Next Article in Journal
Heart Failure Pharmacological Management: Gaps and Current Perspectives
Previous Article in Journal
Advanced Paternal Age Does Not Affect Medically-Relevant Obstetrical and Perinatal Outcomes following IVF or ICSI in Humans with Donated Oocytes
Previous Article in Special Issue
Hypokalemia Duration in the First Year Associated with Subsequent Peritoneal Dialysis-Associated Peritonitis: A Multicenter Retrospective Cohort Study
 
 
Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
Journals
JCM
Volume 12
Issue 3
10.3390/jcm12031018
jcm-logo
Submit to this Journal Review for this Journal Propose a Special Issue
► Article Menu

Article Menu

share Share announcement Help format_quote Cite question_answer Discuss in SciProfiles thumb_up
...
Endorse textsms
...
Comment
first_page
settings
Order Article Reprints
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Review

Comprehensive Management of Blood Pressure in Patients with Septic AKI

by
Junhui Deng
1,
Lina Li
1,
Yuanjun Feng
2 and
Jurong Yang
1,*
1
Department of Nephrology, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 400120, China
2
Department of Renal Rheumatology, Space Hospital Affiliated to Zunyi Medical University, Zunyi 563002, China
*
Author to whom correspondence should be addressed.
J. Clin. Med. 2023, 12(3), 1018; https://doi.org/10.3390/jcm12031018
Submission received: 27 November 2022 / Revised: 18 January 2023 / Accepted: 19 January 2023 / Published: 28 January 2023
(This article belongs to the Special Issue Management of Treatment and Prognosis in Acute Kidney Injury Patients)
Browse Figure
Review Reports Versions Notes

Abstract

:
Acute kidney injury (AKI) is one of the serious complications of sepsis in clinical practice, and is an important cause of prolonged hospitalization, death, increased medical costs, and a huge medical burden to society. The pathogenesis of AKI associated with sepsis is relatively complex and includes hemodynamic abnormalities due to inflammatory response, oxidative stress, and shock, which subsequently cause a decrease in renal perfusion pressure and eventually lead to ischemia and hypoxia in renal tissue. Active clinical correction of hypotension can effectively improve renal microcirculatory disorders and promote the recovery of renal function. Furthermore, it has been found that in patients with a previous history of hypertension, small changes in blood pressure may be even more deleterious for kidney function. Therefore, the management of blood pressure in patients with sepsis-related AKI will directly affect the short-term and long-term renal function prognosis. This review summarizes the pathophysiological mechanisms of microcirculatory disorders affecting renal function, fluid management, vasopressor, the clinical blood pressure target, and kidney replacement therapy to provide a reference for the clinical management of sepsis-related AKI, thereby promoting the recovery of renal function for the purpose of improving patient prognosis.

1. Introduction

Septic shock is a pathological syndrome of life-threatening multiorgan dysfunction caused by a dysregulated host response to infection [1]. Acute kidney injury (AKI) occurs in up to 50% of patients with sepsis, resulting in prolonged hospitalization and a six- to eightfold increase in mortality [2,3,4]. Survivors of AKI are at risk of developing chronic or end-stage renal disease, even with short-term or mild renal impairment, which is a medical burden on society [5,6]. Multiple mechanisms are involved in the development of sepsis-associated AKI, including inflammatory responses, oxidative stress, adaptive responses of renal tubular epithelial cells, and renal hemodynamic abnormalities [7,8,9]. Histological staining of renal tissue from patients who died of sepsis-associated AKI reveals uneven tubular injury, manifested as focal acute tubular injury, and most of the renal tubules were normal [10,11]. This is related to abnormal shunt of renal blood supply due to microcirculation damage, and clinical improvement of blood pressure and optimization of systemic hemodynamic support are essential in patients with AKI or at risk of AKI [12,13]. Statistically, a high proportion of patients diagnosed with sepsis-associated AKI in the intensive care unit have previous chronic hypertension, which is an independent risk factor [14,15]. Because the kidneys of hypertensive patients are more sensitive to abnormal fluctuations in blood pressure [16,17], the management of blood pressure in septic AKI is a great challenge for clinicians. Therefore, this paper summarizes the mechanism of sepsis microcirculation disorder affecting renal function, clinical comprehensive management of blood pressure, and target blood pressure in order to provide references for clinical treatment and urgent clinical research directions.

2. Microcirculatory Disorders

Microcirculation refers to the capillary system that connects the arteries and veins. It is essential to the function of every organ and system in the body for the transport of oxygen and nutrients and the removal of toxins. Impaired microcirculation is a hallmark of septic shock and is the pathophysiological basis for the failure of multiple organs, including the heart, intestines, liver, brain, and kidneys [18,19]. The occurrence of microcirculatory disorders in sepsis involves multiple mechanisms related to endothelial cell injury, blocked intercellular communication, glycocalyx shedding, coagulation dysfunction, leukocyte and platelet adhesion, and altered red blood cell deformability due to severe infection, resulting in reduced microvascular blood flow velocity and microthrombosis, which ultimately disrupt microvascular flow [20,21]. The kidney is particularly rich in microvessels, and impaired microcirculation leads to intrarenal perfusion redistribution, resulting in abnormal blood flow distribution in the renal medulla and renal cortex and decreased oxygenation in tissues, which triggers a vicious cycle of oxidative stress and inflammation [22,23,24]. There is a natural shunt in renal blood flow, with cortical blood perfusion accounting for 80% of renal blood flow (RBF) and a partial pressure of oxygen of approximately 70 mmHg and medullary blood flow accounting for 20% of RBF and a partial pressure of oxygen of approximately 20 mmHg. Compared with the cortex, the medullary circulation is less able to self-regulate against ischemia and hypoxia, making the medulla more sensitive to hypoxia caused by sepsis [25]. This is related to the specific topography of the vascular bundle in the renal medulla, where the thick upper branches of the Henle collaterals are located at the periphery of the vascular bundle, allowing oxygen diffusion to be restricted. In addition, diffuse shunting of oxygen in the renal medulla from the straight ducts down to the upper ducts may reduce oxygen transport [26,27]. Reduced blood flow and decreased oxygenation in the renal medulla may exacerbate tubular epithelial cell injury in the medullary portion, especially in the proximal tubule S3 segment in the outer medulla, leading to increased reactive oxygen species and mitochondrial dysfunction, further leading to reduced renal function [28,29,30].
Hypoxia in the medulla also exacerbates renal injury by involving the tubuloglomerular feedback mechanism (TGF). Hypoxia in the thick ascending branch of the Henle collaterals can lead to decreased production of adenosine triphosphate, which decreases sodium reabsorption, activates TGF, and reduces the glomerular filtration rate by constricting the afferent small arteries, which again triggers a vicious cycle of medullary hypoperfusion and hypoxia [31]. In conclusion, abnormal renal medullary perfusion due to microcirculatory impairment, tissue ischemia and hypoxia, and reaggravation of medullary hypoxia by TGF in sepsis are the main pathological mechanisms for the development of AKI associated with sepsis (Figure 1), and renal medullary hypoxia can be corrected clinically by improving microcirculation, thereby reversing renal impairment.

