Renal autoregulation and blood pressure management in circulatory shock

Post, Emiel Hendrik; Vincent, Jean‐Louis

doi:10.1186/s13054-018-1962-8

Cited by 32 publications

(31 citation statements)

References 83 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The shear stress will stimulate the proinflammatory response which is present on the surface of endothelial cells, increase the expression of endothelial adhesion molecules and their interactions with neutrophils, monocytes that triggers the release of IL-6. [23][24][25][26][27] Our study showed a higher release of IL-6 during pneumoperitoneum insufflation in the standard pressure group than in the low pressure group. Although CO 2 and surgical techniques can contribute to the release of proinflammatory cytokines, 28 our study showed that an acute, slight increase in intraabdominal pressure results in significantly increased IL-6 levels.…”

Section: Discussionmentioning

confidence: 47%

“…23 The renal perfusion is affected by the blood flow and pressure on blood vessels. 24 The impaired blood flow changes the normal blood flow from laminar into turbulent or oscillatory flow that causes the shear stress. The shear stress will stimulate the proinflammatory response which is present on the surface of endothelial cells, increase the expression of endothelial adhesion molecules and their interactions with neutrophils, monocytes that triggers the release of IL-6.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of Low Versus Standard Pressure Pneumoperitoneum on Renal Syndecan-1 Shedding and VEGF Receptor-2 Expression in Living-donor Nephrectomy: A Randomized Controlled Study

Aditianingsih

Mochtar

Lydia

et al. 2020

Preprint

View full text Add to dashboard Cite

Background Laparoscopic nephrectomy is a preferred technique for living kidney donation. However, positive-pressure pneumoperitoneum may have an unfavorable effect on the remaining kidney and other distant organs due to inflamed vascular endothelium and renal tubular cell injury in response to increased systemic inflammation. Early detection of vascular endothelial and renal tubular response is needed to prevent further kidney injury due to increased intraabdominal pressure induced by pneumoperitoneum. Transperitoneal laparoscopic living donor nephrectomy represented a human model of mild increasing intraabdominal pressure. This study aimed to assess the effect of increased intraabdominal pressure on vascular endothelium and renal tubular cells by comparing the effects of low and standard pressure pneumoperitoneum on vascular endothelial growth factor receptor-2 (VEGFR-2) expression and the shedding of syndecan-1 as the early markers to a systemic inflammation. Methods We conducted a prospective randomized study on 44 patients undergoing laparoscopic donor nephrectomy. Subjects were assigned to standard (12 mmHg) or low pressure (8 mmHg) groups. Baseline, intraoperative, and postoperative plasma interleukin-6, syndecan-1, and sVEGFR-2 were quantified by ELISA. Syndecan-1 and VEGFR-2 expression were assessed immunohistochemically in renal cortex tissue. Renal tubule and peritubular capillary ultrastructures were examined using electron microscopy. Perioperative hemodynamic changes, end-tidal CO2, serum creatinine, blood urea nitrogen, and urinary KIM-1 were recorded. Results The low pressure group showed lower intra- and postoperative heart rate, intraoperative plasma IL-6, sVEGFR-2 levels and plasma syndecan-1 than standard pressure group. Proximal tubule syndecan-1 expression was higher in the low pressure group. Proximal-distal tubules and peritubular capillary endothelium VEGFR-2 expression were lower in low pressure group. The low pressure group showed renal tubule and peritubular capillary ultrastructure with intact cell membranes, clear cell boundaries, and intact brush borders, while standard pressure group showed swollen nuclei, tenuous cell membrane, distant boundaries, vacuolizations, and detached brush borders. Conclusion The low pressure pneumoperitoneum attenuated the inflammatory response and resulted in reduction of syndecan-1 shedding and VEGFR-2 expression as the renal tubular and vascular endothelial proinflammatory markers to injury due to a systemic inflammation in laparoscopic nephrectomy. Trial registration ClinicalTrial.gov NCT:03219398, July 17th 2017. Keywords: pneumoperitoneum, renal resistive index, interleukin-6, syndecan-1, sVEGFR-2, laparoscopic nephrectomy

show abstract

Section: Discussionmentioning

confidence: 47%

Section: Discussionmentioning

confidence: 99%

Effects of Low Versus Standard Pressure Pneumoperitoneum on Renal Syndecan-1 Shedding and VEGF Receptor-2 Expression in Living-donor Nephrectomy: A Randomized Controlled Study

Aditianingsih

Mochtar

Lydia

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…The gain quantifies to which extend a change in RBF is caused by a change in RPP. A low transfer gain value implies that oscillations in RPP do not translate into flow fluctuations of similar frequency, that is the kidney is effectively autoregulating in the given frequency band (Post & Vincent, ). The phase indicates the latency between the RBF and RPP signal.…”

Section: Methodsmentioning

confidence: 99%

“…Besides RPP, the influence of β‐blockers on RBF is further complicated by the unknown effect on renal autoregulation in sepsis or septic shock. Renal autoregulation is mediated by vascular reactivity, unlinking RPP from RBF (Post and Vincent, ()). In health, renal autoregulation keeps blood flow at a constant level at perfusion pressures greater than approximately 60–100 mmHg, depending on species (Post, Kellum, Bellomo, & Vincent, ).…”

