Abstract

Endostatin may predict mortality and kidney impairment in general populations as well as in critically ill patients. We decided to explore the possible role of endostatin as a predictor of 30-day mortality, acute kidney injury (AKI), and renal replacement therapy (RRT) in a cohort of unselected intensive care unit (ICU) patients. Endostatin and creatinine in plasma were analyzed and SAPS3 was determined in 278 patients on ICU arrival at admission to a Swedish medium-sized hospital. SAPS3 had the highest predictive value, 0.85 (95% C.I.: 0.8–0.90), for 30-day mortality. Endostatin, in combination with age, predicted 30-day mortality by 0.76 (95% C.I.: 0.70–0.82). Endostatin, together with age and creatinine, predicted AKI with 0.87 (95% C.I.: 0.83–0.91). Endostatin predicted AKI with [0.68 (0.62–0.74)]. Endostatin predicted RRT, either alone [0.82 (95% C.I.: 0.72–0.91)] or together with age [0.81 (95% C.I.: 0.71–0.91)]. The predicted risk for 30-day mortality, AKI, or RRT during the ICU stay, predicted by plasma endostatin, was not influenced by age. Compared to the complex severity score SAPS3, circulating endostatin, combined with age, offers an easily managed option to predict 30-day mortality. Additionally, circulating endostatin combined with creatinine was closely associated with AKI development.

Highlights

  • Patients with multiple organ failure are often treated in intensive care

  • Endostatin is an endogenous inhibitor of angiogenesis

  • The primary aim of this study was, to further elucidate the role of circulating endostatin in an unselected cohort of patients admitted to an intensive care unit (ICU) in a Swedish county hospital, which may differ from patients found in a tertiary care hospital

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Summary

Introduction

Patients with multiple organ failure are often treated in intensive care. The mortality rate in the general intensive care population is high and any possibility to identify patients at risk of developing organ failure, either temporary or definite, might have the ability to counteract severe and prolonged morbidity as well as mortality. Biomarkers could aid clinicians in such decisions, but no biomarker has excellent discrimination capability in intensive care patients. The protein has a molecular weight of approximately 20 kDa and is derived from type XVIII collagen by proteolytic cleavage within its C-terminal end [1]. A study utilizing epitope-defined monoclonal antibodies has shown that glomeruli expressed collagen XVIII in their basement membranes [2]. Acute renal failure induced by ischaemia/reperfusion causes the expression of Biomedicines 2021, 9, 1603.

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