3. Fluid Management

In clinical practice, intractable hypotension due to sepsis is preferentially resuscitated by fluid therapy to achieve the blood pressure target, thereby restoring circulating volume and improving renal perfusion [32]. A retrospective study defined resuscitation goals for patients with sepsis in the ICU as mean arterial pressure greater than 65 mmHg, central venous pressure greater than 8 mmHg, and central venous oxygenation greater than 70%; achieving early resuscitation within 6 h after consultation was associated with a reduction in the development of AKI [33]. The main categories of volume expansion fluid therapy for hypotensive shock are colloids and crystals, and a meta-analysis found that balanced crystalloids and albumin reduced the mortality in patients with sepsis more than hydroxyethyl starch (HES) and saline [34]. The results of this study showed that HES is associated with a higher incidence of AKI and renal replacement (RRT) rate, leading to the recommendation that HES solution be contraindicated in patients with severe sepsis or at risk of AKI [35,36,37]. In a sheep model of septic shock, renal function and cumulative diuresis were preserved in the albumin and crystalloid resuscitation groups, whereas HES resulted in reduced creatinine clearance [38]. However, given the risk of infection, 4% hypotonic albumin is recommended as the concentration [39].
Additionally, 0.9% physiological saline was found to be at risk of causing or exacerbating metabolic acidosis and progression to AKI and RRT in critically ill patients with sepsis [40,41]. However, most patients with sepsis-related AKI experience fluid overload to varying degrees during fluid resuscitation therapy, which can aggravate renal impairment and increase the morbidity and mortality of patients [42,43,44]. In addition to blood pressure, CVP is one of the main clinical indicators of hemodynamics. It usually refers to the pressure in the right atrium and large intrathoracic veins and is important for understanding the effective circulating blood volume and cardiac function [45,46]. A cohort study that included 15 patients with sepsis at the main time indicated that elevated CVP was associated with an increased risk of death and AKI, and in addition, each 1 mmHg increase in CVP was associated with a 6% increase in the odds of AKI [47]. Huo et al. found that a lower CVP level (<13 mmHg) was an independent variable associated with reduced mortality in patients with sepsis-related AKI through a propensity-score-matched analysis of clinical data on adult sepsis from the Medical Information Mart for Intensive Care-IV database [48]. To address fluid overload, clinicians have three primary options: fluid restriction, diuretic pharmacotherapy, or RRT extracorporeal ultrafiltration. Collectively, diuretics should not be used to treat AKI except for fluid overload [49]. Diuretic clearance fluid is harmful in the acute phase of sepsis, and when the patient is stable, fluid overload is harmful and diuretic clearance can be applied [50,51,52]. Kidney replacement therapy (RRT) is an effective treatment for dehydration in patients with hemodynamic instability where fluid overload is not appropriate for diuretics. In conclusion, fluid resuscitation is the primary means to improve sepsis patients and patients with concurrent AKI. In clinical practice, it is necessary to avoid rehydration therapy that is detrimental to the benefit of the kidney, while strictly vigilant against fluid overload. When fluid overload occurs, diuretic medication or RRT may be selected, depending on the patient’s situation.

4. Vasopressor

In septic hypotension, if the blood pressure target cannot be achieved by fluid augmentation, clinicians can also implement resuscitation to improve the microcirculatory perfusion of the kidneys and other organs through the use of a vasopressor. Currently, the commonly used drugs include norepinephrine, dopamine, pressor, and angiotensin II (Table 1).
Norepinephrine increases the arterial pressure through α-adrenergic receptor-mediated vasoconstriction and is the medication of choice for septic hypotension [53,54,55]. Infusion of norepinephrine in a hyperdynamic sheep model of sepsis increased blood flow to the heart, intestine, and kidneys, effectively increasing urine output and improving creatinine clearance [56]. Although it has been reported that norepinephrine can aggravate medulla hypoxia while reviving blood pressure in a sheep sepsis AKI model, it has no significant effect on renal blood flow or renal oxygen delivery [57,58]. Furthermore, systematic reviews and metastudies have found that norepinephrine minimizes arrhythmia compared with other vasopressors and is therefore safe for use in patients with septic shock and AKI [53].
Dopamine is a natural precursor of epinephrine and norepinephrine. It excites mainly the α receptors, β receptors, and peripheral dopamine receptors, and it has shown comparable efficacy with epinephrine in the treatment of infectious shock [59]. Due to its stimulatory effect on dopaminergic receptors, dopamine is suspected to adversely affect the perfusion output of internal organs, such as the kidney [60]. In a prospective, double-blind randomized controlled study, “low-dose” dopamine worsened renal perfusion and increased renal impairment in patients with acute kidney failure in the absence of systemic hemodynamic effects [61]. Dopamine use in septic hypotensive patients was associated with higher rates of mortality, infection, and arrhythmic events compared with norepinephrine and epinephrine [62,63,64,65,66].
Vasopressin increases arterial blood pressure primarily by stimulating the arginine vasopressin receptor 1A (AVPR1A) located on vascular smooth muscle cells to induce vasoconstriction. It is currently recommended as a pressor agent that is unresponsive to norepinephrine, and/or it reduces the dose of norepinephrine required to achieve the blood pressure target [67,68].
In a sheep septic AKI model, vasopressin had better renoprotective effects than norepinephrine [69,70]. In clinical practice, vasopressin increases per beat output, improves renal perfusion in patients with infectious shock, improves renal function, and reduces the use of RRT [71,72]. However, it has also been found that in adults with infectious shock, early administration of vasopressin did not improve the number of days without kidney failure compared with norepinephrine [73]. Therefore, the benefit of vasopressin in septic AKI also needs to be informed by more studies.
Angiotensin II, an endogenous circulating hormone with potent vasoconstrictive effects, effectively increases blood pressure in patients with vasodilatory shock who do not respond to high doses of conventional vasopressors, such as norepinephrine [74]. The decrease in renal arteriolar pressure and sodium in protourine stimulates the secretion of renin by periglomerular cells. Renin acts on angiotensinogen in plasma to produce inactive angiotensin I, which is hydrolyzed to active angiotensin II under the action of angiotensin-converting enzyme. Angiotensin Ⅱ can cause the contraction of the afferent and efferent arterioles, and the efferent arterioles are more sensitive, which increases the pressure in the glomeruli, thus affecting the glomerular filtration rate [75,76]. In a sheep model of septic AKI, angiotensin II was found to restore arterial pressure without exacerbating medullary hypoxia. It significantly increased urine output and normalized creatinine clearance [77,78]. Clinically, in patients with septic acute kidney injury requiring kidney replacement therapy, the 28-day survival and mean arterial pressure response were higher in the angiotensin II group compared with the placebo group, and the release rate from kidney replacement therapy was higher, suggesting that patients with septic AKI requiring kidney replacement therapy may preferentially benefit from angiotensin II [79]. Taken together, we can conclude that angiotensin II appears to be a safe and effective treatment, although more clinical data are still needed to support this.
Table
Table 1. Pharmacological effects and renal effects of the vasopressors.
Table 1. Pharmacological effects and renal effects of the vasopressors.
Drug NameReceptorEffects on Renal FunctionEffect on Urine OutputEffects on the MedullaReference
Norepinephrineα-adrenergic receptorImproveIncreaseExacerbate hypoxia[53,54,55,56,57,58]
Dopamineα receptor, β receptor, and peripheral dopamine receptorWorsenUnknownUnknown[60,61,80,81]
VasopressinAVPR1AImproveIncreaseUnknown[67,68,69,70,71,72]
Angiotensin IIAngiotensin II receptorImproveIncreaseDoes not exacerbate hypoxia[74,77,78]
AVPR1A, arginine vasopressin receptor 1A.

