Influence of fluid resuscitation on renal microvascular PO2 in a normotensive rat model of endotoxemia

Johannes, Tanja; Mik, Egbert G.; Nohé, Boris; Raat, Nicolaas J.H.; Unertl, K.; İnce, Can

doi:10.1186/cc4948

Cited by 52 publications

(15 citation statements)

References 46 publications

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“…Using oxygen-sensitive phosphorescent dyes in the first 1–4 hrs after LPS, Johannes, et al, and Dyson et al, have found that oxygen consumption falls during endotoxemia, albeit not significantly so compared to control animals 12, 13 .…”

Section: Energy Metabolism Solute Transport and Sepsismentioning

confidence: 99%

Mitochondrial Function and Disturbances in the Septic Kidney

Parikh

Yang

et al. 2015

Seminars in Nephrology

150

123

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Per milligram of tissue, only the heart exceeds the kidney’s abundance of mitochondria. Not surprisingly, renal mitochondria are most densely concentrated in the epithelium of the nephron, at sites where the chemical work of moving solutes against electrochemical gradients places large and constant demands for ATP. Derangements of renal epithelial mitochondria appear to be a hallmark for diverse forms of acute kidney injury (AKI). The pathogenesis of multiple-organ dysfunction syndrome (MODS) in sepsis is complex, but a substantial body of experimental and observational human data supports the twin concepts that mitochondrial dysfunction contributes to impaired filtration and that recovery of mitochondrial structure and function is essential for recovery from sepsis-associated AKI. These insights have suggested novel methods to diagnose, stratify, prevent, or even treat this common and deadly complication of critical illness. This review will (1) describe the structure and functions of healthy mitochondria and how renal energy metabolism relates to solute transport; (2) provide an overview of the evidence linking mitochondrial pathology to renal disease; (3) summarize the mitochondrial lesions observed in septic AKI; (4) analyze the role of mitochondrial processes including fission/fusion, mitophagy, and biogenesis in the development of septic AKI and the recovery from this disease; and (5) explore the potential for therapeutically targeting mitochondria to prevent or treat septic AKI.

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Section: Energy Metabolism Solute Transport and Sepsismentioning

confidence: 99%

Mitochondrial Function and Disturbances in the Septic Kidney

Parikh

Yang

et al. 2015

Seminars in Nephrology

150

123

View full text Add to dashboard Cite

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“…This allows for the measurement of oxygen tension (PO 2 ) in the microcirculation [5,6] or interstitium [7,8], depending on the site of injection. The oxygen tension (PO 2 ) can be calculated from the phosphorescence decay kinetics.…”

Section: Biophotonicsmentioning

confidence: 99%

Oxygen‐dependent delayed fluorescence measured in skin after topical application of 5‐aminolevulinic acid

Harms

Boon

Balestra

et al. 2011

Journal of Biophotonics

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Mitochondrial oxygen tension can be measured in vivo by means of oxygen‐dependent quenching of delayed fluorescence of protoporphyrin IX (PpIX). Here we demonstrate that delayed fluorescence is readily observed from skin in rat and man after topical application of the PpIX precursor 5‐aminolevulinic acid (ALA). Delayed fluorescence lifetimes respond to changes in inspired oxygen fraction and blood supply. The signals contain lifetime distributions and the fitting of rectangular distributions to the data appears more adequate than mono‐exponential fitting. The use of topically applied ALA for delayed fluorescence lifetime measurements might pave the way for clinical use of this technique. (© 2011 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)

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“…Furthermore, in a clinical study by Spargias et al , iloprost was successfully used to prevent contrast-mediated nephropathy 9. However, in these studies that reported iloprost to be a renoprotective agent, the selected doses were as low as 1–2 ng/kg/min and the infusion period lasted approximately four to six hours to avoid systemic hypotension, and dosing was not repeated 9,17-19…”

Section: Discussionmentioning

confidence: 99%

Iloprost as an acute kidney injury-triggering agent in severely atherosclerotic patients

Uyar

Yucel

İlin

et al. 2016

CVJA

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SummaryBackgroundIloprost, a stable prostacyclin analog, is used as a rescue therapy for severe peripheral arterial disease (PAD). It has systemic vasodilatory and anti-aggregant effects, with severe vasodilatation potentially causing organ ischaemia when severe atherosclerosis is the underlying cause. In this study, we retrospectively analysed renal outcomes after iloprost infusion therapy in 86 patients.MethodsEighty-six patients with PAD who received iloprost infusion therapy were retrospectively analysed. Clinical and biochemical parameters were recorded before (initial, Cr1), during (third day, Cr2), and after (14th day following the termination of infusion therapy, Cr3) treatment. Acute kidney injury (AKI) was defined according to KDIGO guidelines as a ≥ 0.3 mg/dl (26.52 μmol/l) increase in creatinine levels from baseline within 48 hours.Results:Cr2 (1.46 ± 0.1 mg/dl) (129.06 ± 8.84 μmol/l) and Cr3 (1.53 ± 0.12 mg/dl) (135.25 ± 10.61 μmol/l) creatinine levels were significantly higher compared to the initial value (1.15 ± 0.6 mg/dl) (101.66 ± 53.04 μmol/l). AKI was observed in 36 patients (41.86%) on the third day of iloprost infusion. Logistic regression analysis revealed smoking and not using acetylsalicylic acid as primary predictors (p = 0.02 and p = 0.008, respectively) of AKI during iloprost treatment. On the third infusion day, patients’ urinary output significantly increased (1813.30 ± 1123.46 vs 1545.17 ± 873.00 cm3) and diastolic blood pressure significantly decreased (70.07 ± 15.50 vs 74.14 ± 9.42 mmHg) from their initial values.ConclusionWhile iloprost treatment is effective in patients with PAD who are not suitable for surgery, severe systemic vasodilatation can cause renal ischaemia, resulting in nonoliguric AKI. Smoking, no acetylsalicylic acid use, and lower diastolic blood pressure are the clinical risk factors for AKI during iloprost treatment.

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Influence of fluid resuscitation on renal microvascular PO2 in a normotensive rat model of endotoxemia

Cited by 52 publications

References 46 publications

Mitochondrial Function and Disturbances in the Septic Kidney

Mitochondrial Function and Disturbances in the Septic Kidney

Oxygen‐dependent delayed fluorescence measured in skin after topical application of 5‐aminolevulinic acid

Iloprost as an acute kidney injury-triggering agent in severely atherosclerotic patients

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