidney markers including creatinine, BUN and urea in the early prediction of CSA nephrotoxicity.
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    0
    References
    0
    Citations
    NaN
    KQI
    []