Renal blood flow in sepsis

Langenberg, Christoph; Bellomo, Rinaldo; May, Clive; Wan, Li; Egi, Moritoki; Morgera, Stanislao

doi:10.1186/cc3540

Cited by 228 publications

(83 citation statements)

References 163 publications

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“…This finding is consistent with the recent advances in the pathophysiological understanding of sepsis-induced AKI in humans: the classic paradigm is that decreased blood flow in septic patients is the principal pathophysiological cause of AKI. However, volume resuscitation and renal vasodilators have little effect [30] and renal blood flow was found to be normal or even increased in resuscitated sepsis patients [31,32]. In addition, acute tubular necrosis is rarely found in septic kidneys [33].…”

Section: Discussionmentioning

confidence: 99%

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

Herter

Rossaint²,

Spieker³

et al. 2014

J Innate Immun

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Acute kidney injury (AKI) is a common complication in critically ill patients and is associated with high mortality. Recruitment of neutrophils is a hallmark in the pathogenesis of AKI. Although ischemia-reperfusion injury (IRI) is a frequently used research model of AKI, the clinical relevance of IRI-induced AKI is limited. Epidemiologically, sepsis is the prevailing cause of kidney injury. However, it is still unknown whether these distinct entities of AKI share the same pathophysiological mechanisms. This study was initiated to investigate the molecular mechanisms of neutrophil recruitment into the kidney in a murine model of sepsis-induced AKI. By using a flow cytometry-based method, we show that the two β₂-integrins Mac-1 and LFA-1 as well as E-selectin and P-selectin are involved in neutrophil recruitment into the kidney after induction of sepsis. The molecular mechanisms of neutrophil recruitment were further investigated using intravital microscopy, demonstrating that blocking one of these four molecules reduces the number of adherent leukocytes. This was accompanied by a renal upregulation of E-selectin, P-selectin and ICAM-1 (the counter-receptor of β₂-integrins on endothelial cells) after sepsis induction. We conclude that blocking P-selectin, E-selectin, Mac-1 or LFA-1 protects mice from sepsis-induced AKI.

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Section: Discussionmentioning

confidence: 99%

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

Herter

Rossaint²,

Spieker³

et al. 2014

J Innate Immun

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“…Nevertheless, in spite of conflicting animal studies, Langenberg et al [91] reported only 3 studies in humans that have directly calculated renal blood flow in septic AKI via invasive measurements. All 3 studies demonstrated that septic AKI is characterized by renal arterial vasodilation and preserved overall renal blood flow [92,93,94].…”

Section: Endotoxin Effects On Renal Functionmentioning

confidence: 99%

“…Indeed, glomerular filtration rate and cellular perfusion can diminish even if the overall renal blood flow is improved due to imbalanced vascular resistance between the afferent and efferent arterioles, regional microvascular flow rates, or renal venous congestion [91,96]. Renal and central venous pressures are often augmented in septic patients as a potential effect of the so-called fluid challenge of the first hours after intensive ICU admission.…”

Section: Endotoxin Effects On Renal Functionmentioning

confidence: 99%

Endotoxin Effects on Cardiac and Renal Functions and Cardiorenal Syndromes

et al. 2017

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Gram-negative sepsis is a major cause of morbidity and mortality in critical ill patients. Recent findings in molecular biology and in signaling pathways have enhanced our understanding of its pathogenesis and opened up opportunities of innovative therapeutic approaches. Endotoxin plays a pivotal role in the pathogenesis of multi-organ dysfunction in the setting of gram-negative sepsis. Indeed, heart and kidney impairments seem to be induced by the release of circulating pro-inflammatory and pro-apoptotic mediators triggered by endotoxin interaction with immune cells. These molecules are responsible for cellular apoptosis, autophagy, cell cycle arrest, and microRNAs activation. Therefore, the early identification of sepsis-associated acute kidney injury and heart dysfunction may improve the patient clinical outcome. In this report, we will consider the role of endotoxin in the pathogenesis of sepsis, its effects on both cardiac and renal functions, and the interactions between these 2 systems in the setting of cardiorenal syndromes (CRS), particularly in CRS type 5. Finally, we will discuss the possible role of extracorporeal therapies in reducing endotoxin levels.

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“…We recently performed a comprehensive review of electronic reference libraries, using sepsis and acute renal failure as the key words and limiting it to animal models [12]. We found approximately 160 original articles.…”

Section: The Primacy Of Renal Blood Flowmentioning

confidence: 99%

Septic Acute Kidney Injury: New Concepts

Bellomo

Wan

Langenberg

et al. 2008

Nephron Exp Nephrol

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Acute kidney injury (AKI) is a serious condition that affects many ICU patients. The most common causes of AKI in ICU are severe sepsis and septic shock. The mortality of AKI in septic critically ill patients remains high despite of our increasing ability to support vital organs. This is partly due to our poor understanding of the pathogenesis of sepsis-induced renal dysfunction. However, new concepts are emerging to explain the pathogenesis of septic AKI, which challenge previously held dogma. Throughout the past half century, septic AKI has essentially been considered secondary to kidney ischemia. However, recent models of experimental sepsis have challenged this notion by demonstrating that, in experimental states, which simulate the hemodynamic picture most typically seen in man (e.g. hyperdynamic sepsis) renal blood flow, actually increases as renal vascular resistance decreases. These experimental observations provide proof of concept that septic AKI can occur in the setting of renal hyperemia and that ischemia is not necessary for loss of glomerular filtration rate (GFR) to occur. They also suggest that similar hemodynamic event may occur in man. In addition, preliminary studies in septic sheep show that, when ATP is measured using an implanted phosphorus coil and magnetic resonance technology, renal bioenergetics are preserved in the setting of advanced septic shock. While these findings need to be confirmed, they challenge established paradigms and offer a new conceptual framework of reference for further investigation and intervention in man.

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Renal blood flow in sepsis

Abstract: Introduction To assess changes in renal blood flow (RBF) in human and experimental sepsis, and to identify determinants of RBF.

Cited by 228 publications

References 163 publications

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

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

Endotoxin Effects on Cardiac and Renal Functions and Cardiorenal Syndromes

Septic Acute Kidney Injury: New Concepts

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