Key result
Fatal sepsis is linked to a ~10-fold reduction in renal Ang1 mRNA vs. controls.
Why the study?
Sepsis-induced multi-organ dysfunction syndrome has high mortality and a better understanding of the Angiopoietin/Tie2 system in human organs during sepsis is lacking.
Effect estimate: 10-fold decrease
p-value: p=0.0003
Ang-Tie2 mRNA reductions may contribute to septic AKI; hypothesis-generating for pathway-targeted therapies, should not yet change practice.
Sepsis-induced multi-organ dysfunction syndrome (MODS) still has a high mortality. Improvements await a better understanding of the pathophysiological mechanisms. The angiopoietin (Ang)1/2 and Tie2 (tyrosine kinase with immunoglobulin and epidermal growth factor homology domains 2) ligand/receptor system is an important regulator of endothelial cell responses to severe insults. Plasma Ang2 levels are prognostic in sepsis, but data on Ang/Tie responses in organs in humans are lacking.. We hypothesized that, in kidneys of patients who died of sepsis with acute kidney injury (AKI), the Ang/Tie signaling system is changed in such a way that microvessels become destabilized.
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Aslan et al. (2014) conducted a letter in Lethal human sepsis (n=19). Lethal sepsis vs. Unaffected kidney tissue from renal cell carcinoma patients was evaluated on Renal mRNA expression of Ang1 (10-fold decrease, p=0.0003). In immediate post-mortem renal biopsies of patients dying from sepsis, Ang1 mRNA was decreased 10-fold (P=0.0003) and Tie2 mRNA was significantly reduced (P=0.0004) compared to controls.
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