5. Blood Pressure Target

Sepsis often leads to intractable hypotension, resulting in hypoperfusion and microcirculatory disorders in multiple organs, including the kidneys. Aggressive clinical correction of blood pressure can largely improve renal blood supply and restore renal function [32,82,83]. Mean arterial pressure (MAP) is the average arterial blood pressure during one cardiac cycle. It is widely used as a measure of blood pressure. The latest guidelines on sepsis suggest a MAP garget of 65 mmHg for initial resuscitation in patients with septic shock to reduce the risk of death and end-organ failure [84]. However, it is important to note that even at the same MAP, organs may have different perfusion pressures and pressure–flow rates, with the small postglomerular artery responsible for renal tissue perfusion typically having a lower pressure than systemic arterial blood pressure [85]. Therefore, for patients with sepsis, there are different recommendations for the ideal blood pressure target to help prevent renal impairment or aid recovery (Table 2). A retrospective study from 110 hospitals in the United States evaluated patients with sepsis who were admitted to the intensive care unit (ICU) for more than 24 h from 2010 to 2016. Through multivariate logistic regression analysis, the study found that the time-weighted mean arterial pressure (TWA-MAP) began to be significant for AKI at 65 mmHg, and as MAP decreased from 85 to 55 mmHg, in addition to AKI, patients had a progressive increase in mortality and odds of myocardial injury. Therefore, it is suggested that in septic patients, maintaining MAP well above 65 mmHg may be a more prudent approach to prevent and ameliorate renal injury [86]. In another prospective observational FINNAKI study from 17 hospitals in Finland, 423 patients with severe sepsis from September 2011 to February 2012 were enrolled by screening, of whom 153 (36.2%) presented with AKI, and a significantly higher TWA-MAP of 78.6 mmHg (72.9–85.4 mmHg) was found by between-group analysis in non-AKI patients than in AKI patients. The study indicated that a TWA-MAP cutoff of 73 mmHg best predicted the progression of sepsis-related AKI [87]. Chen et al. conducted a retrospective cohort study of patients admitted to the ICU of Chiayi Chang Gung Memorial Hospital from January 2015 to December 2016, which included 63 critically ill patients with confirmed AKI. They found that the sensitivity and specificity of the total patient mortality at MAP ≤ 77.16 mmHg were 62.50% and 91.30%, respectively, and they concluded that MAP ≤ 77 mmHg can be used as a risk factor for death in patients with AKI [88]. A prospective study, which was approved by the Association des Réanimateurs du Centre-Ouest, France, conducted in two ICUs from October 2007 to April 2009, included and followed 217 patients with septic shock and compared the MAP in the first 24 h after inclusion in patients who developed AKI at 72 h and those who did not develop AKI. The study found that the optimal MAP level to prevent AKI at 72 h after the onset of infectious shock was between 72 and 82 mmHg [89]. A retrospective single-center cohort study from the Mayo Clinic found the lower incidence of AKI in patients with infectious shock when the postresuscitation median MAP was closest to or higher than the preadmission median MAP, suggesting that this MAP should not be a fixed value and that it is necessary to target the preadmission MAP for AKI prevention [90].
For patients with septic shock with a history of hypertension, European experts suggest personalized blood pressure targets, perhaps with a higher MAP leading to better clinical improvement [91]. A study of the blood pressure target in patients with septic AKI with a history of hypertension included 26 patients with a history of chronic hypertension and AKI within the first 24 h of septic shock in two ICUs at the University Hospital of Bordeaux, and the MAP target of 80–85 mmHg was associated with more urine output and lower serum creatinine compared with 65–70 mmHg, confirming the need for higher blood pressure in this group of patients to improve renal perfusion [92]. In a multicenter, open-label trial in France, we randomly assigned 776 patients with septic shock to resuscitation with a mean arterial pressure target of 80 to 85 mmHg (high target group) or 65 to 70 mmHg (low target group). Patients in the high-target group required less renal replacement therapy than those in the low-target group, although the difference in mortality was not associated [93].
In addition to MAP, mean perfusion pressure (MPP) is often used as a clinical indicator of blood pressure. It refers to the difference between the MAP and central venous pressure (CVP) [94]. In a single-center retrospective study conducted in the ICU of Guy’s and St. Thomas’ NHS hospitals, of 2118 ICU patients, 790 patients (37%) developed AKI stage I. AKI I patients with MPP ≤ 59 mmHg were at a significantly increased risk of progression to AKI stage III, and the study concluded that MPP ≤ 59 mmHg was independently associated with AKI progression [95]. In another retrospective analysis of 107 patients hospitalized for infectious shock between August 2010 and June 2013 in the ICU of the tertiary referral university hospital in Melbourne, 55 (51.4%) of whom developed severe AKI, the median MPP decline ratio from premorbidities was 29% in patients who developed severe AKI compared with 24% in non-AKI patients, indicating that a greater MPP decline ratio is associated with the development of septic AKI [96]. A prospective, open-label, before-and-after controlled study conducted in two tertiary ICUs in Australia compared the current standard care and the individualized blood pressure target strategies by screening 62 shocked ICU patients receiving vasopressor medication separately. There was a lower incidence of new significant AKI in the individualized intervention group, indicating that setting an individualized blood pressure target during ICU boosters may prevent AKI and reduce mortality [97]. Taken together, we suggest that clinicians must personalize the management of the patient and could attempt higher blood pressure values in specific cases. Start by targeting 65 mmHg; consider targeting up to 85 mmHg in patients with a previous history of hypertension and monitoring the microcirculation (skin peripheral perfusion) lactate level and urine output to individualize BP targets using fluid infusion and vasoactive drugs.
Table
Table 2. Recommendations for sepsis blood pressure targets by study.
Table 2. Recommendations for sepsis blood pressure targets by study.
NationTimeType of StudyNumber of CasesIndicatorTargetReference
U.S.January 2007 to January 2009Retrospective study233MAPPrehospital MAP[90]
FranceOctober 2007 to April 2009Prospective study217MAP72–82 mmHg[89]
U.S.2010 to 2016Retrospective study8782MAPMuch higher than 65 mmHg[86]
FinlandSeptember 2011 to February 2012Prospective study423MAPAbove 73 mmHg[87]
ChinaJanuary 2015 to December 2016Retrospective study63MAPAbove 77 mmHg[88]
FranceAugust 2016 to July 2017Prospective study26 (with a history of hypertension)MAP80–85 mmHg[92]
U.K.July 2007 to June 2009Retrospective study790MPPAbove 60 mmHg[95]
MAP, mean arterial pressure; MMP, mean perfusion pressure; SBP, systolic blood pressure.

6. Replacement Therapy

Kidney replacement therapy is an effective method to treat internal environment disorders caused by kidney failure in septic patients. It also removes toxins to replace renal function, improves blood pressure by removing inflammatory mediators, and helps ultrafiltrate the overload fluid in oliguric AKI [98,99]. At present, there are many clinical kidney replacement treatment modes, so it is necessary to choose the appropriate treatment mode according to the treatment purpose and condition.
Intermittent hemodialysis (IHD) and continuous renal replacement therapy (CRRT) are often used to address fluid overload, and CRRT was previously thought to be advantageous in septic hemodynamically unstable AKI patients [100,101]. More recently, however, it has been suggested that IHD can also reduce hemodynamic instability and improve prognosis if prescribed accurately [102,103]. In addition, IHD has the advantages of being more practical and cost-effective, eliminating the need for anticoagulation and reducing the risk of bleeding.
Other RRT modalities, such as continuous low-efficiency daily dialysis and prolonged intermittent kidney replacement therapy, have shown both hemodynamic stability and cost-effectiveness and are recommended for use in septicemic patients [104]. Hypotension occurs frequently in patients undergoing CRRT and is independently associated with mortality [105,106]. In a retrospective analysis of 2292 AKI patients undergoing CRRT at three referral hospitals, low MAP at the start of CRRT was associated with high mortality, especially when it was <82.7 mmHg [107]. Therefore, blood pressure management in patients during RRT treatment is even more important, which often requires larger doses of pressor medication because of the clearance of replacement therapy. In terms of alternative therapy doses, a meta-analysis of eight prospective randomized controlled trials found that higher-intensity RRT did not reduce mortality and may actually delay renal recovery compared with standard-intensity RRT [108]. In terms of the timing of treatment, Stéphane Gaudry et al. randomized 620 patients with severe AKI to early RRT treatment or delayed treatment. There was no significant difference in mortality between the two groups, even though delayed treatment avoided the need for kidney replacement therapy in a significant number of patients [109]. However, it has also been found that early initiation of RRT to clear fluid overload is more beneficial to renal function recovery in patients with septic AKI compared with patients with delayed initiation of RRT [110].The Second Affiliated Hospital of Guangzhou Medical University, Guangdong, China, is initiating a large, multicenter, prospective, randomized trial on the timing of initiation of continuous renal replacement therapy for acute kidney injury associated with sepsis in the intensive care unit (ClinicalTrials.gov identifier: NCT03175328); the study will enroll 460 patients with KDIGO 2 sepsis AKI from multicenter China, whose findings will help clinicians choose the right time to initiate CRRT.
Some advanced RRT filters have been shown to be effective in removing proinflammatory cytokines and endotoxins, such as the oXiris blood filter, which effectively removes endotoxins, tumor necrosis factor-α, interleukin-6, interleukin-8, and interferon gamma in patients with sepsis [111]. Two French centers reported experience with the oXiris blood filter in patients with septic shock. Studies found a relative reduction in norepinephrine infusion and an improvement in hemodynamic status, but kidney benefit was inconclusive [112]. High-volume peritoneal dialysis (HVPD) may be considered an alternative form of RRT in AKI [113]. However, it lacks competent control of fluids and can be a backup option for a few special cases.

