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Reduced urinary levels of angiotensin-converting enzyme 2 activity predict acute kidney injury in critically ill patients
Author(s) -
Laurent Bitker,
Sheila K. Patel,
Intissar Bittar,
Glenn M Eastwood,
Rinaldo Bellomo,
Louise M Burrell
Publication year - 2020
Publication title -
critical care and resuscitation/acritical care and resuscitation :
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.991
H-Index - 34
eISSN - 2652-9335
pISSN - 1441-2772
DOI - 10.51893/2020.4.oa7
Subject(s) - medicine , interquartile range , acute kidney injury , odds ratio , intensive care unit , creatinine , receiver operating characteristic , urinary system , renal function , urology , prospective cohort study , urine
Objective: Angiotensin-converting enzyme 2 activity reflects non-classical renin–angiotensin system upregulation. We assessed the association of urinary angiotensin-converting enzyme 2 (uACE2) activity with acute kidney injury (AKI). Design, setting and participants: A prospective observational study in which we measured uACE2 activity in 105 critically ill patients at risk of AKI. We report AKI stage 2 or 3 at 12 hours of urine collection (AKI12h) and AKI stage 2 or 3 at any time during intensive care unit stay in patients free from any stage of AKI at inclusion (AKIICU). AKI prediction was assessed using area under the receiver-operating characteristics curve (AUROC) and net reclassification indices (NRIs). Main outcome measure: AKI stage 2 or 3 at 12 hours of urine collection. Results: Within 12 hours of inclusion, 32 of 105 patients (30%) had developed AKI12h. Corrected uACE2 activity was significantly higher in patients without AKI12h compared with those with AKI12h (median [interquartile range], 13 [6–24] v 7 [4–10] pmol/min/mL per mmol/L of urine creatinine; P 8.7 pmol/min/mL per mmol/L of urine creatinine had a significantly lower risk of AKIICU on log-rank analysis (52% v 84%; P < 0.01). Conclusions: Higher uACE2 activity was associated with a decreased risk of AKI stage 2 or 3. Our findings support future evaluations of the role of the non-classical renin–angiotensin system during AKI.

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