Section: Introductionmentioning

confidence: 99%

β‐Blockade attenuates renal blood flow in experimental endotoxic shock by reducing perfusion pressure

Loon

Rongen

Hoeven³

et al. 2019

Physiol Rep

View full text Add to dashboard Cite

Clinical data suggests that heart rate (HR) control with selective β1‐blockers may improve cardiac function during septic shock. However, it seems counterintuitive to start β‐blocker infusion in a shock state when organ blood flow is already low or insufficient. Therefore, we studied the effects of HR control with esmolol, an ultrashort‐ acting β1‐selective adrenoceptor antagonist, on renal blood flow (RBF) and renal autoregulation during early septic shock. In 10 healthy sheep, sepsis was induced by continuous i.v. administration of lipopolysaccharide, while maintained under anesthesia and mechanically ventilated. After successful resuscitation of the septic shock with fluids and vasoactive drugs, esmolol was infused to reduce HR with 30% and was stopped 30‐min after reaching this target. Arterial and venous pressures, and RBF were recorded continuously. Renal autoregulation was evaluated by the response in RBF to renal perfusion pressure (RPP) in both the time domain and frequency domain. During septic shock, β‐blockade with esmolol significantly increased the pressure dependency of RBF to RPP. Stopping esmolol showed the reversibility of the impaired renal autoregulation. Showing that clinical diligence and caution are necessary when treating septic shock with esmolol in the acute phase since esmolol reduced RPP to critical values thereby significantly reducing RBF.

show abstract

“…What is less well established is the lower limit of MAP beyond which autoregulation breaks down, and when flow becomes directly proportional to the perfusion pressure. Our understanding is currently based on studies of animals , but there appears to be no clear point at which autoregulation ‘breaks down’ (Fig. ) .…”

Section: Renal Perfusionmentioning

confidence: 99%

Pre‐incision hypotension and the association with postoperative acute kidney injury – an opportunity to improve peri‐operative outcomes?

El‐Ghazali

Pandit

2019

Anaesthesia

View full text Add to dashboard Cite

It is well established that intra-operative hypotension is associated with acute kidney injury (AKI), which is in turn associated with postoperative mortality. Recently, Maheshwari et al. investigated the influence of hypotension following induction of anaesthesia, and before the first surgical incision, on the incidence of postoperative AKI [1].From a large retrospective database analysis of more than 42,000 cases, the authors concluded that one-third of hypotensive readings occurred before incision which is arguably a time period under direct control of the anaesthetist. These readings were four times more frequently observed than after the first surgical incision.Hypotension at any time was associated with postoperative AKI. Before anaesthetists change their practice, this instalment of 'Clinical Consequences' will critique and explore the impact of this evidence in depth.The incidence of postoperative AKI can vary depending on the type of surgery, but up to 40% of hospital-acquired AKI may occur in surgical patients [2]. Postoperative AKI is associated with increased mortality, as well as increased financial costs and other complications, such as the need for long-term renal replacement therapy [3][4][5]. Since postoperative AKI is easy to define and measure, perioperative strategies for its prevention seem to be a reasonable target for intervention. The question is, should we place more focus on better monitoring blood pressure and optimising haemodynamic parameters during the period between induction of anaesthesia and the first surgical incision? Renal perfusionIn 2012, the Kidney Disease Improving Global Outcomes (KDIGO) group released their AKI clinical practice guidelines [6]. Acute kidney injury is classified in stages by the degree of increase in serum creatinine and reduction in urine output. It follows that renal function is not a dichotomous (normal vs. deranged), but a continuous parameter. Similarly, the decrease in blood pressure preincision (or specifically the drop in renal perfusion pressure) is also continuous. Yet, logistic regression analysisthe method used by Maheshwari et al. to analyse their datasetrequires that both are converted to binary (dichotomous) measures. They define hypotension as a mean arterial pressure (MAP < 65 mmHg and AKI as KDIGO stage one or higher. It would have perhaps been interesting to inspect the plot of serum creatinine against the actual decrease in pre-induction MAP to look for any suggestion of correlation across the whole range of values, but this was not reported.The blood pressure required to maintain adequate blood flow to vital organs will vary between patients. Blood flow to most organs in health is governed by autoregulatory mechanisms, which are well understood. What is less well established is the lower limit of MAP beyond which autoregulation breaks down, and when flow becomes directly proportional to the perfusion pressure. Our understanding is currently based on studies of animals [7], but there appears to be no clear point at which autoregulation...

show abstract

Renal autoregulation and blood pressure management in circulatory shock

Cited by 32 publications

References 83 publications

Effects of Low Versus Standard Pressure Pneumoperitoneum on Renal Syndecan-1 Shedding and VEGF Receptor-2 Expression in Living-donor Nephrectomy: A Randomized Controlled Study

Effects of Low Versus Standard Pressure Pneumoperitoneum on Renal Syndecan-1 Shedding and VEGF Receptor-2 Expression in Living-donor Nephrectomy: A Randomized Controlled Study

β‐Blockade attenuates renal blood flow in experimental endotoxic shock by reducing perfusion pressure

Pre‐incision hypotension and the association with postoperative acute kidney injury – an opportunity to improve peri‐operative outcomes?

Contact Info

Product

Resources

About