7. Conclusions

Blood pressure control in sepsis directly affects the function of multiple organs, including the kidney, as well as the survival rate of patients. It is one of the difficult problems faced by clinicians. In septic hypotension, abnormal microcirculatory shunts leading to renal medullary ischemia and hypoxia are important pathological processes in AKI, and improving microcirculatory perfusion is the goal-oriented approach to improve renal function. Due to the inconsistency in perfusion pressure, the MAP target for patients with septic AKI is recommended to be set to individualize the blood pressure target based on patient-specific conditions, and more research is needed to determine whether a higher blood pressure is needed. Fluid resuscitation is the primary means of improving hypotensive shock, but decreased urine output after renal impairment often leads to fluid overload and requires RRT to maintain positive volume balance. Poor fluid resuscitation requires the addition of pressor drugs to constrict blood vessels to improve the blood pressure and improve the perfusion to all organs. However, more research evidence is needed to provide a clinical basis for patient treatment, including fluid and vasopressor choice, alternative treatment options, and so on, to achieve better blood pressure management goals, improve kidney function, and reduce mortality.

Author Contributions

Resources, J.Y.; writing—original draft preparation, J.D. and L.L.; writing—review and editing, J.D. and Y.F.; supervision, J.Y.; funding acquisition, J.Y. All authors have read and agreed to the published version of the manuscript.

Funding

This research was funded by the National Natural Science Foundation of China (No. 82270723), and the Chongqing Talent Program Project (cstc2021ycjh-bgzxm0090).

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

Not applicable.

Conflicts of Interest

The authors declare no conflict of interest.

