Tissue oxygen and hemodynamics in renal medulla, cortex, and corticomedullary junction during hemorrhage-reperfusion

Whitehouse, Tony; Stotz, Martin; Taylor, Valerie H.; Stidwill, R; Singer, Mervyn

doi:10.1152/ajprenal.00475.2005

Cited by 61 publications

(47 citation statements)

References 29 publications

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“…86,[100][101][102] In view of tenuous oxygen tensions in mitochondria of parenchymal cells 103 caused by steep oxygen gradients from capillaries across interstitial spaces and cytoplasm, 104 oxygen available for respiration could fall further to precipitously low concentrations when interstitial spaces are widened by edema and inflammation and capillaries regress during fibrosis. Indeed, pathologic hypoxia shown by pimonidazole technique in deep cortex-outer medullary regions during early reperfusion after IRI 105 -persists as fibrosis develops.…”

Section: Cellular Origin Of Interstitial Fibrosis After Akimentioning

confidence: 99%

Failed Tubule Recovery, AKI-CKD Transition, and Kidney Disease Progression

Venkatachalam

Weinberg

Kriz

et al. 2015

Journal of the American Society of Nephrology

574

454

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The transition of AKI to CKD has major clinical significance. As reviewed here, recent studies show that a subpopulation of dedifferentiated, proliferating tubules recovering from AKI undergo pathologic growth arrest, fail to redifferentiate, and become atrophic. These abnormal tubules exhibit persistent, unregulated, and progressively increasing profibrotic signaling along multiple pathways. Paracrine products derived therefrom perturb normal interactions between peritubular capillary endothelium and pericyte-like fibroblasts, leading to myofibroblast transformation, proliferation, and fibrosis as well as capillary disintegration and rarefaction. Although signals from injured endothelium and inflammatory/immune cells also contribute, tubule injury alone is sufficient to produce the interstitial pathology required for fibrosis. Localized hypoxia produced by microvascular pathology may also prevent tubule recovery. However, fibrosis is not intrinsically progressive, and microvascular pathology develops strictly around damaged tubules; thus, additional deterioration of kidney structure after the transition of AKI to CKD requires new acute injury or other mechanisms of progression. Indeed, experiments using an acute-on-chronic injury model suggest that additional loss of parenchyma caused by failed repair of AKI in kidneys with prior renal mass reduction triggers hemodynamically mediated processes that damage glomeruli to cause progression. Continued investigation of these pathologic mechanisms should reveal options for preventing renal disease progression after AKI.

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Section: Cellular Origin Of Interstitial Fibrosis After Akimentioning

confidence: 99%

Failed Tubule Recovery, AKI-CKD Transition, and Kidney Disease Progression

Venkatachalam

Weinberg

Kriz

et al. 2015

Journal of the American Society of Nephrology

574

454

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“…Oxygen pressure in the renal cortex of normal animals is reportedly between 10 and 60 mmHg, whereas the corticomedullary junction and medulla are exposed to marked hypoxia [3][4][5][6][7]. One critical cause of kidney hypoxia, particularly in the medulla, is the arterial-venous oxygen shunt [5,6,8].…”

Section: Hypoxia In the Kidneymentioning

confidence: 99%

Hypoxia and hypoxia-inducible factors in chronic kidney disease

Tanaka

Nangaku

2016

Ren Replace Ther

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It is generally accepted that renal hypoxia plays an important role in the progression of chronic kidney disease (CKD). This review focuses on renal hypoxia and hypoxia-inducible factor (HIF), a master regulator of cellular adaptation to hypoxia, during CKD progression. The kidney, which is physiologically hypoxic, is exposed to increased levels of hypoxia in CKD; insufficient oxygenation in the tubulointerstitium triggers injury and accelerates the deterioration of renal function, culminating in end-stage kidney disease (ESKD). HIF accumulates during specific stages of pathological progression; however, adaptation to hypoxia usually fails. In such cases, decreased vascular endothelial growth factor expression and upregulated antiangiogenic factors result in sustained capillary rarefaction. In addition, oxygen consumption in tubules is primarily increased by enhanced oxidative stress, and the transcriptional activity of HIF becomes suboptimal, which is partly mediated by methylglyoxal in diabetic kidney disease and by indoxyl sulfate, a representative uremic toxin, in advanced CKD. Oxygen-dependent canonical regulators of HIF involve prolyl hydroxylase domain-containing protein (PHD) and factor inhibiting HIF-1 (FIH-1), whereas recent studies have revealed noncanonical and oxygen-independent HIF regulation in the kidney. As a consequence, HIF accumulation usually fails to protect the kidney against hypoxia, which is likely to accelerate progression to ESKD, via several maladaptation mechanisms. The precise roles of HIF and its regulation in CKD warrant further investigation in light of promising data demonstrating that HIF stabilization by PHD inhibitors may be a new therapeutic approach for CKD.

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“…Recently, we [6] and others [7] have used the fluorescence optode technique for studies of intrarenal oxygenation. Renal tissue oxygen tension values obtained using this technique may be less than those obtained using Clark electrodes, particularly in the renal cortex [6].…”

Section: Introductionmentioning

confidence: 99%

Measurement of Renal Tissue Oxygen Tension: Systematic Differences between Fluorescence Optode and Microelectrode Recordings in Anaesthetized Rabbits

et al. 2008

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Background/Aims: The validity of fluorescence optodes for measurement of renal cortical tissue oxygen tension was tested by comparison with Clark electrodes. Methods: We varied renal blood flow and inspired O₂ content in anaesthetized rabbits while simultaneously measuring cortical tissue oxygen tension. Results: Cortical oxygen tension varied with inspired O₂ content. Fluorescence optode measurements were more tightly distributed than those from a Clark electrode. Cumulative frequency distributions for fluorescence optodes were shifted to the left of those for Clark electrodes. The slope of the relationship between oxygen tension in arterial blood and cortical tissue was less for the fluorescence optode than the Clark electrode. Cortical tissue oxygen tension measurements by these two methods were correlated (r² = 0.32; p < 0.001), with no fixed bias but considerable proportional bias. Thus, the slope of the relationship between the two measurements was less than unity (0.57 [0.50–0.69]). Conclusion: Cortical oxygen tension values from fluorescence optodes are less variable but proportionally less than those from Clark electrodes. Theoretical considerations suggest that true interstitial oxygen tension lies somewhere between values provided by the two techniques. Nevertheless, the lesser variability of the fluorescence optode technique may aid detection of physiologically significant changes in intrarenal oxygenation.

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Tissue oxygen and hemodynamics in renal medulla, cortex, and corticomedullary junction during hemorrhage-reperfusion

Cited by 61 publications

References 29 publications

Failed Tubule Recovery, AKI-CKD Transition, and Kidney Disease Progression

Failed Tubule Recovery, AKI-CKD Transition, and Kidney Disease Progression

Hypoxia and hypoxia-inducible factors in chronic kidney disease

Measurement of Renal Tissue Oxygen Tension: Systematic Differences between Fluorescence Optode and Microelectrode Recordings in Anaesthetized Rabbits

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