Renal oxygenation and haemodynamics in acute kidney injury and chronic kidney disease

Singh, Prabhleen; Ricksten, Sven‐Erik; Bragadottir, Gudrun; Redfors, Bengt; Nordquist, Lina

doi:10.1111/1440-1681.12036

Cited by 133 publications

(121 citation statements)

References 107 publications

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“…Renal tissue hypoperfusion and hypoxia are considered to be pivotal links in the pathophysiological chain of events that leads to acute kidney injury (AKI) as well as the one that promotes progression from AKI to chronic kidney diseases (CKD) [1][2][3][4][5][6][7]. Imbalance between renal oxygen supply and demand also appears to play a prominent role in the pathophysiology of diabetic nephropathy [8,9].…”

Section: Introductionmentioning

confidence: 99%

Detailing the Relation Between Renal T2* and Renal Tissue pO2 Using an Integrated Approach of Parametric Magnetic Resonance Imaging and Invasive Physiological Measurements

Pohlmann¹,

Arakelyan²,

Hentschel³

et al. 2014

Investigative Radiology

111

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Objectives: This study is designed to detail the relation between renal T 2 * and renal tissue pO 2 using an integrated approach that combines parametric MRI and quantitative physiological measurements (MR-PHYSIOL). correlations for the outer medulla and showed that extrapolation of results obtained for one renal layer to other renal layers must be made with due caution. For T 2 * to RBF relation significant Spearman correlations were deduced for all renal layers and for all interventions. Materials and Methods

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Section: Introductionmentioning

confidence: 99%

Detailing the Relation Between Renal T2* and Renal Tissue pO2 Using an Integrated Approach of Parametric Magnetic Resonance Imaging and Invasive Physiological Measurements

Pohlmann¹,

Arakelyan²,

Hentschel³

et al. 2014

Investigative Radiology

111

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“…Tubulointerstitial and glomerular hypoxia are important factors that accelerate renal disease (18), and recent studies have observed that activation of Cp expression is mechanistically linked to a hypoxia-inducible factor, where hypoxia response element-dependent gene regulation leads to transcriptional induction of the Cp gene promoter (19). These data, together with the intermittent but recurring hypoxia in the setting of CKD (20), suggest that extrinsic factors, such as hypoxia, may be responsible for modulating Cp levels in patients with CKD. Furthermore, in a rat model of age-associated glomerulosclerosis, caloric restriction prevented elevations in both secreted Cp and Bowman's capsule Cp expression and reduced glomerulosclerosis at 24 months (21).…”

Section: Discussionmentioning

confidence: 99%

Plasma Ceruloplasmin, a Regulator of Nitric Oxide Activity, and Incident Cardiovascular Risk in Patients with CKD

Kennedy

Fan

et al. 2014

Clinical Journal of the American Society of Nephrology

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Background and objectives Increased serum levels of the acute-phase reactant ceruloplasmin predict adverse clinical outcomes in the setting of acute coronary syndromes and heart failure, but their role in patients with CKD is unclear. This study investigated the relationship of ceruloplasmin with clinical outcomes in CKD, especially with regard to traditional cardiac biomarkers.Design, setting, participants, & measurements Serum ceruloplasmin levels in consecutive study participants with CKD (n=654; estimated GFR,60 ml/min per 1.73 m 2 ) as well as a control group of non-CKD participants matched for age and sex (n=250) were measured. Study participants were enrolled during 2001-2006 from a population of patients presenting for elective diagnostic coronary angiography and prospectively followed for 3 years (median follow-up=1095 days) to determine incident major adverse cardiac events (defined as a composite of death, nonfatal myocardial infarction, and stroke).Results Serum ceruloplasmin levels in CKD patients were elevated versus controls (median [interquartile range]; 25.5 [21.8-29.6] versus 22.7 [19.7-26.5] mg/dl; P,0.001) and associated with increased risk of future major adverse cardiac events (hazard ratio, 1.35; 95% confidence interval, 1.0 to 1.82; P=0.04). After adjusting for traditional risk factors, higher serum ceruloplasmin was still associated with higher risk of major adverse cardiac events at 3 years (hazard ratio, 1.61; 95% confidence interval, 1.15 to 2.25; P=0.01). ConclusionIn CKD patients, increased serum ceruloplasmin, a regulator of nitric oxide activity, is associated with increased risk of long-term adverse cardiovascular events, even after multivariable model adjustment for traditional clinical and biologic risk factors.

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“…[4][5][6] In pathology, hypoxic stress increases proinflammatory cytokines and leads to inflammatory cell infiltration and inflammatory injury. 7 Hypoxia is also an acknowledged pathway to renal injury and ischemiareperfusion, which is an inevitable event accompanying renal transplantation and is considered a common cause for delayed graft function and acute renal failure.…”

Section: Introductionmentioning

confidence: 99%

ERK and p38 upregulation versus Bcl-6 downregulation in rat kidney epithelial cells exposed to prolonged hypoxia

Luo

Shi

et al. 2017

cell transplant

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Hypoxia is a common cause of kidney injury and a major issue in kidney transplantation. Mitogen-activated protein kinases (MAPKs) are involved in the cellular response to hypoxia, but the precise roles of MAPKs in renal cell reactions to hypoxic stress are not well known yet. This work was conducted to investigate the regulation of extracellular signal-regulated kinase-1 and -2 (ERK1/2) and p38 and their signaling-relevant molecules in kidney epithelial cells exposed to prolonged hypoxia. Rat kidney epithelial cells Normal Rat Kidney (NRK)-52E were exposed to hypoxic conditions (1% O 2 ) for 24 to 72 h. Cell morphology was examined by light microscopy, and cell viability was checked by 3-The expression of ERK1/2 and p38 MAPK, as well as their signaling-related molecules, was measured by Western blot and real-time polymerase chain (RT-PCR) reaction. At the 1% oxygen level, cell morphology had no appreciable changes compared to the control up to 72 h of exposure under light microscopy, whereas the results of MTS showed a slight but significant reduction in cell viability after 72 h of hypoxia. On the other hand, ERK1/2 and p38 phosphorylation remarkably increased in these cells after 24 to 72 h of hypoxia. In sharp contrast, the expression of transcription factor B-cell lymphoma 6 (Bcl-6) was significantly downregulated in response to hypoxic stress. Other intracellular molecules relevant to the ERK1/2 and p38 signaling pathway, such as protein kinase A, protein kinase C, Bcl-2, nuclear factor erythroid 2-related factor 2, tristetraprolin, and interleukin-10(IL-10), had no significant alterations after 24 to 72 h of hypoxic exposure. We conclude that hypoxic stress increases the phosphorylation of both ERK1/2 and p38 but decreases the level of Bcl-6 in rat kidney epithelial cells.

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Renal oxygenation and haemodynamics in acute kidney injury and chronic kidney disease

Cited by 133 publications

References 107 publications

Detailing the Relation Between Renal T2* and Renal Tissue pO2 Using an Integrated Approach of Parametric Magnetic Resonance Imaging and Invasive Physiological Measurements

Detailing the Relation Between Renal T2* and Renal Tissue pO2 Using an Integrated Approach of Parametric Magnetic Resonance Imaging and Invasive Physiological Measurements

Plasma Ceruloplasmin, a Regulator of Nitric Oxide Activity, and Incident Cardiovascular Risk in Patients with CKD

ERK and p38 upregulation versus Bcl-6 downregulation in rat kidney epithelial cells exposed to prolonged hypoxia

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