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Rinaldo Bellomo - One of the best experts on this subject based on the ideXlab platform.
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Renal Blood Flow fractional excretion of sodium and acute kidney injury time for a new paradigm
Current Opinion in Critical Care, 2012Co-Authors: John R Prowle, Sean M Bagshaw, Rinaldo BellomoAbstract:Purpose of reviewGlobal Renal Blood Flow is considered pivotal to Renal function. Decreased global Renal Blood Flow (decreased perfusion) is further considered the major mechanism of reduced glomerular filtration rate responsible for the development of acute kidney injury (AKI) in critically ill pat
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effect of selective inhibition of Renal inducible nitric oxide synthase on Renal Blood Flow and function in experimental hyperdynamic sepsis
Critical Care Medicine, 2012Co-Authors: Ken Ishikawa, Rinaldo Bellomo, Paolo Calzavacca, Michael Bailey, Clive N MayAbstract:OBJECTIVE Nitric oxide plays an important role in the control of Renal Blood Flow and Renal function. In sepsis, increased levels of inducible nitric oxide synthase produce excessive nitric oxide, which may contribute to the development of acute kidney injury. We, therefore, examined the effects of intraRenal infusion of selective inducible nitric oxide synthase inhibitors in a large animal model of hyperdynamic sepsis in which acute kidney injury occurs in the presence of increased Renal Blood Flow. DESIGN Prospective crossover randomized controlled interventional studies. SETTING University-affiliated research institute. SUBJECTS Twelve unilaterally nephrectomized Merino ewes. INTERVENTION Infusion of a selective (1400W) and a partially selective inducible nitric oxide synthase inhibitor (aminoguanidine) into the Renal artery for 2 hrs after the induction of sepsis, and comparison with a nonselective inhibitor (Nω-nitro-L-arginine methyl ester). MEASUREMENTS AND MAIN RESULTS In sheep with nonhypotensive hyperdynamic sepsis, creatinine clearance halved (32 to 16 mL/min, ratio [95% confidence interval] 0.51 [0.28-0.92]) despite increased Renal Blood Flow (241 to 343 mL/min, difference [95% confidence interval] 102 [78-126]). Infusion of 1400W did not change Renal Blood Flow, urine output, or creatinine clearance, whereas infusion of Nω-nitro-L-arginine methyl ester and a high dose of aminoguanidine normalized Renal Blood Flow, but did not alter creatinine clearance. CONCLUSIONS In hyperdynamic sepsis, intraRenal infusion of a highly selective inducible nitric oxide synthase inhibitor did not reduce the elevated Renal Blood Flow or improve Renal function. In contrast, Renal Blood Flow was reduced by infusion of a nonselective NOS inhibitor or a high dose of a partially selective inducible nitric oxide synthase inhibitor. The Renal vasodilatation in septic acute kidney injury may be due to nitric oxide derived from the endothelial and neural isoforms of nitric oxide synthase, but their blockade did not restore Renal function.
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measurement of Renal Blood Flow by phase contrast magnetic resonance imaging during septic acute kidney injury a pilot investigation
Critical Care Medicine, 2012Co-Authors: John R Prowle, M Molan, Emma Hornsey, Rinaldo BellomoAbstract:Objective:In septic patients, decreased Renal perfusion is considered to play a major role in the pathogenesis of acute kidney injury. However, the accurate measurement of Renal Blood Flow in such patients is problematic and invasive. We sought to overcome such obstacles by measuring Renal Blood flo
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c urrent opinion Renal Blood Flow fractional excretion of sodium and acute kidney injury time for a new paradigm
2012Co-Authors: John R Prowle, Sean M Bagshaw, Rinaldo BellomoAbstract:Purpose of reviewGlobal Renal Blood Flow is considered pivotal to Renal function. Decreased global Renal Blood Flow(decreased perfusion) is further considered the major mechanism of reduced glomerular filtration rateresponsible for the development of acute kidney injury (AKI) in critically ill patients. Additionally, urinarybiochemical tests are widely taught to allow the differential diagnosis of preRenal (functional) AKI andintrinsic [structural AKI (so-called acute tubular necrosis)]. In this review we will examine recent evidenceregarding these two key clinical paradigms.Recent findingsRecent animal experiments and clinical studies in humans using cine-phase contrast magnetic resonancetechnology are not consistent with the decreased perfusion paradigm. They suggest instead that changes inthe intra-Renal circulation including modification in efferent arteriolar function and intra-Renal shunting aremuch more likely to be responsible for AKI, especially in sepsis. Similarly, recent human studies indicatethe urinary biochemistry has limited diagnostic or prognostic ability and is dissociated form biomarker andmicroscopic evidence of tubular injury.SummaryIntra-Renal microcirculatory changes are likely more important than changes in global Blood Flow in thedevelopment of AKI. Urinary biochemistry is not a clinically useful diagnostic or prognostic tool in criticallyill patients at risk of or with AKI.Keywordsacute kidney injury, fractional excretion of sodium, fractional excretion of urea, Renal Blood Flow, urinalysis