References

  1. Singer, M.; Deutschman, C.S.; Seymour, C.W.; Shankar-Hari, M.; Annane, D.; Bauer, M.; Bellomo, R.; Bernard, G.R.; Chiche, J.D.; Coopersmith, C.M.; et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA 2016, 315, 801–810. [Google Scholar] [CrossRef]
  2. Bagshaw, S.M.; George, C.; Bellomo, R. Early acute kidney injury and sepsis: A multicentre evaluation. Crit. Care 2008, 12, R47. [Google Scholar] [CrossRef] [Green Version]
  3. Bagshaw, S.M.; Uchino, S.; Bellomo, R.; Morimatsu, H.; Morgera, S.; Schetz, M.; Tan, I.; Bouman, C.; Macedo, E.; Gibney, N.; et al. Septic acute kidney injury in critically ill patients: Clinical characteristics and outcomes. Clin. J. Am. Soc. Nephrol. CJASN 2007, 2, 431–439. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  4. Gómez, H.; Kellum, J.A. Sepsis-induced acute kidney injury. Curr. Opin. Crit. Care 2016, 22, 546–553. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  5. Bellomo, R.; Kellum, J.A.; Ronco, C.; Wald, R.; Martensson, J.; Maiden, M.; Bagshaw, S.M.; Glassford, N.J.; Lankadeva, Y.; Vaara, S.T.; et al. Acute kidney injury in sepsis. Intensive Care Med. 2017, 43, 816–828. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  6. Coca, S.G.; Yusuf, B.; Shlipak, M.G.; Garg, A.X.; Parikh, C.R. Long-term risk of mortality and other adverse outcomes after acute kidney injury: A systematic review and meta-analysis. Am. J. Kidney Dis. Off. J. Natl. Kidney Found. 2009, 53, 961–973. [Google Scholar] [CrossRef] [Green Version]
  7. Gomez, H.; Ince, C.; De Backer, D.; Pickkers, P.; Payen, D.; Hotchkiss, J.; Kellum, J.A. A unified theory of sepsis-induced acute kidney injury: Inflammation, microcirculatory dysfunction, bioenergetics, and the tubular cell adaptation to injury. Shock 2014, 41, 3–11. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  8. Zarbock, A.; Gomez, H.; Kellum, J.A. Sepsis-induced acute kidney injury revisited: Pathophysiology, prevention and future therapies. Curr. Opin. Crit. Care 2014, 20, 588–595. [Google Scholar] [CrossRef]
  9. Deng, J.; Tan, W.; Luo, Q.; Lin, L.; Zheng, L.; Yang, J. Long Non-coding RNA MEG3 Promotes Renal Tubular Epithelial Cell Pyroptosis by Regulating the miR-18a-3p/GSDMD Pathway in Lipopolysaccharide-Induced Acute Kidney Injury. Front. Physiol. 2021, 12, 663216. [Google Scholar] [CrossRef]
  10. Lerolle, N.; Nochy, D.; Guérot, E.; Bruneval, P.; Fagon, J.Y.; Diehl, J.L.; Hill, G. Histopathology of septic shock induced acute kidney injury: Apoptosis and leukocytic infiltration. Intensive Care Med. 2010, 36, 471–478. [Google Scholar] [CrossRef]
  11. Takasu, O.; Gaut, J.P.; Watanabe, E.; To, K.; Fagley, R.E.; Sato, B.; Jarman, S.; Efimov, I.R.; Janks, D.L.; Srivastava, A.; et al. Mechanisms of cardiac and renal dysfunction in patients dying of sepsis. Am. J. Respir. Crit. Care Med. 2013, 187, 509–517. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  12. Mårtensson, J.; Bellomo, R. Pathophysiology of Septic Acute Kidney Injury. Contrib. Nephrol. 2016, 187, 36–46. [Google Scholar] [CrossRef]
  13. Bavishi, C.; Bangalore, S.; Messerli, F.H. Outcomes of Intensive Blood Pressure Lowering in Older Hypertensive Patients. J. Am. Coll. Cardiol. 2017, 69, 486–493. [Google Scholar] [CrossRef] [PubMed]
  14. Wang, X.; Tao, Y.H.; Yang, J.; Wang, S.W.; Zhou, J.J.; Yang, L.C. Risk Factors for Sepsis Associated-Acute Kidney Injury in Intensive Care Unit Patients. Sichuan Da Xue Xue Bao. Yi Xue Ban = J. Sichuan Univ. Med. Sci. Ed. 2020, 51, 708–713. [Google Scholar] [CrossRef]
  15. Iram, H.; Ali, M.; Kumar, V.; Ejaz, A.; Solangi, S.A.; Junejo, A.M.; Solangi, S.A.; Un Nisa, N. Frequency of Risk Factors and Outcome of Hospital-Acquired Acute Kidney Injury. Cureus 2020, 12, e12001. [Google Scholar] [CrossRef] [PubMed]
  16. James, M.T.; Grams, M.E.; Woodward, M.; Elley, C.R.; Green, J.A.; Wheeler, D.C.; de Jong, P.; Gansevoort, R.T.; Levey, A.S.; Warnock, D.G.; et al. A Meta-analysis of the Association of Estimated GFR, Albuminuria, Diabetes Mellitus, and Hypertension With Acute Kidney Injury. Am. J. Kidney Dis. Off. J. Natl. Kidney Found. 2015, 66, 602–612. [Google Scholar] [CrossRef] [Green Version]
  17. Bo, S.; Gruden, G.; Charbonnier, E.; Martorana, M.; Gambino, R.; Cassader, M.; Gentile, L.; Cavallo-Perin, P.; Durazzo, M. High-normal blood pressure and impaired renal function. A prospective study in a population-based cohort. Minerva Med. 2014, 105, 211–219. [Google Scholar]
  18. De Backer, D.; Ricottilli, F.; Ospina-Tascón, G.A. Septic shock: A microcirculation disease. Curr. Opin. Anaesthesiol. 2021, 34, 85–91. [Google Scholar] [CrossRef]
  19. Furst, B.; Bughrara, N.; Musuku, S.R. Macrocirculation and Microcirculation in Septic Shock. Anesth. Analg. 2021, 133, e37–e38. [Google Scholar] [CrossRef]
  20. De Backer, D.; Donadello, K.; Taccone, F.S.; Ospina-Tascon, G.; Salgado, D.; Vincent, J.L. Microcirculatory alterations: Potential mechanisms and implications for therapy. Ann. Intensive Care 2011, 1, 27. [Google Scholar] [CrossRef] [Green Version]
  21. Ertmer, C.; Rehberg, S. Pathophysiology of sepsis. Dtsch. Med. Wochenschr. 1946 2016, 141, 1067–1073. [Google Scholar] [CrossRef]
  22. Evans, R.G.; Gardiner, B.S.; Smith, D.W.; O’Connor, P.M. Intrarenal oxygenation: Unique challenges and the biophysical basis of homeostasis. Am. J. Physiol.-Ren. Physiol. 2008, 295, F1259–F1270. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  23. Pallone, T.L.; Edwards, A.; Mattson, D.L. Renal medullary circulation. Compr. Physiol. 2012, 2, 97–140. [Google Scholar] [CrossRef] [PubMed]
  24. Evans, R.G.; Ince, C.; Joles, J.A.; Smith, D.W.; May, C.N.; O’Connor, P.M.; Gardiner, B.S. Haemodynamic influences on kidney oxygenation: Clinical implications of integrative physiology. Clin. Exp. Pharm. Physiol. 2013, 40, 106–122. [Google Scholar] [CrossRef] [PubMed]
  25. Regner, K.R.; Zuk, A.; Van Why, S.K.; Shames, B.D.; Ryan, R.P.; Falck, J.R.; Manthati, V.L.; McMullen, M.E.; Ledbetter, S.R.; Roman, R.J. Protective effect of 20-HETE analogues in experimental renal ischemia reperfusion injury. Kidney Int. 2009, 75, 511–517. [Google Scholar] [CrossRef] [Green Version]
  26. Fry, B.C.; Edwards, A.; Sgouralis, I.; Layton, A.T. Impact of renal medullary three-dimensional architecture on oxygen transport. Am. J. Physiol.-Ren. Physiol. 2014, 307, F263–F272. [Google Scholar] [CrossRef] [Green Version]
  27. Pannabecker, T.L.; Layton, A.T. Targeted delivery of solutes and oxygen in the renal medulla: Role of microvessel architecture. Am. J. Physiol.-Ren. Physiol. 2014, 307, F649–F655. [Google Scholar] [CrossRef] [Green Version]
  28. Devarajan, P. Update on mechanisms of ischemic acute kidney injury. J. Am. Soc. Nephrol. JASN 2006, 17, 1503–1520. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  29. Regner, K.R.; Roman, R.J. Role of medullary blood flow in the pathogenesis of renal ischemia-reperfusion injury. Curr. Opin. Nephrol. Hypertens. 2012, 21, 33–38. [Google Scholar] [CrossRef] [Green Version]
  30. Lee, C.J.; Gardiner, B.S.; Evans, R.G.; Smith, D.W. A model of oxygen transport in the rat renal medulla. Am. J. Physiol.-Ren. Physiol. 2018, 315, F1787–F1811. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  31. Marcoux, A.A.; Tremblay, L.E.; Slimani, S.; Fiola, M.J.; Mac-Way, F.; Haydock, L.; Garneau, A.P.; Isenring, P. Anatomophysiology of the Henle’s Loop: Emphasis on the Thick Ascending Limb. Compr. Physiol. 2021, 12, 3119–3139. [Google Scholar] [CrossRef] [PubMed]
