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Clinical and subclinical acute kidney injury in multidrug‐resistant septic patients treated with colistimethate sodium: Incidence and clinical outcomes
Author(s) -
Thammathiwat Theerachai,
Tiranathanagul Khajohn,
Srisawat Nattachai,
Susantitaphong Paweena,
Praditpornsilpa Kearkiat,
EiamOng Somchai
Publication year - 2020
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/nep.13663
Subject(s) - medicine , subclinical infection , acute kidney injury , incidence (geometry) , creatinine , sepsis , lipocalin , nephrotoxicity , urinary system , prospective cohort study , gastroenterology , kidney , physics , optics
Aim Colistimethate sodium (CMS) has been postulated as the principal cause of high incidence of clinical acute kidney injury (AKI) in multidrug‐resistance (MDR) septic patients with normal baseline serum creatinine (sCr) who were treated with CMS. This prospective observational study was conducted to examine the incidence and clinical outcomes of clinical and subclinical AKI in MDR septic patients receiving CMS. Methods Forty‐two MDR septic patients with normal sCr who required CMS were included. Clinical AKI was diagnosed by increased sCr levels according to the KDIGO2012 criteria while subclinical AKI was identified by elevated levels of urinary neutrophil gelatinase‐associated lipocalin (uNGAL > 150 ng/mL) or urinary liver‐type fatty‐acid‐binding protein (uL‐FABP > 10.5 ng/mL). Results Clinical AKI was noted in 47.6% of patients on day 5 and 38.1% on day 7 after initiating CMS. By using uL‐FABP, subclinical AKI was observed in 45.2% and 54.8% on day 5 and 7, respectively. At baseline prior to CMS treatment, subclinical AKI was already present in 90%. The baseline uL‐FABP was superior to the baseline uNGAL in early prediction of clinical AKI on day 5. The subclinical AKI patients had comparable worse outcomes as clinical AKI patients. Conclusion The incidence of subclinical AKI in MDR septic patients before CMS treatment was extremely high. The baseline uL‐FABP provided the best predictive capacity of clinical AKI. The causes of clinical AKI might include the persistence of sepsis process, subclinical AKI and CMS nephrotoxicity. Proper management of subclinical AKI patients before CMS initiation should be concerned to prevent further renal damage and improve patient and renal outcomes.