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the impact of intraRenal nitric oxide synthase inhibition on Renal Blood Flow and function in mild and severe hyperdynamic sepsis
Critical Care Medicine, 2011Co-Authors: Ken Ishikawa, Rinaldo Bellomo, Clive N MayAbstract:Objective: In experimental hyperdynamic sepsis, Renal function deteriorates despite Renal vasodilatation and increased Renal Blood Flow. Because nitric oxide is increased in sepsis and participates in Renal Blood Flow control, we investigated the effects of intraRenal Nω-nitro-l-arginine methyl ester, a nonspecific nitric oxide synthase inhibitor, in mild and severe sepsis. Design: Prospective crossover and randomized control interventional studies. Setting: University-affiliated research institute. Subjects: Thirty-two merino ewes. Intervention: Examination of responses to intraRenal infusion of Nω-nitro-l-arginine methyl ester for 8 hrs in unilaterally nephrectomized normal sheep and in sheep administered Escherichia coli. Measurements and Main Results: In normal sheep, Nω-nitro-l-arginine methyl ester decreased Renal Blood Flow (301 ± 30 to 228 ± 26 mL/min) and creatinine clearance (40.0 ± 5.8 to 31.1 ± 2.8 mL/min), whereas plasma creatinine increased, but fractional excretion of sodium was unchanged. In sheep with nonhypotensive hyperdynamic sepsis, plasma creatinine increased and there were decreases in creatinine clearance (34.5 ± 4.6 to 20.1 ± 3.7 mL/min) and fractional excretion of sodium despite increased Renal Blood Flow. Infusion of Nω-nitro-l-arginine methyl ester normalized Renal Blood Flow and increased urine output, but creatinine clearance did not improve and plasma creatinine and fractional excretion of sodium increased. In sheep with severe hypotensive sepsis, creatinine clearance decreased further (31.1 ± 5.4 to 16.0 ± 1.7 mL/min) despite increased Renal Blood Flow. Infusion of Nω-nitro-l-arginine methyl ester restored mean arterial pressure and reduced Renal Blood Flow but did not improve plasma creatinine or creatinine clearance. Conclusions: In hyperdynamic sepsis, with or without hypotension, creatinine clearance decreased despite increasing Renal Blood Flow. IntraRenal Nω-nitro-l-arginine methyl ester infusion reduced Renal Blood Flow but did not improve creatinine clearance. These data indicate that septic acute kidney injury is not the result of decreased Renal Blood Flow nor is it improved by nonspecific nitric oxide synthase inhibition.
Clive N May - One of the best experts on this subject based on the ideXlab platform.
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effect of selective inhibition of Renal inducible nitric oxide synthase on Renal Blood Flow and function in experimental hyperdynamic sepsis
Critical Care Medicine, 2012Co-Authors: Ken Ishikawa, Rinaldo Bellomo, Paolo Calzavacca, Michael Bailey, Clive N MayAbstract:OBJECTIVE Nitric oxide plays an important role in the control of Renal Blood Flow and Renal function. In sepsis, increased levels of inducible nitric oxide synthase produce excessive nitric oxide, which may contribute to the development of acute kidney injury. We, therefore, examined the effects of intraRenal infusion of selective inducible nitric oxide synthase inhibitors in a large animal model of hyperdynamic sepsis in which acute kidney injury occurs in the presence of increased Renal Blood Flow. DESIGN Prospective crossover randomized controlled interventional studies. SETTING University-affiliated research institute. SUBJECTS Twelve unilaterally nephrectomized Merino ewes. INTERVENTION Infusion of a selective (1400W) and a partially selective inducible nitric oxide synthase inhibitor (aminoguanidine) into the Renal artery for 2 hrs after the induction of sepsis, and comparison with a nonselective inhibitor (Nω-nitro-L-arginine methyl ester). MEASUREMENTS AND MAIN RESULTS In sheep with nonhypotensive hyperdynamic sepsis, creatinine clearance halved (32 to 16 mL/min, ratio [95% confidence interval] 0.51 [0.28-0.92]) despite increased Renal Blood Flow (241 to 343 mL/min, difference [95% confidence interval] 102 [78-126]). Infusion of 1400W did not change Renal Blood Flow, urine output, or creatinine clearance, whereas infusion of Nω-nitro-L-arginine methyl ester and a high dose of aminoguanidine normalized Renal Blood Flow, but did not alter creatinine clearance. CONCLUSIONS In hyperdynamic sepsis, intraRenal infusion of a highly selective inducible nitric oxide synthase inhibitor did not reduce the elevated Renal Blood Flow or improve Renal function. In contrast, Renal Blood Flow was reduced by infusion of a nonselective NOS inhibitor or a high dose of a partially selective inducible nitric oxide synthase inhibitor. The Renal vasodilatation in septic acute kidney injury may be due to nitric oxide derived from the endothelial and neural isoforms of nitric oxide synthase, but their blockade did not restore Renal function.