  32. Cinel, I.; Kasapoglu, U.S.; Gul, F.; Dellinger, R.P. The initial resuscitation of septic shock. J. Crit. Care 2020, 57, 108–117. [Google Scholar] [CrossRef] [PubMed]
  33. Kiers, H.D.; Griesdale, D.E.; Litchfield, A.; Reynolds, S.; Gibney, R.T.; Chittock, D.; Pickkers, P.; Sweet, D.D. Effect of early achievement of physiologic resuscitation goals in septic patients admitted from the ward on the kidneys. J. Crit. Care 2010, 25, 563–569. [Google Scholar] [CrossRef] [PubMed]
  34. Tseng, C.H.; Chen, T.T.; Wu, M.Y.; Chan, M.C.; Shih, M.C.; Tu, Y.K. Resuscitation fluid types in sepsis, surgical, and trauma patients: A systematic review and sequential network meta-analyses. Crit. Care 2020, 24, 693. [Google Scholar] [CrossRef]
  35. Li, B.; Zhao, H.; Zhang, J.; Yan, Q.; Li, T.; Liu, L. Resuscitation Fluids in Septic Shock: A Network Meta-Analysis of Randomized Controlled Trials. Shock 2020, 53, 679–685. [Google Scholar] [CrossRef]
  36. Brunkhorst, F.M.; Engel, C.; Bloos, F.; Meier-Hellmann, A.; Ragaller, M.; Weiler, N.; Moerer, O.; Gruendling, M.; Oppert, M.; Grond, S.; et al. Intensive insulin therapy and pentastarch resuscitation in severe sepsis. N. Engl. J. Med. 2008, 358, 125–139. [Google Scholar] [CrossRef] [Green Version]
  37. Reinhart, K.; Perner, A.; Sprung, C.L.; Jaeschke, R.; Schortgen, F.; Johan Groeneveld, A.B.; Beale, R.; Hartog, C.S. Consensus statement of the ESICM task force on colloid volume therapy in critically ill patients. Intensive Care Med. 2012, 38, 368–383. [Google Scholar] [CrossRef]
  38. Kampmeier, T.G.; Arnemann, P.H.; Hessler, M.; Bockbreder, K.; Wald, A.; Morelli, A.; Rehberg, S.W.; Ertmer, C. Effects of resuscitation with human albumin 5%, hydroxyethyl starch 130/0.4 6%, or crystalloid on kidney damage in an ovine model of septic shock. Br. J. Anaesth. 2018, 121, 581–587. [Google Scholar] [CrossRef] [Green Version]
  39. Finfer, S.; Bellomo, R.; Boyce, N.; French, J.; Myburgh, J.; Norton, R. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N. Engl. J. Med. 2004, 350, 2247–2256. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  40. Yunos, N.M.; Bellomo, R.; Hegarty, C.; Story, D.; Ho, L.; Bailey, M. Association between a chloride-liberal vs chloride-restrictive intravenous fluid administration strategy and kidney injury in critically ill adults. JAMA 2012, 308, 1566–1572. [Google Scholar] [CrossRef] [Green Version]
  41. Yunos, N.M.; Kim, I.B.; Bellomo, R.; Bailey, M.; Ho, L.; Story, D.; Gutteridge, G.A.; Hart, G.K. The biochemical effects of restricting chloride-rich fluids in intensive care. Crit. Care Med. 2011, 39, 2419–2424. [Google Scholar] [CrossRef]
  42. Zhang, L.; Chen, Z.; Diao, Y.; Yang, Y.; Fu, P. Associations of fluid overload with mortality and kidney recovery in patients with acute kidney injury: A systematic review and meta-analysis. J. Crit. Care 2015, 30, 860.e7–860.e13. [Google Scholar] [CrossRef] [PubMed]
  43. Selewski, D.T.; Goldstein, S.L. The role of fluid overload in the prediction of outcome in acute kidney injury. Pediatr. Nephrol. 2018, 33, 13–24. [Google Scholar] [CrossRef] [PubMed]
  44. Montomoli, J.; Donati, A.; Ince, C. Acute Kidney Injury and Fluid Resuscitation in Septic Patients: Are We Protecting the Kidney? Nephron 2019, 143, 170–173. [Google Scholar] [CrossRef] [PubMed]
  45. Gelman, S. Venous function and central venous pressure: A physiologic story. Anesthesiology 2008, 108, 735–748. [Google Scholar] [CrossRef] [Green Version]
  46. Reems, M.M.; Aumann, M. Central venous pressure: Principles, measurement, and interpretation. Compend. Contin. Educ. Vet. 2012, 34, E1. [Google Scholar] [PubMed]
  47. Chen, C.Y.; Zhou, Y.; Wang, P.; Qi, E.Y.; Gu, W.J. Elevated central venous pressure is associated with increased mortality and acute kidney injury in critically ill patients: A meta-analysis. Crit. Care 2020, 24, 80. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  48. Huo, Y.; Wang, X.; Li, B.; Rello, J.; Kim, W.Y.; Wang, X.; Hu, Z. Impact of central venous pressure on the mortality of patients with sepsis-related acute kidney injury: A propensity score-matched analysis based on the MIMIC IV database. Ann. Transl. Med. 2022, 10, 199. [Google Scholar] [CrossRef]
  49. Nadeau-Fredette, A.C.; Bouchard, J. Fluid management and use of diuretics in acute kidney injury. Adv. Chronic Kidney Dis. 2013, 20, 45–55. [Google Scholar] [CrossRef]
  50. Malbrain, M.L.; Marik, P.E.; Witters, I.; Cordemans, C.; Kirkpatrick, A.W.; Roberts, D.J.; Van Regenmortel, N. Fluid overload, de-resuscitation, and outcomes in critically ill or injured patients: A systematic review with suggestions for clinical practice. Anaesthesiol. Intensive Ther. 2014, 46, 361–380. [Google Scholar] [CrossRef]
  51. Kirkpatrick, A.W.; Roberts, D.J.; De Waele, J.; Jaeschke, R.; Malbrain, M.L.; De Keulenaer, B.; Duchesne, J.; Bjorck, M.; Leppaniemi, A.; Ejike, J.C.; et al. Intra-abdominal hypertension and the abdominal compartment syndrome: Updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med. 2013, 39, 1190–1206. [Google Scholar] [CrossRef] [PubMed]
  52. Kirkpatrick, A.W.; Roberts, D.J.; Jaeschke, R.; De Waele, J.J.; De Keulenaer, B.L.; Duchesne, J.; Bjorck, M.; Leppäniemi, A.; Ejike, J.C.; Sugrue, M.; et al. Methodological background and strategy for the 2012-2013 updated consensus definitions and clinical practice guidelines from the abdominal compartment society. Anaesthesiol. Intensive Ther. 2015, 47, S63–S77. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  53. Ruslan, M.A.; Baharuddin, K.A.; Noor, N.M.; Yazid, M.B.; Noh, A.Y.M.; Rahman, A. Norepinephrine in Septic Shock: A Systematic Review and Meta-analysis. West. J. Emerg. Med. 2021, 22, 196–203. [Google Scholar] [CrossRef] [PubMed]
  54. Hamzaoui, O.; Scheeren, T.W.L.; Teboul, J.L. Norepinephrine in septic shock: When and how much? Curr. Opin. Crit. Care 2017, 23, 342–347. [Google Scholar] [CrossRef]
  55. Bellomo, R.; Giantomasso, D.D. Noradrenaline and the kidney: Friends or foes? Crit. Care 2001, 5, 294–298. [Google Scholar] [CrossRef]
  56. Di Giantomasso, D.; May, C.N.; Bellomo, R. Norepinephrine and vital organ blood flow during experimental hyperdynamic sepsis. Intensive Care Med. 2003, 29, 1774–1781. [Google Scholar] [CrossRef]
  57. Lankadeva, Y.R.; Kosaka, J.; Evans, R.G.; Bailey, S.R.; Bellomo, R.; May, C.N. Intrarenal and urinary oxygenation during norepinephrine resuscitation in ovine septic acute kidney injury. Kidney Int. 2016, 90, 100–108. [Google Scholar] [CrossRef]
  58. Calzavacca, P.; Evans, R.G.; Bailey, M.; Bellomo, R.; May, C.N. Variable responses of regional renal oxygenation and perfusion to vasoactive agents in awake sheep. Am. J. Physiol.-Regul. Integr. Comp. Physiol. 2015, 309, R1226–R1233. [Google Scholar] [CrossRef] [Green Version]
  59. Du, Y.; Wang, L.; Shi, H.; Gao, M. Comparison of clinical effect of dopamine and norepinephrine in the treatment of septic shock. Pak. J. Pharm. Sci. 2015, 28, 1461–1464. [Google Scholar]
  60. De Backer, D.; Scolletta, S. Clinical management of the cardiovascular failure in sepsis. Curr. Vasc. Pharmacol. 2013, 11, 222–242. [Google Scholar]
  61. Lauschke, A.; Teichgräber, U.K.; Frei, U.; Eckardt, K.U. ‘Low-dose’ dopamine worsens renal perfusion in patients with acute renal failure. Kidney Int. 2006, 69, 1669–1674. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  62. De Backer, D.; Aldecoa, C.; Njimi, H.; Vincent, J.L. Dopamine versus norepinephrine in the treatment of septic shock: A meta-analysis. Crit. Care Med. 2012, 40, 725–730. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  63. Ventura, A.M.; Shieh, H.H.; Bousso, A.; Góes, P.F.; de Cássia, F.O.F.I.; de Souza, D.C.; Paulo, R.L.; Chagas, F.; Gilio, A.E. Double-Blind Prospective Randomized Controlled Trial of Dopamine Versus Epinephrine as First-Line Vasoactive Drugs in Pediatric Septic Shock. Crit. Care Med. 2015, 43, 2292–2302. [Google Scholar] [CrossRef] [PubMed]
