Renal cortical and medullary blood flow during modest saline loading in humans

Damkjær, Mads; Vafaee, Manouchehr Seyedi; Braad, Poul-Erik; Petersen, Henrik; Høilund-Carlsen, Poul Fl.; Bie, Peter

doi:10.1111/j.1748-1716.2012.02436.x

Cited by 14 publications

(21 citation statements)

References 75 publications

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“…108,109 Thus, changes in body fluid volume status should affect the determinants of kidney tissue PO 2 , but the overall effect on kidney oxygenation will depend on the balance of effects on kidney oxygen delivery and consumption, which cannot necessarily be predicted from first principles. For example, extracellular fluid volume expansion (saline loading) can, 110 although perhaps not always, 111,112 lead to increased RBF and medullary perfusion and so increased oxygen delivery. It also inhibits tubular sodium reabsorption and so decreases oxygen consumption.…”

Section: Contrast-induced Nephropathymentioning

confidence: 99%

Haemodynamic influences on kidney oxygenation: Clinical implications of integrative physiology

Evans

İnce

Joles

et al. 2013

Clin Exp Pharma Physio

222

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SUMMARY1. Renal blood flow, local tissue perfusion and blood oxygen content are the major determinants of oxygen delivery to kidney tissue. Arterial pressure and segmental vascular resistance influence kidney oxygen consumption through effects on glomerular filtration rate and sodium reabsorption.2. Diffusive shunting of oxygen from arteries to veins in the cortex and from descending to ascending vasa recta in the medulla limits oxygen delivery to renal tissue. Oxygen shunting depends on the vascular network, renal haemodynamics and kidney oxygen consumption. Consequently, the impact of changes in renal haemodynamics on tissue oxygenation cannot necessarily be predicted intuitively and, instead, requires the integrative approach offered by computational modelling and multiple measuring modalities.3. Tissue hypoxia is a hallmark of acute kidney injury (AKI) arising from multiple initiating insults, including ischaemia-reperfusion injury, radiocontrast administration, cardiopulmonary bypass surgery, shock and sepsis. Its pathophysiology is defined by inflammation and/or ischaemia resulting in alterations in renal tissue oxygenation, nitric oxide bioavailability and oxygen radical homeostasis. This sequence of events appears to cause renal microcirculatory dysfunction, which may then be exacerbated by the inappropriate use of therapies common in peri-operative medicine, such as fluid resuscitation.4. The development of new ways to prevent and treat AKI requires an integrative approach that considers not just the molecular mechanisms underlying failure of filtration and tissue damage, but also the contribution of haemodynamic factors that determine kidney oxygenation. The development of bedside monitors allowing continuous surveillance of renal haemodynamics, oxygenation and function should facilitate better prevention, detection and treatment of AKI.

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Section: Contrast-induced Nephropathymentioning

confidence: 99%

Haemodynamic influences on kidney oxygenation: Clinical implications of integrative physiology

Evans

İnce

Joles

et al. 2013

Clin Exp Pharma Physio

222

239

View full text Add to dashboard Cite

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“…It requires a comprehensive approach using multi‐faceted measuring modalities including non‐invasive imaging such as ultrasound, computer tomography and magnetic resonance imaging (Damkjaer et al . , Pohlmann et al . , Brabrand et al .…”

mentioning

confidence: 99%

How bold is blood oxygenation level‐dependent (BOLD) magnetic resonance imaging of the kidney? Opportunities, challenges and future directions

