Renal Endothelial Injury and Microvascular Dysfunction in Acute Kidney Injury

Verma, Sudhanshu Kumar; Molitoris, Bruce A.

doi:10.1016/j.semnephrol.2015.01.010

Cited by 183 publications

(159 citation statements)

References 117 publications

Supporting

Mentioning

136

Contrasting

Unclassified

Order By: Relevance

“…They are known to facilitate leukocyte binding to the endothelium in areas of inflammation and promote microvascular dysfunction and tissue injury (37). We observed increased VCAM-1 protein levels in the kidney after VILI compared with sham and CLP kidneys.…”

Section: Discussionmentioning

confidence: 51%

See 1 more Smart Citation

Ventilator-induced lung injury increases expression of endothelial inflammatory mediators in the kidney

Hepokoski

Englert

Baron

et al. 2017

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

In critical illness, such as sepsis or the acute respiratory distress syndrome, acute kidney injury (AKI) is common and associated with increased morbidity and mortality. Mechanical ventilation in critical illnesses is also a risk factor for AKI, but it is potentially modifiable. Injurious ventilation strategies may lead to the systemic release of inflammatory mediators from the lung due to ventilator induced lung injury (VILI). The systemic consequences of VILI are difficult to differentiate clinically from other systemic inflammatory syndromes, such as sepsis. The purpose of this study was to identify unique changes in the expression of inflammatory mediators in kidney tissue in response to VILI compared with systemic sepsis to gain insight into direct effects of VILI on the kidney. Four groups of mice were compared—mice with sepsis from cecal ligation and puncture (CLP), mice subjected to injurious mechanical ventilation with high tidal volumes (VILI), mice exposed to CLP followed by VILI (CLP+VILI), and sham controls. Protein expression of common inflammatory mediators in kidneys was analyzed using a proteome array and confirmed by Western blot analysis or ELISA. VEGF and VCAM-1 were found to be significantly elevated in kidneys from VILI mice compared with sham and CLP. Angiopoietin-2 was significantly increased in CLP+VILI compared with CLP alone and was also correlated with higher levels of AKI biomarker, neutrophil gelatinase-associated lipocalin. These results suggest that VILI alters the renal expression of VEGF, VCAM-1, and angiopoietin-2, and these proteins warrant further investigation as potential biomarkers and therapeutic targets.

show abstract

Section: Discussionmentioning

confidence: 51%

“…VCAM-1 and other adhesion molecules are increasingly expressed following endothelial activation by circulating cytokines (including VEGF) (37,40). They are known to facilitate leukocyte binding to the endothelium in areas of inflammation and promote microvascular dysfunction and tissue injury (37).…”

Section: Discussionmentioning

confidence: 99%

Ventilator-induced lung injury increases expression of endothelial inflammatory mediators in the kidney

Hepokoski

Englert

Baron

et al. 2017

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

show abstract

“…Release of large number of inflammatory factors can damage the endothelial cells of patients with sepsis, activate the coagulation system to a hyper-coagulable state, induce formation of renal micro vascular thrombosis and affect renal perfusion [14]. In addition, endotoxemia increases reactive oxygen species (ROS) generated by mitochondrial respiratory chain and decreases enzyme activities in tubular epithelial cell.…”

Section: Discussionmentioning

confidence: 99%

Clinical effect of combined ulinastatin and continuous renal replacement therapy on management of severe sepsis with acute kidney injury

Fang¹,

Zhao²

2017

Trop. J. Pharm Res

View full text Add to dashboard Cite

Purpose: To explore the effect of a combination of ulinastatin and continuous renal replacement therapy (CRRT) for the treatment of severe sepsis with acute kidney injury (SAKI Results: Levels of interleukin-6 (IL-6), tumor necrosis factor α (TNFα), serum C-reactive protein (CRP), procalcitonin (PCT), malondialdehyde (MDA), cystatin, blood urea nitrogen (BUN), prothrombin time (PT), activated partial thromboplastin time (APTT), serum creatinine (SCr) and urinary kidney injury molecule-1 (Kim-1) in the treatment group were significantly lower than those in the control group after ulinastatin treatment (p < 0.05). However, superoxide dismutase (SOD), fibrinogen (Fib) and total antioxidant capacity (T-AOC) in the treatment group were significantly higher in the control group after treatment (p < 0.05). No serious adverse drug reactions were seen in the two groups. In addition, there were no significant differences in 28-day mortality between the two groups. Conclusion: These results suggest that ulinastatin combined with CRRT effectively decreases serum levels of inflammation in SAKI patients through a mechanism involving improvement of antioxidant capacity, reduction of oxidative stress, and enhancement of renal and coagulation functions.

show abstract

“…Several mechanisms have been implicated in intervention-related AKI pathophysiology(12) (13,14). Pre-existing renal disease (15,16), diabetes, hypertension (17), smoking, cardiovascular disease, nephrotoxic medication or contrast administration have been identified as common risk-factors (4,14,15).…”

Section: Introductionmentioning

confidence: 99%

Pre-operative Functional Cardiovascular Reserve Is Associated with Acute Kidney Injury after Intervention

Saratzis

Shakespeare

Jones

et al. 2017

European Journal of Vascular and Endovascular Surgery

View full text Add to dashboard Cite

What this paper addsThe impact of cardiovascular reserve on acute kidney injury (AKI) after endovascular surgery remains unclear, mostly due to the difficulties in assessing cardiovascular reserve. We are still unsure whether AKI is related mostly to pre-existing occult co-morbidities, such as cardiovascular disease, or procedure-related parameters. Hence, developing an adequate renoprotective strategy is not an easy task. In this analysis, we have shown that development of AKI after intervention is associated with pre-operative cardiovascular reserve, independent of other risk-factors and procedural parameters. This offers insight in what drives AKI development after endovascular intervention and where/how preventative measures should focus.

show abstract

Renal Endothelial Injury and Microvascular Dysfunction in Acute Kidney Injury

Cited by 183 publications

References 117 publications

Ventilator-induced lung injury increases expression of endothelial inflammatory mediators in the kidney

Ventilator-induced lung injury increases expression of endothelial inflammatory mediators in the kidney

Clinical effect of combined ulinastatin and continuous renal replacement therapy on management of severe sepsis with acute kidney injury

Pre-operative Functional Cardiovascular Reserve Is Associated with Acute Kidney Injury after Intervention

Contact Info

Product

Resources

About