Renal Decapsulation Prevents Intrinsic Renal Compartment Syndrome in Ischemia-Reperfusion–Induced Acute Kidney Injury: A Physiologic Approach*

Cruces, Pablo; Lillo, Pablo; Salas, Camila; Lillo, Felipe; González, Carlos; Pacheco, Alejandro; Hurtado, Daniel E.

doi:10.1097/ccm.0000000000002830

Cited by 23 publications

(17 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Two beneficial effects of decapsulation have been previously described. One is the suppression of RIHP 26 , 27 , and the other is the improvement of renal tissue hypoxia 28 . Our results indicated that tubulointerstitial injury was dependent on RIHP.…”

Section: Discussionmentioning

confidence: 99%

Pathophysiological and molecular mechanisms involved in renal congestion in a novel rat model

Shimada

Hirose

Takahashi

et al. 2018

Sci Rep

View full text Add to dashboard Cite

Increased central venous pressure in congestive heart failure causes renal dysfunction; however, the underlying mechanisms are unclear. We created a rat renal congestion model and investigated the effect of renal congestion on hemodynamics and molecular mechanisms. The inferior vena cava (IVC) between the renal veins was ligated by suture in male Sprague-Dawley rats to increase upstream IVC pressure and induce congestion in the left kidney only. Left kidney congestion reduced renal blood flow, glomerular filtration rate, and increased renal interstitial hydrostatic pressure. Tubulointerstitial and glomerular injury and medullary thick ascending limb hypoxia were observed only in the congestive kidneys. Molecules related to extracellular matrix expansion, tubular injury, and focal adhesion were upregulated in microarray analysis. Renal decapsulation ameliorated the tubulointerstitial injury. Electron microscopy captured pericyte detachment in the congestive kidneys. Transgelin and platelet-derived growth factor receptors, as indicators of pericyte-myofibroblast transition, were upregulated in the pericytes and the adjacent interstitium. With the compression of the peritubular capillaries and tubules, hypoxia and physical stress induce pericyte detachment, which could result in extracellular matrix expansion and tubular injury in renal congestion.

show abstract

Section: Discussionmentioning

confidence: 99%

Pathophysiological and molecular mechanisms involved in renal congestion in a novel rat model

Shimada

Hirose

Takahashi

et al. 2018

Sci Rep

View full text Add to dashboard Cite

show abstract

“…As in other forms of ARDS, use of high positive end-expiratory pressure and/or tidal volumes increases intrathoracic pressure, right atrial pressure and right ventricular afterload, and can decrease cardiac output 140 . Right-sided heart dysfunction and increased venous pressures can result in increased interstitial and tubular hydrostatic pressure within the encapsulated kidney, which decreases net GFR and oxygen delivery to the kidney 146 . The observed association between mechanical ventilation or use of vasopressors with the risk of AKI further suggests that haemodynamic factors contribute to COVID-19 AKI 5 , 147 , 148 .…”

Section: Pathophysiology Of Covid-19 Akimentioning

confidence: 99%

Pathophysiology of COVID-19-associated acute kidney injury

et al. 2021

View full text Add to dashboard Cite

Although respiratory failure and hypoxaemia are the main manifestations of COVID-19, kidney involvement is also common. Available evidence supports a number of potential pathophysiological pathways through which acute kidney injury (AKI) can develop in the context of SARS-CoV-2 infection. Histopathological findings have highlighted both similarities and differences between AKI in patients with COVID-19 and in those with AKI in non-COVID-related sepsis. Acute tubular injury is common, although it is often mild, despite markedly reduced kidney function. Systemic haemodynamic instability very likely contributes to tubular injury. Despite descriptions of COVID-19 as a cytokine storm syndrome, levels of circulating cytokines are often lower in patients with COVID-19 than in patients with acute respiratory distress syndrome with causes other than COVID-19. Tissue inflammation and local immune cell infiltration have been repeatedly observed and might have a critical role in kidney injury, as might endothelial injury and microvascular thrombi. Findings of high viral load in patients who have died with AKI suggest a contribution of viral invasion in the kidneys, although the issue of renal tropism remains controversial. An impaired type I interferon response has also been reported in patients with severe COVID-19. In light of these observations, the potential pathophysiological mechanisms of COVID-19-associated AKI may provide insights into therapeutic strategies.

show abstract

“…This method can be applied to models of kidney diseases such as ischemia/reperfusion injury and polycystic kidney disease [18,19]. It also has disadvantages: it is limited to extracellular regions, it is difficult to use in clinical applications because of its invasiveness, and the oxygen tension and renal flow results might be affected by renal decapsulation [20]. Therefore, other hypoxia detection methods are currently under development: blood oxygen level–dependent magnetic resonance imaging (BOLD-MRI), nitroimidazole probes, and phosphorescence lifetime measurement [17].…”

Section: Measurement Of Oxygen Status In the Kidneymentioning

confidence: 99%

The role of oxidative stress and hypoxia in renal disease

Honda

Hirakawa

Nangaku

2019

Kidney Res Clin Pract

118

View full text Add to dashboard Cite

Oxygen is required to sustain aerobic organisms. Reactive oxygen species (ROS) are constantly released during mitochondrial oxygen consumption for energy production. Any imbalance between ROS production and its scavenger system induces oxidative stress. Oxidative stress, a critical contributor to tissue damage, is well-known to be associated with various diseases. The kidney is susceptible to hypoxia, and renal hypoxia is a common final pathway to end stage kidney disease, regardless of the underlying cause. Renal hypoxia aggravates oxidative stress, and elevated oxidative stress, in turn, exacerbates renal hypoxia. Oxidative stress is also enhanced in chronic kidney disease, especially diabetic kidney disease, through various mechanisms. Thus, the vicious cycle between oxidative stress and renal hypoxia critically contributes to the progression of renal injury. This review examines recent evidence connecting chronic hypoxia and oxidative stress in renal disease and subsequently describes several promising therapeutic approaches against oxidative stress.

show abstract

Renal Decapsulation Prevents Intrinsic Renal Compartment Syndrome in Ischemia-Reperfusion–Induced Acute Kidney Injury: A Physiologic Approach*

Abstract: Our results strongly suggest that renal decapsulation prevents the onset of an intrinsic renal compartment syndrome after ischemic acute kidney injury.

Cited by 23 publications

References 30 publications

Pathophysiological and molecular mechanisms involved in renal congestion in a novel rat model

Pathophysiological and molecular mechanisms involved in renal congestion in a novel rat model

Pathophysiology of COVID-19-associated acute kidney injury

The role of oxidative stress and hypoxia in renal disease

Contact Info

Product

Resources

About