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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005397naa a2200409 4500
001oai:lup.lub.lu.se:f1df978b-1f77-4fec-bbbc-4c6b57294604
003SwePub
008181019s2018 | |||||||||||000 ||eng|
0247 a https://lup.lub.lu.se/record/f1df978b-1f77-4fec-bbbc-4c6b572946042 URI
0247 a https://doi.org/10.1097/CCM.00000000000029962 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
1001 a Fisher, Janeu Lund University,Lunds universitet,Translationell Sepsisforskning,Forskargrupper vid Lunds universitet,Translational Sepsis research,Lund University Research Groups,Skåne University Hospital4 aut0 (Swepub:lu)med-jfi
2451 0a Is heparin-binding protein inhibition a mechanism of albumin's efficacy in human septic shock?
264 1c 2018
520 a Objectives: Our objectives were to determine first whether albumin prevents heparin-binding protein-induced increased endothelial cell permeability and renal cell inflammation and second, whether a plasma heparin-binding protein-to-albumin ratio predicts risk of acute kidney injury, fluid balance, and plasma cytokine levels in septic shock. Design: In vitro human endothelial and renal cell model and observation cohort of septic shock. Settings: Research laboratory and multicenter clinical trial (Vasopressin and Septic Shock Trial). Patients: Adult septic shock (norepinephrine dose > 5 μg/min for > 6 hr). Interventions: In vitro: heparin-binding protein (or thrombin) was added with or without albumin to 1) human endothelial cell monolayers to assess permeability and 2) to human renal tubular epithelial cells to assess inflammation. Measurements and Main Results: Transendothelial electrical resistance - a marker of permeability - of human endothelial cells was measured using a voltohmmeter. We measured plasma heparin-binding protein-to-albumin ratio and a panel of cytokines in septic shock patients (n = 330) to define an heparin-binding protein-to-albumin ratio that predicts risk of acute kidney injury. Albumin inhibited heparin-binding protein (and thrombin-induced) increased endothelial cell permeability at a threshold concentration of 20-30 g/L but increased renal tubular cell interleukin-6 release. Patients who developed or had worsened acute kidney injury had significantly higher heparin-binding protein-to-albumin ratio (1.6 vs 0.89; p < 0.001) and heparin-binding protein (38.2 vs 20.8 ng/mL; p < 0.001) than patients without acute kidney injury. The highest heparin-binding protein-to-albumin ratio (> 3.05), heparin-binding protein quartiles (> 69.8), and heparin-binding protein > 30 ng/mL were significantly associated with development or worsening of acute kidney injury (p < 0.001) in unadjusted and adjusted analyses and were robust to sensitivity analyses for death as a competing outcome. Heparin-binding protein and heparin-binding protein-to-albumin ratio were directly associated with positive fluid balance (p < 0.001) and with key inflammatory cytokines. Increasing quartiles of heparin-binding protein-to-albumin ratio and heparin-binding protein (but not albumin) were highly significantly associated with days alive and free of acute kidney injury and renal replacement therapy (p < 0.001), vasopressors (p < 0.001), ventilation (p < 0.001), and with 28-day mortality. Conclusions: Albumin inhibits heparin-binding protein-induced increased human endothelial cell permeability and heparin-binding protein greater than 30 ng/mL and heparin-binding protein-to-albumin ratio greater than 3.01 - but not serum albumin - identified patients at increased risk for acute kidney injury in septic shock.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Infektionsmedicin0 (SwePub)302092 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Infectious Medicine0 (SwePub)302092 hsv//eng
653 a albumin
653 a biomarker
653 a heparin-binding protein
653 a septic shock
7001 a Linder, Adamu Lund University,Lunds universitet,Translationell Sepsisforskning,Forskargrupper vid Lunds universitet,Translational Sepsis research,Lund University Research Groups,Skåne University Hospital4 aut0 (Swepub:lu)infe-lad
7001 a Bentzer, Peteru Lund University,Lunds universitet,Cirkulationsfysiologi vid kritisk sjukdom,Forskargrupper vid Lunds universitet,Fluid resuscitation in critical illness,Lund University Research Groups,Helsingborg Hospital4 aut0 (Swepub:lu)mphy-pbe
7001 a Boyd, Johnu University of British Columbia,St. Paul’s Hospital4 aut
7001 a Kong, Hyejin Juliau University of British Columbia,St. Paul’s Hospital4 aut
7001 a Lee, Terryu St. Paul’s Hospital,University of British Columbia4 aut
7001 a Walley, Keith R.u St. Paul’s Hospital,University of British Columbia4 aut
7001 a Russell, James A.u St. Paul’s Hospital,University of British Columbia4 aut
7102 a Translationell Sepsisforskningb Forskargrupper vid Lunds universitet4 org
7730 t Critical Care Medicineg 46:5, s. 364-374q 46:5<364-374x 0090-3493
8564 u http://dx.doi.org/10.1097/CCM.0000000000002996y FULLTEXT
8564 8u https://lup.lub.lu.se/record/f1df978b-1f77-4fec-bbbc-4c6b57294604
8564 8u https://doi.org/10.1097/CCM.0000000000002996

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