et al. 2014

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Renal tissue hypoperfusion and hypoxia are key elements in the pathophysiology of acute kidney injury and its progression to chronic kidney disease. Yet, in vivo assessment of renal haemodynamics and tissue oxygenation remains a challenge. Many of the established approaches are invasive, hence not applicable in humans. Blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI) offers an alternative. BOLD-MRI is non-invasive and indicative of renal tissue oxygenation. Nonetheless, recent (pre-) clinical studies revived the question as to how bold renal BOLD-MRI really is. This review aimed to deliver some answers. It is designed to inspire the renal physiology, nephrology and imaging communities to foster explorations into the assessment of renal oxygenation and haemodynamics by exploiting the powers of MRI. For this purpose, the specifics of renal oxygenation and perfusion are outlined. The fundamentals of BOLD-MRI are summarized. The link between tissue oxygenation and the oxygenation-sensitive MR biomarker T2∗ is outlined. The merits and limitations of renal BOLD-MRI in animal and human studies are surveyed together with their clinical implications. Explorations into detailing the relation between renal T2∗ and renal tissue partial pressure of oxygen (pO2 ) are discussed with a focus on factors confounding the T2∗ vs. tissue pO2 relation. Multi-modality in vivo approaches suitable for detailing the role of the confounding factors that govern T2∗ are considered. A schematic approach describing the link between renal perfusion, oxygenation, tissue compartments and renal T2∗ is proposed. Future directions of MRI assessment of renal oxygenation and perfusion are explored.

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“…It was suggested that increased oxidative stress in the renal medulla decreases medullary perfusion and thereby increases sodium reabsorption during hypertension . We have adapted imaging technology to quantify regional renal blood flows in man allowing imaging procedures to be added to measurements of haemodynamic, hormonal and renal responses to volume expansion. For the present study, we hypothesized that in patients with mild essential hypertension, but no measurable target organ damage, the response of local renal flow to saline loading differs from baseline and from the response of normotensive subjects.…”

Section: Introductionmentioning

confidence: 99%

The exaggerated natriuresis of essential hypertension occurs independently of changes in renal medullary blood flow

et al. 2019

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Aims:In patients with essential hypertension, abnormal renal sodium handling includes exaggerated natriuresis in response to extracellular volume expansion. We tested the hypothesis that exaggerated natriuresis is associated with increases in medullary and/or cortical renal blood flow. Methods: Patients with mild essential hypertension, but no signs of end organ damage, and control subjects were studied after 4 days of dietary standardization (<60 mmol Na + day −1 ) preceded in patients by a 14-day drug washout period. On the study day, subjects received a 4-hour intravenous volume expansion with saline (2.1% of body mass). Renal medullary and cortical blood flows were measured by PET scanning using H 2 15 O as tracer; anatomical regions of interest were defined by contrast-enhanced CT scanning. Results: In patients, arterial blood pressure increased during volume expansion (107 ± 2-114 ± 3 mm Hg, P < 0.05) in contrast to the control group (92 ± 2-92 ± 2 mm Hg). Renal sodium excretion increased more in patients than in controls (+133 ± 31 µmol min −1 vs +61 ± 14 µmol min −1 , respectively, P < 0.05) confirming exaggerated natriuresis. During volume expansion, renal medullary blood flow did not change significantly in patients (2.8 ± 0.4-2.5 ± 0.5 mL (g tissue) −1 min −1 ) or in controls (3.2 ± 0.3-3.1 ± 0.2 mL (g tissue) −1 min −1 ). In control subjects, renal cortical blood flow fell during volume expansion (4.1 ± 0.3-3.7 ± 0.2 mL (g tissue) −1 min −1 , P < 0.05) in contrast to patients in which deviations remained insignificant. Conclusion: Exaggerated natriuresis, a hallmark of essential hypertension, is not mediated by increases in regional, renal blood flow. K E Y W O R D S hypertension, low salt diet, renal blood flow, renal haemodynamics, sodium sensitivity, volume expansion See Editorial Commentary: Castrop, H. 2019. Renal medullary blood flow and essential hypertension. Acta Physiol. 226, e13289.

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Renal cortical and medullary blood flow during modest saline loading in humans

Abstract: In normal humans, changes in RMBF are not necessarily involved in the natriuretic response to modest saline loading. This result is in line with data from conscious rodents.

Cited by 14 publications

References 75 publications

Haemodynamic influences on kidney oxygenation: Clinical implications of integrative physiology

Haemodynamic influences on kidney oxygenation: Clinical implications of integrative physiology

How bold is blood oxygenation level‐dependent (BOLD) magnetic resonance imaging of the kidney? Opportunities, challenges and future directions

The exaggerated natriuresis of essential hypertension occurs independently of changes in renal medullary blood flow

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