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the impact of intraRenal nitric oxide synthase inhibition on Renal Blood Flow and function in mild and severe hyperdynamic sepsis
Critical Care Medicine, 2011Co-Authors: Ken Ishikawa, Rinaldo Bellomo, Clive N MayAbstract:Objective: In experimental hyperdynamic sepsis, Renal function deteriorates despite Renal vasodilatation and increased Renal Blood Flow. Because nitric oxide is increased in sepsis and participates in Renal Blood Flow control, we investigated the effects of intraRenal Nω-nitro-l-arginine methyl ester, a nonspecific nitric oxide synthase inhibitor, in mild and severe sepsis. Design: Prospective crossover and randomized control interventional studies. Setting: University-affiliated research institute. Subjects: Thirty-two merino ewes. Intervention: Examination of responses to intraRenal infusion of Nω-nitro-l-arginine methyl ester for 8 hrs in unilaterally nephrectomized normal sheep and in sheep administered Escherichia coli. Measurements and Main Results: In normal sheep, Nω-nitro-l-arginine methyl ester decreased Renal Blood Flow (301 ± 30 to 228 ± 26 mL/min) and creatinine clearance (40.0 ± 5.8 to 31.1 ± 2.8 mL/min), whereas plasma creatinine increased, but fractional excretion of sodium was unchanged. In sheep with nonhypotensive hyperdynamic sepsis, plasma creatinine increased and there were decreases in creatinine clearance (34.5 ± 4.6 to 20.1 ± 3.7 mL/min) and fractional excretion of sodium despite increased Renal Blood Flow. Infusion of Nω-nitro-l-arginine methyl ester normalized Renal Blood Flow and increased urine output, but creatinine clearance did not improve and plasma creatinine and fractional excretion of sodium increased. In sheep with severe hypotensive sepsis, creatinine clearance decreased further (31.1 ± 5.4 to 16.0 ± 1.7 mL/min) despite increased Renal Blood Flow. Infusion of Nω-nitro-l-arginine methyl ester restored mean arterial pressure and reduced Renal Blood Flow but did not improve plasma creatinine or creatinine clearance. Conclusions: In hyperdynamic sepsis, with or without hypotension, creatinine clearance decreased despite increasing Renal Blood Flow. IntraRenal Nω-nitro-l-arginine methyl ester infusion reduced Renal Blood Flow but did not improve creatinine clearance. These data indicate that septic acute kidney injury is not the result of decreased Renal Blood Flow nor is it improved by nonspecific nitric oxide synthase inhibition.
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Renal Blood Flow during acute Renal failure in man
Blood Purification, 2009Co-Authors: John R Prowle, Clive N May, Ken Ishikawa, Rinaldo BellomoAbstract:Background: In the critically ill, ischemia secondary to decreased Renal Blood Flow (RBF) is believed to be central to the pathogenesis of acute Renal failure (ARF); however, the sci
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an assessment of the accuracy of Renal Blood Flow estimation by doppler ultrasound
Intensive Care Medicine, 2008Co-Authors: Li Wan, Clive N May, Natalie Yang, Cheeyan Hiew, Anthony Schelleman, Lynne Johnson, Rinaldo BellomoAbstract:Background Knowledge of Renal Blood Flow is considered important in the management of critically ill patients with acute Renal failure. Renal Doppler ultrasound has been used to estimate Renal Blood Flow. Its accuracy, however, has not been formally assessed.
