Adhesion Molecules Involved in Neutrophil Recruitment during Sepsis-Induced Acute Kidney Injury

Herter, Jan M.; Rossaint, Jan; Spieker, Tilmann; Zarbock, Alexander

doi:10.1159/000358238

Cited by 64 publications

(51 citation statements)

References 40 publications

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“…Activated endothelial cells up-regulate the expression of adhesion molecules and release additional pro-inflammatory mediators. E-selectin, specifically induced on the endothelium upon inflammatory stimulation, has been demonstrated to play a major role in leukocyte recruitment into the kidney during the late stages of sepsis-induced AKI [38*]. Experimental data highlight the importance of leukocyte recruitment into the kidney [38*] especially in later stages of AKI.…”

Section: Inflammation Propagates Renal Damage During Sepsismentioning

confidence: 99%

“…E-selectin, specifically induced on the endothelium upon inflammatory stimulation, has been demonstrated to play a major role in leukocyte recruitment into the kidney during the late stages of sepsis-induced AKI [38*]. Experimental data highlight the importance of leukocyte recruitment into the kidney [38*] especially in later stages of AKI. Although not seen in all models of sepsis-induced AKI [39] elimination of neutrophils or blocking adhesion molecules that are required for neutrophil recruitment into the kidney completely abolished sepsis-induced AKI in a cecal ligation and puncture (CLP)-induced sepsis model [38*].…”

Section: Inflammation Propagates Renal Damage During Sepsismentioning

confidence: 99%

“…Experimental data highlight the importance of leukocyte recruitment into the kidney [38*] especially in later stages of AKI. Although not seen in all models of sepsis-induced AKI [39] elimination of neutrophils or blocking adhesion molecules that are required for neutrophil recruitment into the kidney completely abolished sepsis-induced AKI in a cecal ligation and puncture (CLP)-induced sepsis model [38*]. This observation can be explained by the fact that adherent and transmigrated neutrophils release reactive oxygen species, proteases, elastases, myeloperoxidase, and other enzymes that damage the tissue.…”

Section: Inflammation Propagates Renal Damage During Sepsismentioning

confidence: 99%

See 2 more Smart Citations

Sepsis-induced acute kidney injury revisited

Zarbock

Gómez

Kellum

2014

Current Opinion in Critical Care

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287

119

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Purpose of review Acute kidney injury (AKI) is a common complication in critically ill patients and is associated with increased morbidity and mortality. Sepsis is the most common cause of AKI. Considerable evidence now suggests that the pathogenic mechanisms of sepsis-induced AKI are different from those seen in other etiologies of AKI. This review focuses on the recent advances in this area and discusses possible therapeutic interventions that might derive from these new insights into the pathogenesis of sepsis-induced AKI. Recent findings The traditional paradigm that sepsis-induced AKI arises from ischemia has been challenged by recent evidence that total renal blood flow (RBF) in is not universally impaired during sepsis, and AKI can develop in the presence of normal or even increased RBF. Animal and human studies suggest that adaptive responses of tubular epithelial cells to injurious signals are responsible for renal dysfunction. Simultaneously occurring renal inflammation and microcirculatory dysfunction further amplify these mechanisms. Summary An understanding of the pathologic mechanisms of sepsis-induced AKI emphasizes the important role of maladaptive responses to the septic insult. Preventive and therapeutic measures should be based on counteracting these maladaptive responses of tubular epithelial cells, inflammation, and microvascular dysfunction.

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Section: Inflammation Propagates Renal Damage During Sepsismentioning

confidence: 99%

Section: Inflammation Propagates Renal Damage During Sepsismentioning

confidence: 99%

Section: Inflammation Propagates Renal Damage During Sepsismentioning

confidence: 99%

See 1 more Smart Citation

Sepsis-induced acute kidney injury revisited

Zarbock

Gómez

Kellum

2014

Current Opinion in Critical Care

Self Cite

287

119

View full text Add to dashboard Cite

show abstract

“…Genetic polymorphisms in the ABO gene have been associated with circulating levels of glycoproteins important in endothelial function and inflammation, including soluble intercellular adhesion molecule-1 (ICAM-1), thrombomodulin, vWF, and the selectins (12,(20)(21)(22)(23). These same proteins have been implicated in the pathogenesis of AKI (24)(25)(26)(27)(28). Although non-O blood types are reported risk factors for MI, VTE, and ARDS, it is unknown if ABO blood type is associated with AKI risk (13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

The ABO Histo-Blood Group and AKI in Critically Ill Patients with Trauma or Sepsis

Reilly

Anderson

Mangalmurti

et al. 2015

Clinical Journal of the American Society of Nephrology

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Background and objective ABO blood types are determined by antigen modifications on glycoproteins and glycolipids and associated with altered plasma levels of inflammatory and endothelial injury markers implicated in AKI pathogenesis. We sought to determine the association of ABO blood types with AKI risk in critically ill patients with trauma or sepsis.Design, setting, participants, & measurements We conducted two prospective cohort studies at an urban, academic, level I trauma center and tertiary referral center; 497 patients with trauma admitted to the surgical intensive care unit between 2005 and 2010 with an injury severity score .15 and 759 patients with severe sepsis admitted to the medical intensive care unit between 2008 and 2013 were followed for 6 days for the development of incident AKI. AKI was defined by Acute Kidney Injury Network creatinine and dialysis criteria.Results Of 497 patients with trauma, 134 developed AKI (27%). In multivariable analysis, blood type A was associated with higher AKI risk relative to type O among patients of European descent (n=229; adjusted risk, 0.28 versus 0.14; risk difference, 0.14; 95% confidence interval, 0.03 to 0.24; P=0.02). Of 759 patients with sepsis, AKI developed in 326 (43%). Blood type A again conferred higher AKI risk relative to type O among patients of European descent (n=437; adjusted risk, 0.53 versus 0.40; risk difference, 0.14; 95% confidence interval, 0.04 to 0.23; P=0.01). Findings were similar when analysis was restricted to those patients who did not develop acute respiratory distress syndrome or were not transfused. We did not detect a significant association between blood type and AKI risk among individuals of African descent in either cohort.Conclusions Blood type A is independently associated with AKI risk in critically ill patients with trauma or severe sepsis of European descent, suggesting a role for ABO glycans in AKI susceptibility.

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“…Neutrophils originate from stem cells in the bone marrow where growth factors induce sequential expression of genes, resulting in a distinct phenotype, not least characterized by its different sets of cytoplasmic granule containing preformed host defense proteins ready to be released at sites of inflammation [1] . Being transported in the bloodstream, specific adhesion molecules expressed by endothelial cells and chemotactic gradients are important for neutrophil recruitment and activation [2][3][4][5] .…”

mentioning

confidence: 99%