期刊论文详细信息
Kidney and Blood Pressure Research
Dexamethasone Modifies Cystatin C-Based Diagnosis of Acute Kidney Injury During Cisplatin-Based Chemotherapy
Mohamed F.3  Buckley N.A.3  Pianta T.J.4  Succar L.2  Chin M.2  Davidson T.6  Endre Z.H.1  Pickering J.W.5 
[1] Prince of Wales Clinical School, University of New South Wales, Sydney, NSW, Australia$$Medicine, University of Otago, Christchurch, New Zealand$$;Prince of Wales Clinical School, University of New South Wales, Sydney, NSW, Australia$$;Prince of Wales Clinical School, University of New South Wales, Sydney, NSW, Australia$$Clinical Pharmacology, University of Sydney, Sydney, NSW, Australia$$;Prince of Wales Clinical School, University of New South Wales, Sydney, NSW, Australia$$Northern Clinical School, University of Melbourne, Melbourne, VIC, Australia$$;Medicine, University of Otago, Christchurch, New Zealand$$;Anatomical Pathology, SEALS, Prince of Wales Hospital, Randwick, NSW, Australia$$
关键词: Cystatin C;    Creatinine;    Acute kidney injury;    Biomarkers;    Dexamethasone;   
DOI  :  10.1159/000469715
来源: S Karger AG
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【 摘 要 】

Background/Aims: Plasma cystatin C (pCysC) may be superior to serum creatinine (sCr) as a surrogate of GFR. However, the performance of pCysC for diagnosing acute kidney injury (AKI) after cisplatin-based chemotherapy is potentially affected by accompanying corticosteroid anti-emetic therapy and hydration. Methods: In a prospective observational study pCysC, sCr, urinary kidney injury molecule-1 (KIM-1), and urinary clusterin were measured over 2 weeks in 27 patients given first-cycle chemotherapy. The same variables were measured over 2 weeks in Sprague–Dawley rats given a single intraperitoneal injection of dexamethasone, cisplatin, or both, and in controls. Results: In patients, pCysC increases were greater than sCr 41% vs. 16%, mean paired difference 25% (95% CI: 16–34%)], relative increases were ≥ 50% in 9 patients (35%) for pCysC compared with 2 (8%) for sCr (p = 0.04) and increases in sCr were accompanied by increased KIM-1 and clusterin excretion, but increases in pCysC alone were not. In rats, dexamethasone administration produced dose-dependent increases in pCysC (and augmented cisplatin-induced increases in pCysC), but did not augment histological injury, increases in sCr, or KIM-1 and clusterin excretion. Conclusions: In the presence of dexamethasone, elevation of pCysC does not reliably diagnose AKI after cisplatin-based chemotherapy.

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