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Renal Blood Flow and function during recovery from experimental septic acute kidney injury
Intensive Care Medicine, 2007Co-Authors: Christoph Langenberg, Clive N May, Li Wan, Moritoki Egi, Rinaldo BellomoAbstract:To measure Renal Blood Flow (RBF) and Renal function during recovery from experimental septic acute kidney injury (AKI). Controlled experimental study. Nine merino ewes. University physiology laboratory. We recorded systemic and Renal hemodynamics during a 96-h observation period (control) via implanted transit-time Flow probes. We then compared this period with 96 h of septic AKI (48 h of Escherichia coli infusion) and subsequent recovery (48 h of observation after stopping E. coli). Compared with the control period, E. coli infusion induced hyperdynamic sepsis (increased cardiac output and decreased Blood pressure) and septic AKI (serum creatinine 65.4 ± 8.7 vs. 139.9 ± 33.0 μmol/l; creatinine clearance 73.8 ± 12.2 vs. 40.2 ± 17.2 ml/min; p < 0.05) with a mortality of 22%. RBF increased (278.8 ± 33.9 vs. 547.9 ± 124.8 ml/min; p < 0.05) as did Renal vascular conductance (RVC). During recovery, we observed a decrease in RVC and RBF with all values returning to control levels. Indices of tubular function [fractional excretion of sodium (FENa) and urea (FEUn) and urinary sodium concentration (UNa)], which had been affected by sepsis, returned to control values after 18 h of recovery, as did serum creatinine. Infusion of E. coli induced a hyperdynamic circulatory state with hyperemic AKI. Recovery was associated with relative Renal vasoconstriction and reduction in RBF and RVC back to control levels. Indices of tubular function normalized more rapidly than changes in RBF.
P E De Jong - One of the best experts on this subject based on the ideXlab platform.
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feasibility of measuring Renal Blood Flow by phase contrast magnetic resonance imaging in patients with autosomal dominant polycystic kidney disease
European Radiology, 2016Co-Authors: Edwin M Spithoven, Carlo A J M Gaillard, Esther Meijer, C Borns, Wendy E Boertien, Peter Kappert, Marcel J W Greuter, E Van Der Jagt, Priya Vart, P E De JongAbstract:Objectives Renal Blood Flow (RBF) has been shown to predict disease progression in autosomal dominant polycystic kidney disease (ADPKD). We investigated the feasibility and accuracy of phase-contrast RBF by MRI (RBFMRI) in ADPKD patients with a wide range of estimated glomerular filtration rate (eGFR) values.
John R Prowle - One of the best experts on this subject based on the ideXlab platform.
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Renal Blood Flow fractional excretion of sodium and acute kidney injury time for a new paradigm
Current Opinion in Critical Care, 2012Co-Authors: John R Prowle, Sean M Bagshaw, Rinaldo BellomoAbstract:Purpose of reviewGlobal Renal Blood Flow is considered pivotal to Renal function. Decreased global Renal Blood Flow (decreased perfusion) is further considered the major mechanism of reduced glomerular filtration rate responsible for the development of acute kidney injury (AKI) in critically ill pat
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measurement of Renal Blood Flow by phase contrast magnetic resonance imaging during septic acute kidney injury a pilot investigation
Critical Care Medicine, 2012Co-Authors: John R Prowle, M Molan, Emma Hornsey, Rinaldo BellomoAbstract:Objective:In septic patients, decreased Renal perfusion is considered to play a major role in the pathogenesis of acute kidney injury. However, the accurate measurement of Renal Blood Flow in such patients is problematic and invasive. We sought to overcome such obstacles by measuring Renal Blood flo
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c urrent opinion Renal Blood Flow fractional excretion of sodium and acute kidney injury time for a new paradigm
2012Co-Authors: John R Prowle, Sean M Bagshaw, Rinaldo BellomoAbstract:Purpose of reviewGlobal Renal Blood Flow is considered pivotal to Renal function. Decreased global Renal Blood Flow(decreased perfusion) is further considered the major mechanism of reduced glomerular filtration rateresponsible for the development of acute kidney injury (AKI) in critically ill patients. Additionally, urinarybiochemical tests are widely taught to allow the differential diagnosis of preRenal (functional) AKI andintrinsic [structural AKI (so-called acute tubular necrosis)]. In this review we will examine recent evidenceregarding these two key clinical paradigms.Recent findingsRecent animal experiments and clinical studies in humans using cine-phase contrast magnetic resonancetechnology are not consistent with the decreased perfusion paradigm. They suggest instead that changes inthe intra-Renal circulation including modification in efferent arteriolar function and intra-Renal shunting aremuch more likely to be responsible for AKI, especially in sepsis. Similarly, recent human studies indicatethe urinary biochemistry has limited diagnostic or prognostic ability and is dissociated form biomarker andmicroscopic evidence of tubular injury.SummaryIntra-Renal microcirculatory changes are likely more important than changes in global Blood Flow in thedevelopment of AKI. Urinary biochemistry is not a clinically useful diagnostic or prognostic tool in criticallyill patients at risk of or with AKI.Keywordsacute kidney injury, fractional excretion of sodium, fractional excretion of urea, Renal Blood Flow, urinalysis
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cine phase contrast magnetic resonance imaging for the measurement of Renal Blood Flow
Contributions To Nephrology, 2010Co-Authors: John R Prowle, M Molan, Emma Hornsey, Rinaldo BellomoAbstract:During critical illness, reductions in Renal Blood Flow (RBF) are believed to be a major cause of kidney dysfunction, and therapy is often aimed at restoration of RBF. Despite this, our ability to measure RBF during critical illness has been limited by the invasiveness of the available techniques. Cine Phase-Contrast Magnetic Resonance Imaging (CPC-MRI) represents an entirely noninvasive, contrast-free method of measuring Blood Flow with the potential of enabling the measurement of Blood Flow to major organs including the kidney. We have recently assessed the feasibility of measuring RBF by means of CPC-MRI in 2 critically ill patients with septic acute kidney injury and were able to compare such measurements to those obtained in a normal volunteer.