  64. Xu, B.; Peter, O. Dopamine versus noradrenaline in septic shock. Australas. Med. J. 2011, 4, 571–574. [Google Scholar] [CrossRef]
  65. Kohn-Loncarica, G.; Fustiñana, A.; Santos, C.; Lantelli, G.P.; Rowensztein, H.; González-Dambrauskas, S. Clinical outcome of children with fluid-refractory septic shock treated with dopamine or epinephrine. A retrospective study at a pediatric emergency department in Argentina. Rev. Bras. Ter. Intensiv. 2020, 32, 551–556. [Google Scholar] [CrossRef]
  66. Belletti, A.; Benedetto, U.; Biondi-Zoccai, G.; Leggieri, C.; Silvani, P.; Angelini, G.D.; Zangrillo, A.; Landoni, G. The effect of vasoactive drugs on mortality in patients with severe sepsis and septic shock. A network meta-analysis of randomized trials. J. Crit. Care 2017, 37, 91–98. [Google Scholar] [CrossRef] [Green Version]
  67. Russell, J.A. Bench-to-bedside review: Vasopressin in the management of septic shock. Crit. Care 2011, 15, 226. [Google Scholar] [CrossRef] [Green Version]
  68. Der-Nigoghossian, C.; Hammond, D.A.; Ammar, M.A. Narrative Review of Controversies Involving Vasopressin Use in Septic Shock and Practical Considerations. Ann. Pharmacother. 2020, 54, 706–714. [Google Scholar] [CrossRef]
  69. Di Giantomasso, D.; Morimatsu, H.; Bellomo, R.; May, C.N. Effect of low-dose vasopressin infusion on vital organ blood flow in the conscious normal and septic sheep. Anaesth. Intensive Care 2006, 34, 427–433. [Google Scholar] [CrossRef] [Green Version]
  70. Okazaki, N.; Iguchi, N.; Evans, R.G.; Hood, S.G.; Bellomo, R.; May, C.N.; Lankadeva, Y.R. Beneficial Effects of Vasopressin Compared With Norepinephrine on Renal Perfusion, Oxygenation, and Function in Experimental Septic Acute Kidney Injury. Crit. Care Med. 2020, 48, e951–e958. [Google Scholar] [CrossRef]
  71. Wang, J.; Shi, M.; Huang, L.; Li, Q.; Meng, S.; Xu, J.; Xue, M.; Xie, J.; Liu, S.; Huang, Y. Addition of terlipressin to norepinephrine in septic shock and effect of renal perfusion: A pilot study. Ren. Fail. 2022, 44, 1207–1215. [Google Scholar] [CrossRef] [PubMed]
  72. Huang, H.; Wu, C.; Shen, Q.; Xu, H.; Fang, Y.; Mao, W. The effect of early vasopressin use on patients with septic shock: A systematic review and meta-analysis. Am. J. Emerg. Med. 2021, 48, 203–208. [Google Scholar] [CrossRef]
  73. Gordon, A.C.; Mason, A.J.; Thirunavukkarasu, N.; Perkins, G.D.; Cecconi, M.; Cepkova, M.; Pogson, D.G.; Aya, H.D.; Anjum, A.; Frazier, G.J.; et al. Effect of Early Vasopressin vs Norepinephrine on Kidney Failure in Patients With Septic Shock: The VANISH Randomized Clinical Trial. JAMA 2016, 316, 509–518. [Google Scholar] [CrossRef]
  74. Khanna, A.; English, S.W.; Wang, X.S.; Ham, K.; Tumlin, J.; Szerlip, H.; Busse, L.W.; Altaweel, L.; Albertson, T.E.; Mackey, C.; et al. Angiotensin II for the Treatment of Vasodilatory Shock. N. Engl. J. Med. 2017, 377, 419–430. [Google Scholar] [CrossRef] [PubMed]
  75. Nishiyama, A.; Kobori, H. Independent regulation of renin-angiotensin-aldosterone system in the kidney. Clin. Exp. Nephrol. 2018, 22, 1231–1239. [Google Scholar] [CrossRef] [Green Version]
  76. Patzak, A.; Lai, E.; Persson, P.B.; Persson, A.E. Angiotensin II-nitric oxide interaction in glomerular arterioles. Clin. Exp. Pharm. Physiol. 2005, 32, 410–414. [Google Scholar] [CrossRef] [PubMed]
  77. Lankadeva, Y.R.; Kosaka, J.; Evans, R.G.; Bellomo, R.; May, C.N. Urinary Oxygenation as a Surrogate Measure of Medullary Oxygenation during Angiotensin II Therapy in Septic Acute Kidney Injury. Crit. Care Med. 2018, 46, e41–e48. [Google Scholar] [CrossRef] [PubMed]
  78. Wan, L.; Langenberg, C.; Bellomo, R.; May, C.N. Angiotensin II in experimental hyperdynamic sepsis. Crit. Care 2009, 13, R190. [Google Scholar] [CrossRef] [Green Version]
  79. Tumlin, J.A.; Murugan, R.; Deane, A.M.; Ostermann, M.; Busse, L.W.; Ham, K.R.; Kashani, K.; Szerlip, H.M.; Prowle, J.R.; Bihorac, A.; et al. Outcomes in Patients with Vasodilatory Shock and Renal Replacement Therapy Treated with Intravenous Angiotensin II. Crit. Care Med. 2018, 46, 949–957. [Google Scholar] [CrossRef]
  80. Wen, L.; Xu, L. The efficacy of dopamine versus epinephrine for pediatric or neonatal septic shock: A meta-analysis of randomized controlled studies. Ital. J. Pediatr. 2020, 46, 6. [Google Scholar] [CrossRef] [Green Version]
  81. Baske, K.; Saini, S.S.; Dutta, S.; Sundaram, V. Epinephrine versus dopamine in neonatal septic shock: A double-blind randomized controlled trial. Eur. J. Pediatr. 2018, 177, 1335–1342. [Google Scholar] [CrossRef] [PubMed]
  82. Kellum, J.A.; Chawla, L.S.; Keener, C.; Singbartl, K.; Palevsky, P.M.; Pike, F.L.; Yealy, D.M.; Huang, D.T.; Angus, D.C. The Effects of Alternative Resuscitation Strategies on Acute Kidney Injury in Patients with Septic Shock. Am. J. Respir. Crit. Care Med. 2016, 193, 281–287. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  83. Maiden, M.J.; Otto, S.; Brealey, J.K.; Finnis, M.E.; Chapman, M.J.; Kuchel, T.R.; Nash, C.H.; Edwards, J.; Bellomo, R. Structure and Function of the Kidney in Septic Shock. A Prospective Controlled Experimental Study. Am. J. Respir. Crit. Care Med. 2016, 194, 692–700. [Google Scholar] [CrossRef] [PubMed]
  84. Evans, L.; Rhodes, A.; Alhazzani, W.; Antonelli, M.; Coopersmith, C.M.; French, C.; Machado, F.R.; McIntyre, L.; Ostermann, M.; Prescott, H.C.; et al. Surviving sepsis campaign: International guidelines for management of sepsis and septic shock 2021. Intensive Care Med. 2021, 47, 1181–1247. [Google Scholar] [CrossRef] [PubMed]
  85. Kato, R.; Pinsky, M.R. Personalizing blood pressure management in septic shock. Ann. Intensive Care 2015, 5, 41. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  86. Maheshwari, K.; Nathanson, B.H.; Munson, S.H.; Khangulov, V.; Stevens, M.; Badani, H.; Khanna, A.K.; Sessler, D.I. The relationship between ICU hypotension and in-hospital mortality and morbidity in septic patients. Intensive Care Med. 2018, 44, 857–867. [Google Scholar] [CrossRef] [Green Version]
  87. Poukkanen, M.; Wilkman, E.; Vaara, S.T.; Pettilä, V.; Kaukonen, K.M.; Korhonen, A.M.; Uusaro, A.; Hovilehto, S.; Inkinen, O.; Laru-Sompa, R.; et al. Hemodynamic variables and progression of acute kidney injury in critically ill patients with severe sepsis: Data from the prospective observational FINNAKI study. Crit. Care 2013, 17, R295. [Google Scholar] [CrossRef] [Green Version]
  88. Ko, C.H.; Lan, Y.W.; Chen, Y.C.; Cheng, T.T.; Yu, S.F.; Cidem, A.; Liu, Y.H.; Kuo, C.W.; Yen, C.C.; Chen, W.; et al. Effects of Mean Artery Pressure and Blood pH on Survival Rate of Patients with Acute Kidney Injury Combined with Acute Hypoxic Respiratory Failure: A Retrospective Study. Medicina 2021, 57, 1243. [Google Scholar] [CrossRef]
  89. Badin, J.; Boulain, T.; Ehrmann, S.; Skarzynski, M.; Bretagnol, A.; Buret, J.; Benzekri-Lefevre, D.; Mercier, E.; Runge, I.; Garot, D.; et al. Relation between mean arterial pressure and renal function in the early phase of shock: A prospective, explorative cohort study. Crit. Care 2011, 15, R135. [Google Scholar] [CrossRef] [Green Version]
