Renal ischemia/reperfusion leads to macrophage-mediated increase in pulmonary vascular permeability

Kramer, Andrew A.; Postler, Gilbert; Salhab, Khaled F.; Mendez, Cynthia; Carey, Larry C.; Rabb, Hamid

doi:10.1046/j.1523-1755.1999.00460.x

Cited by 247 publications

(183 citation statements)

References 26 publications

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“…However, several studies have investigated the effects on the lung of ischemia-reperfusion injury in other organs. Renal ischemia-reperfusion, for instance, induces histologic lung damage and increases pulmonary vascular permeability and expression of proinflammatory cytokines in lung tissue (11,32). Some studies also demonstrate a link between intestinal ischemia-reperfusion injury and lung damage (12,33).…”

Section: Discussionmentioning

confidence: 99%

Hypoxic–ischemic brain damage induces distant inflammatory lung injury in newborn piglets

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Hypoxic–ischemic brain damage induces distant inflammatory lung injury in newborn piglets

et al. 2015

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“…Proinflammatory cytokines such as IL-6, IL-8 and TNF-α are increased in patients with AKI, 16 and increased levels of IL-6 and IL-8 predicted prolonged mechanical ventilation in patients with AKI. 15 The inflammatory nature of AKI and the resultant effect on the lungs is highlighted by studies in animal models demonstrating that inflammatory genes are up-regulated in the kidney and lung 32 and that anti-inflammatory treatment with IL-6 inhibition, 33 α-MSH 34 or a p38 MAP kinase inhibitor 35 protect against lung injury in animal models of AKI. Because ESRD is generally regarded as an immune-deficient state, 21 it is possible that the proinflammatory cytokine production may be dampened in patients with ESRD.…”

Section: Discussionmentioning

confidence: 99%

In Critically Ill Patients Requiring CRRT, AKI Is Associated with Increased Respiratory Failure and Death Versus ESRD

et al. 2011

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Background/aims: To compare outcomes of critically ill patients with acute kidney injury (AKI) requiring continuous renal replacement therapy (CRRT) versus those with pre-existing end-stage renal disease (ESRD) requiring CRRT to identify factors that contribute to the increased mortality seen in AKI patients. Methods: Retrospective cohort of 257 intensive care unit (ICU) patients who received CRRT. AKI is defined as requiring CRRT with an admission serum creatinine ≤1 mg/dL; ESRD is defined as chronic dialysis dependence. Primary outcome was hospital mortality. Multivariate logistic regression was performed to determine the impact of APACHE II score, intubation, vasopressors, infection, diabetes, hypertension, gender, and race on mortality. Results: Of 257 patients requiring CRRT, 28 had ESRD and 108 had AKI. Hospital mortality was higher in patients with AKI versus ESRD (69% vs. 39%, p = 0.0032). Severity of illness using APACHE II was similar in AKI and ESRD. Patients with AKI were more likely to require mechanical ventilation (89% vs. 57%, p = 0.0003). After multivariate analysis, the requirement for mechanical ventilation was the single factor associated with increased hospital mortality [odds ratio (OR): 3.1]. Conclusions: In ICU patients requiring CRRT, patients with AKI have a higher mortality than patients with ESRD due to an increased need for mechanical ventilation.

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“…How such changes cause volume dysregulation, however, remains to be determined. Furthermore, regional endothelial injury may activate endothelial cells in remote organs, such as the lungs, leading to acute lung injury, which further contributes to renal damage via systemic hypoxia (113). In addition, the injury of endothelial cells may induce a procoagulative response and thereby contribute to vascular obstruction and deficits in renal perfusion (114,115).…”

Section: Endothelial Injurymentioning

confidence: 99%

Renal Hypoxia and Dysoxia After Reperfusion of the Ischemic Kidney

Legrand

Mik

Johannes³

et al. 2008

Mol Med

238

169

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Ischemia is the most common cause of acute renal failure. Ischemic-induced renal tissue hypoxia is thought to be a major component in the development of acute renal failure in promoting the initial tubular damage. Renal oxygenation originates from a balance between oxygen supply and consumption. Recent investigations have provided new insights into alterations in oxygenation pathways in the ischemic kidney. These findings have identified a central role of microvascular dysfunction related to an imbalance between vasoconstrictors and vasodilators, endothelial damage and endothelium-leukocyte interactions, leading to decreased renal oxygen supply. Reduced microcirculatory oxygen supply may be associated with altered cellular oxygen consumption (dysoxia), because of mitochondrial dysfunction and activity of alternative oxygen-consuming pathways. Alterations in oxygen utilization and/or supply might therefore contribute to the occurrence of organ dysfunction. This view places oxygen pathways' alterations as a potential central player in the pathogenesis of acute kidney injury. Both in regulation of oxygen supply and consumption, nitric oxide seems to play a pivotal role. Furthermore, recent studies suggest that, following acute ischemic renal injury, persistent tissue hypoxia contributes to the development of chronic renal dysfunction. Adaptative mechanisms to renal hypoxia may be ineffective in more severe cases and lead to the development of chronic renal failure following ischemia-reperfusion. This paper is aimed at reviewing the current insights into oxygen transport pathways, from oxygen supply to oxygen consumption in the kidney and from the adaptation mechanisms to renal hypoxia. Their role in the development of ischemia-induced renal damage and ischemic acute renal failure are discussed.

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Renal ischemia/reperfusion leads to macrophage-mediated increase in pulmonary vascular permeability

Abstract: Increased PVP develops after isolated renal IRI, and macrophage-derived products are mediators in this response. These findings have implications for understanding the mechanisms underlying respiratory dysfunction associated with acute renal failure.

Cited by 247 publications

References 26 publications

Hypoxic–ischemic brain damage induces distant inflammatory lung injury in newborn piglets

Hypoxic–ischemic brain damage induces distant inflammatory lung injury in newborn piglets

In Critically Ill Patients Requiring CRRT, AKI Is Associated with Increased Respiratory Failure and Death Versus ESRD

Renal Hypoxia and Dysoxia After Reperfusion of the Ischemic Kidney

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