The Microcirculation of the Septic Kidney

Zafrani, Lara; Payen, Didier; Azoulay, Élie; İnce, Can

doi:10.1016/j.semnephrol.2015.01.008

Cited by 49 publications

(36 citation statements)

References 83 publications

(85 reference statements)

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“…Conversely, our data revealed no substantial changes in T 1 relaxation times in the SAKI kidneys, suggesting that the inflammatory responses in the renal cells in our model were not severe and the effect of water content changes on APTw and rNOEw signal can be considered negligible. Many recent studies have indicated that renal microcirculation plays a more important role in the development of SAKI, and severe sepsis is always associated with reduced functional capillary density and renal blood volume (RBV) and increased blood flow heterogeneit . Gupta et al reported that RBV in LPS‐treated rats (3 h after i.v.…”

Section: Discussionmentioning

confidence: 99%

CEST MRI of sepsis‐induced acute kidney injury

et al. 2018

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Sepsis-induced acute kidney injury (SAKI) is a major complication of kidney disease associated with increased mortality and faster progression. Therefore, the development of imaging biomarkers to detect septic AKI is of great clinical interest. In this study, we aimed to characterize the endogenous chemical exchange saturation transfer (CEST) MRI contrast in the lipopolysaccharide (LPS)-induced SAKI mouse model and to investigate the use of CEST MRI for detecting such injury. We used a SAKI mouse model that was generated by i.p. injection of 10 mg/kg LPS. The resulting kidney injury was confirmed by the elevation of serum creatinine and histology. MRI assessments were performed 24 h after LPS injection, including CEST MRI at different B strengths (1, 1.8 and 3 μT), T mapping, T mapping and conventional magnetization transfer contrast (MTC) MRI. The CEST MRI results were analyzed using Z-spectra, in which the normalized water signal saturation (S /S ) is measured as a function of saturation frequency. Substantial decreases in CEST contrast were observed at both 3.5 and - 3.5 ppm frequency offset from water at all B powers, with the most significant difference obtained at a B of 1.8 μT. The average S /S differences between injured and normal kidneys were 0.07 (0.55 ± 0.04 versus 0.62 ± 0.04, P = 0.0028) and 0.07 (0.50 ± 0.04 versus 0.57 ± 0.03, P = 0.0008) for 3.5 and - 3.5 ppm, respectively. In contrast, the T and T relaxation times and MTC contrast in the injured kidneys did not show a significant change compared with the normal control. Our results showed that CEST MRI is more sensitive to the pathological changes in injured kidneys than the changes in T , T and MTC effect, indicating its potential clinical utility for molecular imaging of renal diseases.

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Section: Discussionmentioning

confidence: 99%

CEST MRI of sepsis‐induced acute kidney injury

et al. 2018

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“…The renal microcirculation is disturbed in a similar fashion during sepsis-induced AKI [12,16,17], even with normal or increased global organ RBF [18]. Multiple mechanisms seem to frame this characteristic microcirculatory derangement, including endothelial dysfunction, impaired red blood cell deformability, damage and shedding of the glycocalyx layer, increased leukocyte activation, adhesion and recruitment, platelet adhesion, and activation of the coagulation cascade with fibrin deposition [15,19] (Fig. 1).…”

Section: Novel Concepts In the Pathophysiology Of Sepsis-induced Acutmentioning

confidence: 99%

“…DAMPs, damage-associated molecular patterns; eNOS, endothelial-derived nitric oxide synthase; iNOS, inducible nitric oxide synthase; NO, nitric oxide. Adapted with permission from [19]. …”

Section: Figurementioning

confidence: 99%

Sepsis-induced acute kidney injury

Gómez

Kellum²

2016

Current Opinion in Critical Care

256

174

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Purpose of review Sepsis is a common and frequently fatal condition in which mortality has been consistently linked to increasing organ dysfunction. For example, acute kidney injury (AKI) occurs in 40–50% of septic patients and increases mortality six to eight-fold. However, the mechanisms by which sepsis causes organ dysfunction are not well understood and hence current therapy remains reactive and nonspecific. Recent findings Recent studies have challenged the previous notion that organ dysfunction is solely secondary to hypoperfusion, by showing, for example, that AKI occurs in the setting of normal or increased renal blood flow; and that it is characterized not by acute tubular necrosis or apoptosis, but rather by heterogeneous areas of colocalized sluggish peritubular blood flow and tubular epithelial cell oxidative stress. Evidence has also shown that microvascular dysfunction, inflammation, and the metabolic response to inflammatory injury are fundamental pathophysiologic mechanisms that may explain the development of sepsis-induced AKI. Summary The implications of these findings are significant because in the context of decades of negative clinical trials in the field, the recognition that other mechanisms are at play opens the possibility to better understand the processes of injury and repair, and provides an invaluable opportunity to design mechanism-targeted therapeutic interventions.

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“…The peritubular capillary bed comes from the efferent arteriole and becomes the vasa recta capillaries in the medulla, for which blood flow runs in opposition to the ultrafiltrate in the adjacent tubules. 4 Tissue Hypoxia and Alterations of the Renal Microcirculation During AKI Oxygen delivery and consumption determine renal tissue oxygenation, which is necessary for function of sodium-potassium pumps that themselves require oxygen-dependent adenosine triphospahte (ATP) production. 5,6 In the kidney, oxygen tension is low, ranging from 70 mm Hg (cortex) to 20 mm Hg (medulla).…”

Section: Anatomy Of the Renal Circulationmentioning

confidence: 99%