Toni Jäntti1, Tuukka Tarvasmäki2, Veli-Pekka Harjola3, Kari Pulkki4, Heidi Turkia4, Tuija Sabell2, Heli Tolppanen2, Raija Jurkko2, Mari Hongisto3, Anu Kataja5, Alessandro Sionis6, Jose Silva-Cardoso7, Marek Banaszewski8, Salvatore DiSomma9, Alexandre Mebazaa10, Mikko Haapio11, Johan Lassus2. 1. Department of Cardiology, Heart and Lung Center, Helsinki University Hospital, University of Helsinki, 00029 HUS, Helsinki, Finland. toni.jantti@fimnet.fi. 2. Department of Cardiology, Heart and Lung Center, Helsinki University Hospital, University of Helsinki, 00029 HUS, Helsinki, Finland. 3. Emergency Medicine, Department of Emergency Medicine and Services, Helsinki University Hospital, University of Helsinki, Helsinki, Finland. 4. HUSLAB Diagnostic Services, Helsinki University Hospital and University of Helsinki, Helsinki, Finland. 5. Internal Medicine, Department of Internal Medicine and Rehabilitation, Helsinki University Hospital, University of Helsinki, Helsinki, Finland. 6. Intensive Cardiac Care Unit, Cardiology Department, Hospital de La Santa Creu I Sant Pau, Biomedical Research Institute IIB-SantPau, Universidad Autónoma de Barcelona, Barcelona, Spain. 7. CINTESIS, Department of Cardiology, São João Hospital Center, and Porto Medical School, University of Porto, Porto, Portugal. 8. Intensive Cardiac Therapy Clinic, National Institute of Cardiology, Warsaw, Poland. 9. Department of Medical Sciences and Translational Medicine, Sant'Andrea Hospital, University of Rome Sapienza, Rome, Italy. 10. INSERM U942, Department of Anesthesia and Critical Care, Hôpital Lariboisière, APHP, University Paris Diderot, Paris, France. 11. Nephrology, Department of Nephrology, Abdominal Center, Helsinki University Hospital, University of Helsinki, Helsinki, Finland.
Abstract
BACKGROUND: Acute kidney injury (AKI) is a frequent form of organ injury in cardiogenic shock. However, data on AKI markers such as plasma proenkephalin (P-PENK) and neutrophil gelatinase-associated lipocalin (P-NGAL) in cardiogenic shock populations are lacking. The objective of this study was to assess the ability of P-PENK and P-NGAL to predict acute kidney injury and mortality in cardiogenic shock. RESULTS: P-PENK and P-NGAL were measured at different time points between baseline and 48 h in 154 patients from the prospective CardShock study. The outcomes assessed were AKI defined by an increase in creatinine within 48 h and all-cause 90-day mortality. Mean age was 66 years and 26% were women. Baseline levels of P-PENK and P-NGAL (median [interquartile range]) were 99 (71-150) pmol/mL and 138 (84-214) ng/mL. P-PENK > 84.8 pmol/mL and P-NGAL > 104 ng/mL at baseline were identified as optimal cut-offs for AKI prediction and independently associated with AKI (adjusted HRs 2.2 [95% CI 1.1-4.4, p = 0.03] and 2.8 [95% CI 1.2-6.5, p = 0.01], respectively). P-PENK and P-NGAL levels at baseline were also associated with 90-day mortality. For patients with oliguria < 0.5 mL/kg/h for > 6 h before study enrollment, 90-day mortality differed significantly between patients with low and high P-PENK/P-NGAL at baseline (5% vs. 68%, p < 0.001). However, the biomarkers provided best discrimination for mortality when measured at 24 h. Identified cut-offs of P-PENK24h > 105.7 pmol/L and P-NGAL24h > 151 ng/mL had unadjusted hazard ratios of 5.6 (95% CI 3.1-10.7, p < 0.001) and 5.2 (95% CI 2.8-9.8, p < 0.001) for 90-day mortality. The association remained significant despite adjustments with AKI and two risk scores for mortality in cardiogenic shock. CONCLUSIONS: High levels of P-PENK and P-NGAL at baseline were independently associated with AKI in cardiogenic shock patients. Furthermore, oliguria before study inclusion was associated with worse outcomes only if combined with high baseline levels of P-PENK or P-NGAL. High levels of both P-PENK and P-NGAL at 24 h were found to be strong and independent predictors of 90-day mortality. TRIAL REGISTRATION: NCT01374867 at www.clinicaltrials.gov , registered 16 Jun 2011-retrospectively registered.
BACKGROUND:Acute kidney injury (AKI) is a frequent form of organ injury in cardiogenic shock. However, data on AKI markers such as plasma proenkephalin (P-PENK) and neutrophil gelatinase-associated lipocalin (P-NGAL) in cardiogenic shock populations are lacking. The objective of this study was to assess the ability of P-PENK and P-NGAL to predict acute kidney injury and mortality in cardiogenic shock. RESULTS:P-PENK and P-NGAL were measured at different time points between baseline and 48 h in 154 patients from the prospective CardShock study. The outcomes assessed were AKI defined by an increase in creatinine within 48 h and all-cause 90-day mortality. Mean age was 66 years and 26% were women. Baseline levels of P-PENK and P-NGAL (median [interquartile range]) were 99 (71-150) pmol/mL and 138 (84-214) ng/mL. P-PENK > 84.8 pmol/mL and P-NGAL > 104 ng/mL at baseline were identified as optimal cut-offs for AKI prediction and independently associated with AKI (adjusted HRs 2.2 [95% CI 1.1-4.4, p = 0.03] and 2.8 [95% CI 1.2-6.5, p = 0.01], respectively). P-PENK and P-NGAL levels at baseline were also associated with 90-day mortality. For patients with oliguria < 0.5 mL/kg/h for > 6 h before study enrollment, 90-day mortality differed significantly between patients with low and high P-PENK/P-NGAL at baseline (5% vs. 68%, p < 0.001). However, the biomarkers provided best discrimination for mortality when measured at 24 h. Identified cut-offs of P-PENK24h > 105.7 pmol/L and P-NGAL24h > 151 ng/mL had unadjusted hazard ratios of 5.6 (95% CI 3.1-10.7, p < 0.001) and 5.2 (95% CI 2.8-9.8, p < 0.001) for 90-day mortality. The association remained significant despite adjustments with AKI and two risk scores for mortality in cardiogenic shock. CONCLUSIONS: High levels of P-PENK and P-NGAL at baseline were independently associated with AKI in cardiogenic shockpatients. Furthermore, oliguria before study inclusion was associated with worse outcomes only if combined with high baseline levels of P-PENK or P-NGAL. High levels of both P-PENK and P-NGAL at 24 h were found to be strong and independent predictors of 90-day mortality. TRIAL REGISTRATION: NCT01374867 at www.clinicaltrials.gov , registered 16 Jun 2011-retrospectively registered.
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