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Renal Blood Flow during acute Renal failure in man
Blood Purification, 2009Co-Authors: John R Prowle, Clive N May, Ken Ishikawa, Rinaldo BellomoAbstract:Background: In the critically ill, ischemia secondary to decreased Renal Blood Flow (RBF) is believed to be central to the pathogenesis of acute Renal failure (ARF); however, the sci
Christoph Langenberg - One of the best experts on this subject based on the ideXlab platform.
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Renal Blood Flow and function during recovery from experimental septic acute kidney injury
Intensive Care Medicine, 2007Co-Authors: Christoph Langenberg, Clive N May, Li Wan, Moritoki Egi, Rinaldo BellomoAbstract:To measure Renal Blood Flow (RBF) and Renal function during recovery from experimental septic acute kidney injury (AKI). Controlled experimental study. Nine merino ewes. University physiology laboratory. We recorded systemic and Renal hemodynamics during a 96-h observation period (control) via implanted transit-time Flow probes. We then compared this period with 96 h of septic AKI (48 h of Escherichia coli infusion) and subsequent recovery (48 h of observation after stopping E. coli). Compared with the control period, E. coli infusion induced hyperdynamic sepsis (increased cardiac output and decreased Blood pressure) and septic AKI (serum creatinine 65.4 ± 8.7 vs. 139.9 ± 33.0 μmol/l; creatinine clearance 73.8 ± 12.2 vs. 40.2 ± 17.2 ml/min; p < 0.05) with a mortality of 22%. RBF increased (278.8 ± 33.9 vs. 547.9 ± 124.8 ml/min; p < 0.05) as did Renal vascular conductance (RVC). During recovery, we observed a decrease in RVC and RBF with all values returning to control levels. Indices of tubular function [fractional excretion of sodium (FENa) and urea (FEUn) and urinary sodium concentration (UNa)], which had been affected by sepsis, returned to control values after 18 h of recovery, as did serum creatinine. Infusion of E. coli induced a hyperdynamic circulatory state with hyperemic AKI. Recovery was associated with relative Renal vasoconstriction and reduction in RBF and RVC back to control levels. Indices of tubular function normalized more rapidly than changes in RBF.
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Renal Blood Flow in experimental septic acute Renal failure
Kidney International, 2006Co-Authors: Christoph Langenberg, Clive N May, Li Wan, Moritoki Egi, Rinaldo BellomoAbstract:Reduced Renal Blood Flow (RBF) is considered central to the pathogenesis of septic acute Renal failure (ARF). However, no controlled experimental studies have continuously assessed RBF during the development of severe septic ARF. We conducted a sequential animal study in seven female Merino sheep. Flow probes were implanted around the pulmonary and left Renal arteries. Two weeks later, systemic hemodynamics and RBF were monitored continuously during a 48-h control period and, after a week, during a 48-h period of hyperdynamic sepsis induced by continuous Escherichia coli infusion. Infusion of E. coli induced hyperdynamic sepsis with significantly increased cardiac output (3.8±0.4 vs 9.8±1.1 l/min; P P P P P μ mol/l; P P P E. coli induced hyperdynamic sepsis and ARF. Septic ARF in this setting was associated with a marked increase in RBF and with Renal vasodilatation.
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Renal Blood Flow in sepsis
Critical Care, 2005Co-Authors: Christoph Langenberg, Rinaldo Bellomo, Clive N May, Li Wan, Moritoki Egi, Stanislao MorgeraAbstract:Introduction To assess changes in Renal Blood Flow (RBF) in human and experimental sepsis, and to identify determinants of RBF.