  90. Moman, R.N.; Ostby, S.A.; Akhoundi, A.; Kashyap, R.; Kashani, K. Impact of individualized target mean arterial pressure for septic shock resuscitation on the incidence of acute kidney injury: A retrospective cohort study. Ann. Intensive Care 2018, 8, 124. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  91. Cecconi, M.; De Backer, D.; Antonelli, M.; Beale, R.; Bakker, J.; Hofer, C.; Jaeschke, R.; Mebazaa, A.; Pinsky, M.R.; Teboul, J.L.; et al. Consensus on circulatory shock and hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Intensive Care Med. 2014, 40, 1795–1815. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  92. Dewitte, A.; Labat, A.; Duvignaud, P.A.; Bouche, G.; Joannes-Boyau, O.; Ripoche, J.; Hilbert, G.; Gruson, D.; Rubin, S.; Ouattara, A.; et al. High mean arterial pressure target to improve sepsis-associated acute kidney injury in patients with prior hypertension: A feasibility study. Ann. Intensive Care 2021, 11, 139. [Google Scholar] [CrossRef] [PubMed]
  93. Asfar, P.; Meziani, F.; Hamel, J.F.; Grelon, F.; Megarbane, B.; Anguel, N.; Mira, J.P.; Dequin, P.F.; Gergaud, S.; Weiss, N.; et al. High versus low blood-pressure target in patients with septic shock. N. Engl. J. Med. 2014, 370, 1583–1593. [Google Scholar] [CrossRef]
  94. Panwar, R.; Lanyon, N.; Davies, A.R.; Bailey, M.; Pilcher, D.; Bellomo, R. Mean perfusion pressure deficit during the initial management of shock—An observational cohort study. J. Crit. Care 2013, 28, 816–824. [Google Scholar] [CrossRef]
  95. Ostermann, M.; Hall, A.; Crichton, S. Low mean perfusion pressure is a risk factor for progression of acute kidney injury in critically ill patients—A retrospective analysis. BMC Nephrol. 2017, 18, 151. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  96. Wong, B.T.; Chan, M.J.; Glassford, N.J.; Mårtensson, J.; Bion, V.; Chai, S.Y.; Oughton, C.; Tsuji, I.Y.; Candal, C.L.; Bellomo, R. Mean arterial pressure and mean perfusion pressure deficit in septic acute kidney injury. J. Crit. Care 2015, 30, 975–981. [Google Scholar] [CrossRef] [PubMed]
  97. Panwar, R.; Van Haren, F.; Cazzola, F.; Nourse, M.; Brinkerhoff, G.; Quail, A. Standard care versus individualized blood pressure targets among critically ill patients with shock: A multicenter feasibility and preliminary efficacy study. J. Crit. Care 2022, 70, 154052. [Google Scholar] [CrossRef]
  98. Romagnoli, S.; Ricci, Z.; Ronco, C. CRRT for sepsis-induced acute kidney injury. Curr. Opin. Crit. Care 2018, 24, 483–492. [Google Scholar] [CrossRef]
  99. Gibney, N.; Cerda, J.; Davenport, A.; Ramirez, J.; Singbartl, K.; Leblanc, M.; Ronco, C. Volume management by renal replacement therapy in acute kidney injury. Int. J. Artif. Organs 2008, 31, 145–155. [Google Scholar] [CrossRef]
  100. Legrand, M.; Darmon, M.; Joannidis, M.; Payen, D. Management of renal replacement therapy in ICU patients: An international survey. Intensive Care Med. 2013, 39, 101–108. [Google Scholar] [CrossRef]
  101. Summary of Recommendation Statements. Kidney Int. Suppl. 2012, 2, 8–12. [CrossRef] [PubMed] [Green Version]
  102. Schortgen, F.; Soubrier, N.; Delclaux, C.; Thuong, M.; Girou, E.; Brun-Buisson, C.; Lemaire, F.; Brochard, L. Hemodynamic tolerance of intermittent hemodialysis in critically ill patients: Usefulness of practice guidelines. Am. J. Respir. Crit. Care Med. 2000, 162, 197–202. [Google Scholar] [CrossRef] [PubMed]
  103. Vodovar, D.; Mégarbane, B. Extracorporeal Kidney-Replacement Therapy for Acute Kidney Injury. N. Engl. J. Med. 2022, 386, 2250. [Google Scholar] [CrossRef] [PubMed]
  104. Fathima, N.; Kashif, T.; Janapala, R.N.; Jayaraj, J.S.; Qaseem, A. Single-best Choice Between Intermittent Versus Continuous Renal Replacement Therapy: A Review. Cureus 2019, 11, e5558. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  105. Shawwa, K.; Kompotiatis, P.; Jentzer, J.C.; Wiley, B.M.; Williams, A.W.; Dillon, J.J.; Albright, R.C.; Kashani, K.B. Hypotension within one-hour from starting CRRT is associated with in-hospital mortality. J. Crit. Care 2019, 54, 7–13. [Google Scholar] [CrossRef] [PubMed]
  106. Santiago, M.J.; López-Herce, J.; Urbano, J.; Solana, M.J.; del Castillo, J.; Sánchez, A.; Bellón, J.M. Continuous renal replacement therapy in children after cardiac surgery. J. Thorac. Cardiovasc. Surg. 2013, 146, 448–454. [Google Scholar] [CrossRef] [Green Version]
  107. Kim, Y.; Yun, D.; Kwon, S.; Jin, K.; Han, S.; Kim, D.K.; Oh, K.H.; Joo, K.W.; Kim, Y.S.; Kim, S.; et al. Target value of mean arterial pressure in patients undergoing continuous renal replacement therapy due to acute kidney injury. BMC Nephrol. 2021, 22, 20. [Google Scholar] [CrossRef]
  108. Wang, Y.; Gallagher, M.; Li, Q.; Lo, S.; Cass, A.; Finfer, S.; Myburgh, J.; Bouman, C.; Faulhaber-Walter, R.; Kellum, J.A.; et al. Renal replacement therapy intensity for acute kidney injury and recovery to dialysis independence: A systematic review and individual patient data meta-analysis. Nephrol. Dial. Transplant. 2018, 33, 1017–1024. [Google Scholar] [CrossRef] [Green Version]
  109. Gaudry, S.; Hajage, D.; Schortgen, F.; Martin-Lefevre, L.; Pons, B.; Boulet, E.; Boyer, A.; Chevrel, G.; Lerolle, N.; Carpentier, D.; et al. Initiation Strategies for Renal-Replacement Therapy in the Intensive Care Unit. N. Engl. J. Med. 2016, 375, 122–133. [Google Scholar] [CrossRef]
  110. Xing, Z.Q.; Liu, D.W.; Wang, X.T.; Long, Y.; Zhang, H.M.; Pan, P.; Su, L.X. Early initiation renal replacement therapy for fluid management to reduce central venous pressure is more conducive to renal function recovery in patients with acute kidney injury. Chin. Med. J. 2019, 132, 1328–1335. [Google Scholar] [CrossRef]
  111. Hellman, T.; Uusalo, P.; Järvisalo, M.J. Renal Replacement Techniques in Septic Shock. Int. J. Mol. Sci. 2021, 22, 10238. [Google Scholar] [CrossRef] [PubMed]
  112. Schwindenhammer, V.; Girardot, T.; Chaulier, K.; Grégoire, A.; Monard, C.; Huriaux, L.; Illinger, J.; Leray, V.; Uberti, T.; Crozon-Clauzel, J.; et al. oXiris® Use in Septic Shock: Experience of Two French Centres. Blood Purif. 2019, 47 (Suppl. S3), 29–35. [Google Scholar] [CrossRef] [PubMed]
  113. Gabriel, D.P.; Caramori, J.T.; Martim, L.C.; Barretti, P.; Balbi, A.L. High volume peritoneal dialysis vs daily hemodialysis: A randomized, controlled trial in patients with acute kidney injury. Kidney Int. Suppl. 2008, 73, S87–S93. [Google Scholar] [CrossRef] [PubMed]
Jcm 12 01018 g001 550
Figure 1. Pathophysiological mechanism of microcirculatory dysfunction affecting renal function in sepsis. TGF, tubuloglomerular feedback mechanism.
Figure 1. Pathophysiological mechanism of microcirculatory dysfunction affecting renal function in sepsis. TGF, tubuloglomerular feedback mechanism.
Jcm 12 01018 g001
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.

Share and Cite

MDPI and ACS Style

Deng, J.; Li, L.; Feng, Y.; Yang, J. Comprehensive Management of Blood Pressure in Patients with Septic AKI. J. Clin. Med. 2023, 12, 1018. https://doi.org/10.3390/jcm12031018

AMA Style

Deng J, Li L, Feng Y, Yang J. Comprehensive Management of Blood Pressure in Patients with Septic AKI. Journal of Clinical Medicine. 2023; 12(3):1018. https://doi.org/10.3390/jcm12031018

Chicago/Turabian Style

Deng, Junhui, Lina Li, Yuanjun Feng, and Jurong Yang. 2023. "Comprehensive Management of Blood Pressure in Patients with Septic AKI" Journal of Clinical Medicine 12, no. 3: 1018. https://doi.org/10.3390/jcm12031018

APA Style

Deng, J., Li, L., Feng, Y., & Yang, J. (2023). Comprehensive Management of Blood Pressure in Patients with Septic AKI. Journal of Clinical Medicine, 12(3), 1018. https://doi.org/10.3390/jcm12031018

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop