Neurocrit Care

https://doi.org/10.1007/s12028-021-01345-7

REVIEW ARTICLE

Acute Kidney Injury at the Neurocritical Care

Unit
Gonzalo Ramírez‑Guerrero1,2,3*  , Romyna Baghetti‑Hernández1,3 and Claudio Ronco4,5,6

© 2021 Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society

Abstract 
Neurocritical care has advanced substantially in recent decades, allowing doctors to treat patients with more com‑
plicated conditions who require a multidisciplinary approach to achieve better clinical outcomes. In neurocritical
patients, nonneurological complications such as acute kidney injury (AKI) are independent predictors of worse clinical
outcomes. Different research groups have reported an AKI incidence of 11.6% and an incidence of stage 3 AKI, accord‑
ing to the Kidney Disease: Improving Global Outcomes, that requires dialysis of 3% to 12% in neurocritical patients.
These patients tend to be younger, have less comorbidity, and have a different risk profile, given the diagnostic and
therapeutic procedures they undergo. Trauma-induced AKI, sepsis, sympathetic overstimulation, tubular epitheliopa‑
thy, hyperchloremia, use of nephrotoxic drugs, and renal hypoperfusion are some of the causes of AKI in neurocritical
patients. AKI is the result of a sum of events, although the mechanisms underlying many of them remain uncertain;
however, two important causes that merit mention are direct alteration of the physiological brain–kidney connection
and exposure to injury as a result of the specific medical management and well-established therapies that neurocriti‑
cal patients are subjected to. This review will focus on AKI in neurocritical care patients. Specifically, it will discuss its
epidemiology, causes, associated mechanisms, and relationship to the brain–kidney axis. Additionally, the use and
risks of extracorporeal therapies in this group of patients will be reviewed.
Keywords:  Acute kidney injury, Critical care, Renal replacement therapy, Traumatic brain injury, Subarachnoid
hemorrhage, Cerebral hemorrhage, Stroke, Dialysis

Introduction mortality can be as high as 60–80% [4]. This is a frequent

Neurocritical care has advanced substantially in recent scenario; there are reports of additional organ dysfunc-
decades. New neuromonitoring techniques, therapies, tion apart from central nervous system (CNS) lesions in
and endovascular procedures have emerged [1] to meet up to 81% of patients [5].
the needs of patients with more complicated conditions This review will focus on AKI in neurocritical care
who require a multidisciplinary approach to achieve bet- patients. Specifically, it will discuss its epidemiology,
ter clinical outcomes. causes, associated mechanisms, and relationship to the
Acute kidney injury (AKI) is a systemic disease that brain–kidney axis. Additionally, the use and risks of
is one of the most frequent and severe complications in extracorporeal therapies in this group of patients will be
patients who are critically ill because of its high morbidity reviewed.
and mortality and economic impact [2, 3]. The increased
mortality associated with it is even higher when it is pre- Epidemiology and Outcomes of AKI in Neurocritical
sent along with dysfunction of another organ; in this case, Pathologies
Nonneurological complications in neurocritical
patients are known to be independent predictors of
*Correspondence: [email protected] worse clinical outcomes [6]. There are few reports on
1
Critical Care Unit, Carlos Van Buren Hospital, Valparaíso, Chile
Full list of author information is available at the end of the article the incidence, prognosis, and risk factors of AKI in
neurocritical patients or on individual pathologies, such nomogram specified ten risk factors for predicting the
as acute ischemic stroke (AIS) [7], traumatic brain injury occurrence of AKI, with an area under the curve of 0.87.
(TBI) [8], intracerebral hemorrhage (ICH), or subarach- The risk factors included are Glasgow Coma Scale classi-
noid hemorrhage (SAH) [9]. Neurocritical patients tend fication; hypertension; coronary disease; pneumonia and
to be younger, have less comorbidity, and have a different heart failure in the first 7 days of hospitalization; and use
risk profile, given the diagnostic and therapeutic proce- of furosemide, torsemide, dopamine, and norepineph-
dures they undergo. rine [21]. Covic et al. [11] reported the independent risk
Different research groups have reported an AKI inci- factors of AKI of older age, reduced glomerular filtra-
dence of 11.6% in neurocritical patients in general, with tion rate (GFR), and type of AIS. One of the most often
rates that vary according to the specific pathology: an reported risk factors for the onset of AKI in neurocritical
incidence of 9.2% has been reported in patients with TBI and nonneurocritical patients is the presence of chronic
[10], 14.5% to 20.9% in patients with AIS, 19% in patients kidney disease [12].
with ICH, and 12% to 23.1% in patients with SAH [9–15] These severity scores have the limitation of limited
(Table 1). AKI can result in an up to fivefold increase in external validation, which suggests a poor capacity to dis-
mortality in direct relation to its severity, lead to poorer cern at-risk patients.
functional recovery, and increase the possibility of mod-
erate-to-severe disability at hospital discharge [9, 12, 16,
17]. An incidence of 3% to 12% of stage 3 AKI, accord- Physiopathology of AKI in Neurocritical Care Unit
ing to the Kidney Diseases: Improving Global Outcomes Patients
[18], has been reported to require dialysis; this is linked The Brain–Kidney Connection
to higher mortality rates (50% to 70%) and severe disabil- The brain and kidneys share a complex crosstalk to main-
ity because of a lower possibility of intrahospital rehabili- tain homeostasis. The term crosstalk refers to organ
tation in this subgroup of patients [12, 19]. interaction via biological communication through central
and peripheral pathways (Fig. 1) [22]. Given this relation-
Risk Factors of AKI in Neurocritical Care Unit ship, AKI can generate anatomical, functional, and bio-
Patients chemical changes in the brain, such as changes in the
Acute kidney injury risk prediction is fundamental for concentration of neurotransmitters and cytokines, acid–
planning diagnostic and therapeutic procedures in neu- base homeostasis, and drug metabolism; this can cause
rocritical patients. Multiple specific renal severity scores direct and indirect injuries [23]. Concomitantly, effer-
have been published (Liaño, Bullock, and Chertow, ent impulses from the CNS can increase renal sympa-
among others) [20], but only one nomogram for neuro- thetic activity causing renin secretion, increasing tubular
critical patients has been reported [21]. An et  al.’s [21] sodium absorption, and decreasing renal blood flow [24].

Table 1  Studies showing incidence of AKI in neurological diseases

Study Year published Patients (n) Diseases Incidence Diagnosis criteria

Tsagalis [7] 2009 1,350 Stroke 14.29% AKIN

Corral [8] 2012 224 TBI 8% RIFLE
Zacharia [9] 2009 787 SAH 23.1% RIFLE
Moore [10] 2010 207 TBI 9.2% RIFLE
Covic [11] 2008 1,090 Stroke 14.5% RIFLE
Büttner [12] 2020 681 Alla 11.6% AKIN
Zorrilla-Vaca [13],b 2017 5,147,754/615,623 Stroke/ICH 12.9%/19% AKIN
Tujjar [14] 2017 202 SAH 12% AKIN
Wang [15] 2018 647 Stroke 20.9% KDIGO
LI [16] 2011 136 TBI 23% AKIN
Sadan [54] 2017 1,267 SAH 16.7% KDIGO
Eagles [87] 2019 413 SAH 38% KDIGO
AKI acute kidney injury, AKIN acute kidney injury network, CNS central nervous system, ICH intracerebral hemorrhage, KDIGO Kidney Disease: Improving Global
Outcomes, RIFLE Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease, SAH subarachnoid hemorrhage, TBI traumatic brain injury
a
  Neurologic autoimmune disorder, intracranial hemorrhage, infection of the CNS, ischemic stroke, tumor, others
b
 Meta-analysis
 Fig. 1  Kidney–brain axis interaction. Role of acute kidney injury and acute brain injury in inflammation, sympathetic nervous system, uremic state,
and diseases related to these mechanisms. DAMPs, damage-associated molecular patterns, GFR, glomerular filtration rate, PAMPs, pathogen-associ‑
ated molecular patterns, SAH, subarachnoid hemorrhage, TBI, traumatic brain injury

Inflammation cause of BBB alteration [27, 28] through facilitation of an

Experimental evidence from an animal model of AKI has influx of water and solutes. Only in AKI models—not in
modeled the brain–kidney axis in regard to inflamma- other models of systemic inflammation—has an increase
tion. High levels of inflammatory cytokines in the brain been observed in the cerebral cortex and corpus callosum
and cellular inflammation in astrocytes and microglia, of keratinocyte-derived chemoattractants and granulo-
together with anatomic and functional injuries, increased cyte colony-stimulating factor, along with specific mark-
blood–brain barrier (BBB) permeability and pyknosis in ers of brain inflammation and extravasation of Evans
neuronal cells [25]. The mechanism that underlies the blue dye in the brain [25]. In animal models, a direct
increase in BBB permeability is not well described. AKI effect of TNF-α and an indirect effect of the upregulation
increases proinflammatory cytokines and decreases their of matrix metalloproteinase 9 has been demonstrated,
clearance, thus increasing the inflammatory response which can alter endothelial tight junctions with water and
[26]. This suggests that this inflammatory state, as well as protein extravasation, resulting in vasogenic edema [29,
other states by entities such as sepsis or liver failure, is a 30]. This is enhanced through aquaporins-4 expression
that is 2.5 times higher than normal, an increase induced parallelism between the vascular beds of both organs to
by the kidney disease [31]. ensure adequate perfusion [36, 37] and close manage-
This inflammatory state is also triggered from the brain ment of sodium correction, fluid tonicity, and water bal-
to the kidney. Evidence from brain-dead kidney donors ance [38].
has shown greater renal inflammation, with infiltration This cerebrovascular and renal regulation is altered
of T-lymphocytes and macrophages. After perfusing in neurocritical patients. It has been observed that sus-
these kidneys, cytokine release was observed, which is a tained cerebral autoregulation in patients with neurocrit-
stimulating factor of granulocyte colonies, IL-6, IL-9, and ical pathologies is associated with renal hyperfiltration
MCP-1 [32]. and that loss of cerebral autoregulation may contribute to
an alteration of renal autoregulation, generating a decline
Neurotransmitter alteration in creatinine clearance and increasing susceptibility of
Neurotransmitter transport is also affected when there developing AKI [39].
is an alteration of BBB permeability. Animal studies have Kidney hyperfiltration is a frequent finding in neuro-
shown that AKI interferes with the Na + independent critical care patients and this phenomenon has implica-
cationic amino acid transporter (CAT1/SLC7A1), which tions on drug pharmacokinetics [39–41]. Several authors
regulates the influence of L-arginine and thus taurine, have reported faster elimination of levetiracetam after
alanine, glycine, and creatine. This generates accumula- neurologic injury, with the consequent risk of underdos-
tion and/or depletion of amino acids and neurotransmit- ing for treatment or prophylaxis [42, 43]. The mecha-
ters in CNS as well as others that are strictly regulated nisms that promote increased renal clearance remain
to maintain low concentrations in cerebral tissue, such as poorly understood. Some of those which have been pro-
glutamate, glycine, and gamma-aminobutyric acid [33]. posed are aggressive fluid resuscitation and vasopressor
Metabolic acidosis generated by AKI plays a role in support, systemic inflammation after trauma, cytokine
altering neurotransmitter homeostasis and the traffic of storm, hypertonic solutions, increased atrial natriuretic
neurotransmitters between astrocytes and neurons. Cell peptide and brain–kidney crosstalk in an inflammatory
acidification increases the oxidative deamination of glu- state, and increased sympathetic nervous system activity
tamate through glutamate dehydrogenase, generating as common pathways [27, 44–48].
an excess of ammonia and, in consequence, altering the
cycle of neurotransmitters [27, 34, 35]. Causes of AKI in neurocritical care unit patients
TBI‑induced AKI
Blood flow dysregulation Acute kidney injury develops without severe episodes of
The brain and kidney have a vascular autoregulation systemic hypoperfusion and nephrotoxin exposure [49].
mechanism which maintains blood flow constant despite The mechanisms proposed in the literature were the fol-
variations in blood pressure; there is a hemodynamic lowing (Table 2):

Table 2  Relevant mechanisms in AKI

AKI in TBI AKI in SAH AKI in AIS and ICH

Sepsis-associated AKI Sepsis-associated AKI Sepsis-associated AKI

Trauma-related AKI Induced hydroelectrolytic disorders Renal hypoperfusion
Hemorrhagic shock Hypernatremia
Rhabdomyolysis Hyperchloremia
Oxidative stress
DAMPs/ PAMPs
Sympathetic hyperstimulation Contrast induced AKI Contrast associated AKI
Hyperactivity of SNS
Activation of HPA axis
Tubular epitheliopathy Osmotic nephrosis Osmotic nephrosis
Osmotic nephrosis Drug-induced AIN: Drug-induced AIN:
Levetiracetam [88–90] Levetiracetam [88–90]
Phenytoin [90] Phenytoin [90]
Drug-induced AIN: – –
Levetiracetam [88–90]
Phenytoin [90]
AIN acute interstitial nephritis, AIS acute ischemic stroke, AKI acute kidney injury, DAMPs damage-associated molecular patterns, HPA hypothalamic–pituitary–adrenal
axis, ICH intracerebral hemorrhage, PAMPs pathogen-associated molecular patterns, SAH subarachnoid hemorrhage, SNS sympathetic nervous system, TBI traumatic
brain injury
 1. Activation of the brain–kidney axis: intensive care unit admission [14] because of intensive
care unit-specific interventions and medical manage-
a. Sympathetic renal stimulation by sympa- ment strategies, such as use of hyperosmolar therapy and
thetic efferents, which induce the release of potential exposure to nephrotoxic agents such as intrave-
noradrenaline and adrenaline by the adrenal nous contrast media [52] (Table 2). The mechanisms are
gland. Catecholamines stimulate beta 1 adrener- the following:
gic receptors, increasing renin secretion by the
juxtaglomerular cells, which increases ­Na+ and 1. Hypernatremia and hyperchloremia due to use of
water reabsorption in addition to producing a hypertonic saline therapy:
vasopressor effect. Catecholamines also stimu- a. Hypertonic saline therapy is often used to con-
late alpha 1 adrenergic receptors in the kidney trol intracranial hypertension and hyponatremia.
vasculature, decreasing renal blood flow, GFR, Hypernatremia and hyperchloremia produce
and urine output [50]. intravascular dehydration and vasoconstric-
b. Activation of the hypothalamic–pituitary–adre- tion either directly or through tubuloglomerular
nal axis as a direct trauma-induced result that feedback mechanisms [52]. A randomized trial
increases endogenous catecholamines [50]. comparing a low-chloride (NaCl/Na-acetate)
versus high-chloride hypertonic solution (NaCl)
2. Functional alterations and apoptosis of renal tubular for patients who required hyperosmolar therapy
epithelial cells secondary to a systemic inflammatory for SAH revealed that the rate of AKI was higher
reaction in severe brain injury: in the NaCl group (53.3% vs. 11.8%, p = 0.01)
a. Increased proteinuria and plasma neutrophil and suggested that patients with a chloride level
gelatinase-associated lipocalin  (NGAL) have of 109 mmol/L or above are those at highest risk
been shown in one in vitro study. These markers for AKI [53, 54].
of tubular damage correlated with inflammatory 2. Contrast-induced AKI:
mediators, suggesting that acute brain damage a. The patient population with SAH has an
generates tubular injury. The cellular mechanism increased risk of contrast-induced nephropa-
proposed is based on the inflammatory media- thy through multiple exposures to IV contrast
tors such as IL-6, MCP-1, and MIP1 beta con- media secondary to the diagnosis and treatment
tained in the plasma of patients with TBI, which of intracranial aneurysm, such as computed
are involved in neutrophil adhesion to tubu- tomography angiography and coil embolization
lar epithelial cells. This injures the epithelium [55].
through the disassembly of tight junctions and
the degradation of elastases and matrix metallo-
proteinases [49]. AKI in AIS and Intracerebral Hemorrhage
3. Autonomic nervous system dysregulation: The mechanisms were the following:

a. An imbalance in the parasympathetic and sym- 1. Intensive reduction of systolic blood pressure in ICH:
pathetic pathway in patients with severe TBI a. As recommended by current guidelines, an
results in hyperactivity of the sympathetic nerv- acute reduction of systolic blood pressure to
ous system, causing a hyperadrenergic state or 140 mm Hg can improve functional outcomes in
paroxysmal sympathetic hyperactivity, as this patients with ICH [56], but it is strongly associ-
clinical condition is known. Any anatomical ated with AKI [57].
injury to areas that control the autonomic nerv- 2. Contrast-associated AKI in endovascular thrombec-
ous system can result in autonomic dysregula- tomy in AIS:
tion (hypothalamus, nucleus of the solitary tract, a. Additional exposure to contrast media in addi-
areas A1 to A5 of the medulla, and subforni- tion to what is received during diagnostic imag-
cal organ) and the increased sympathetic tone ing techniques along with use of intraarterial
results in renal vasoconstriction and decreased contrast increase the risk of contrast-associated
renal perfusion [51]. AKI more than intravenous contrast media. It
occurs in 1 out of 30 patients [58].
AKI in Subarachnoid Hemorrhage 3. Infusion rate of mannitol used to decrease intracra-
In contrast to TBI-induced AKI, SAH is not an early nial pressure in patients with ICH:
complication. Most episodes occur  > 
1  week after
 a. Mannitol accumulation in the extracellular space could explain this are increased oxygen consumption
causes an increase in local renal osmolality and secondary to ICP surges (associated with brain hyper-
osmotic nephrosis, renal vasoconstriction, and metabolism and increased oxygen consumption) and
deterioration of the GFR [59]. limited brain oxygen diffusion due to increased brain
water content [69].
One of the problems with IHD that is associated
Renal Replacement Therapy in Neurocritical Care with the rapid removal of urea, sodium, and other
Despite the undisputed benefit of renal replacement ther- osmoles from the vascular compartment is the com-
apy (RRT) in encephalopathy due to retention of nitrogen partmentalization of these osmoles at the intracranial
products and toxic drugs, metabolic acidosis, and sodium level. As this area has a slower removal rate, an osmo-
and water balance, these therapies may pose a risk to lar gradient is generated between the two compart-
neurocritical patients. They may cause dialysis-associated ments, which triggers the diffusion of water into the
neurovascular injury and affect the treatment prescribed brain and a significant increase in ICP during treat-
by the rest of the neurocritical unit team, regardless of ment [70, 71]. This phenomenon of dialysis disequilib-
the type of therapy used. rium syndrome and cerebral vasogenic edema [72] can
Intermittent and continuous therapies have been found be explained through different mechanisms. First, the
to be equally effective regarding mortality and/or dialysis reverse urea effect occurs, which is slower removal of
dependence, but reports have shown significant differ- urea from cerebrospinal fluid than from the blood dur-
ences in neurocritical patients [60]. The mechanism and ing IHD, causing the aforementioned gradient. This is
speed at which blood purification occurs is the major dif- subsequently supported by findings of urea transport-
ference between the two types of therapies: the goal of ers, which are downregulated in uremic states, caus-
removal uremic solutes through diffusion is achieved in a ing a reduced adaptive response in the brain to rapid
short period of time in the case of intermittent therapies changes in plasma urea and accentuated by overregula-
[61]. tion of aquaporin channels, increasing water entry into
This scenario affects the brain–kidney connection the brain regardless of the degree of urea reduction [31,
because of an effective therapy. The neurological conse- 70, 73, 74]. The second mechanism underlying dialysis
quences include de novo cerebral edema or an increase of disequilibrium syndrome is the hypothesis of idiogenic
existing edema, herniation, neurological impairment, or osmoles, in which osmotically active molecules (not
death; thus, neurocritical patients merit special consid- including urea, ­Na+, ­K+, or ­Cl−) contribute to cerebral
eration when planning RRT [62]. Our therapeutic goals edema [75]. The third mechanism is the hypothesis of
must be to prevent secondary damage by maintaining paradoxical CNS acidosis, in which the decreased brain
proper cerebral blood flow (CBF) and cerebral perfusion pH produced by the correction of systemic acidosis
pressure (CPP) together with intracranial pressure (ICP) through RRT with elevated bicarbonate concentrations
control, which may be significantly affected by these in the dialysate generates an osmotic gradient through
therapies, with their consequent prognostic implications the release of intracellular protein-bound sodium and
[63]. Continuous RRT (CRRT) has proven to be associ- potassium. This mechanism is accentuated by a reduc-
ated with better mean blood pressure, cardiac output, tion in CPP caused by the therapy, causing cerebral
and oxygen delivery outcomes compared with intermit- hypoxia and cerebral acidosis with the production of
tent hemodialysis (IHD). It offers a better hemodynamic local vasodilators, increasing vasogenic edema [76, 77].
profile and, therefore, better CPP and CBF control, which Unlike CRRT, IHD treatments can worsen the clinical
leads it to be associated with better neurological out- conditions of patients with cerebral edema because of
comes [63, 64]. a postdialytic influx of fluid into the brain (Fig.  2) [78].
Significant changes in the density of white and gray Therefore, CRRT should be the first option in these
matter have been observed after an IHD session in all patients (Table  3). Moreover, it has been suggested that
patients with increased water content in the brain, but citrate may provide neuroprotection by attenuating
these changes were not observed after CRRT [65]. In hypoxic brain injury through its effects on astrocytes and
addition, IHD has also been shown to lead to decreased oxidative phosphorylation [79].
circulating blood volume and decreased CBF, as has Nevertheless, if only IHD is available, the initial decline
been demonstrated by transcranial Doppler imaging. in osmolality should be moderated by slower dialysate
Furthermore, the absolute brain tissue oxygen tension and blood flows coupled with a smaller dialyzer sur-
level was lower during IHD [66, 67] and hypotension face, a high dialysate sodium content, and daily treat-
was more frequently reported as a complication of IHD ment to reduce changes in serum urea [80]. These factors
compared to CRRT [68]. Possible mechanisms that must be taken into account independently of the type of
 Fig. 2  Kidney–brain axis interaction and renal replacement therapy. AQ-4, aquaporin 4, BBB, blood–brain barrier, BUN, blood urea nitrogen, CNS,
central nervous system, Nt, neurotransmitters, UT, urea transporter

Table 3  Central nervous system effects of CRRT versus IHD this must be managed through the dialysate/replenished
IHD CRRT​
fluid in order to achieve the desired goal. Practical algo-
rithms, such as those reported by Dangoisse et al. [82]. or
Decreased circulatory blood volume Prefixed sodium formulas according to the sodium kinetic model can be
Decreased CBF Hypophosphatemia used. The must be modified for a single-pool, fixed-vol-
induced hypoxia due
to high affinity
ume equation to quantify the changes of natremia during
Decreased PbtO2 Anticoagulation
CRRT.
Increased ICP –   
Na(t) = Na0 + Nadial/RF) −Na0 × 1−e−Dt/V (1)

Cerebral vasodilation –
Changes in density of white and gray matter –
DDS/DANI –
where ­Nadial/RF is the sodium concentration in the solu-
tions; ­Na0 is the patient’s initial sodium level; D is the
CBF cerebral blood flow, CRRT​ continuous renal replacement therapy, DANI
dialysis-associated neurovascular injury, DDS dialysis disequilibrium syndrome,
effective sodium dialysance, which is almost the same as
ICP intracranial pressure, IHD intermittent hemodialysis, PbtO2 brain tissue effective urea clearance; t is the time from the beginning
oxygenation of CRRT; and V is the total volume of body water, esti-
mated via the Watson formula and with estimated edema
volume added on [83].
technique used and the patient’s plasma osmolality and
sodium and blood urea nitrogen (BUN) levels should be
routinely monitored. Hypophosphatemia and RRT​
Another key factor to consider during CRRT is the pres-
Natremia and CRRT​ ence of hypophosphatemia, which has been reported
A controlled correction of natremia or maintaining a in around 80% of patients who undergo these proce-
target natremia is essential when prescribing CRRT, dures [84]. Hypophosphatemia produces a decrease in
given that despite the safety elements mentioned above 2,3-diphosphoglycerate in erythrocytes, increasing the
regarding IHD, cases of significant reductions in osmo- affinity of hemoglobin for oxygen and causing a reduc-
larity—up to 35 mOsm/kg within the first 24 h of start- tion in intracellular adenosine triphosphate [85]. This
ing CRRT—have been observed [81]. A problem with disorder caused by CRRT can alter the multimodal moni-
CRRT replacement solutions is that the sodium in them toring values in the case of brain tissue oxygen tension
is prefixed, ranging from 136 to 140 mmol/L. Therefore, by causing hypoxia due to high affinity. Therefore, when
it is present, supplementation with 1.2 to 2  mmol/L of
phosphorus in the replenishment/dialysis solutions is an Declarations
option [86]. Conflict of interest
Regardless of the cause that leads to starting RRT, The authors report no conflicts of interest. The authors declare that they have
nephrologists must be extremely cautious with find- no known competing financial interests or personal relationships that could
have appeared to influence the work reported in this article. The authors alone
ings that suggest edema, dialysate composition, and are responsible for the content and writing of this article.
changes in plasma osmolality. They must consider not
only sodium and BUN but also the goals set by the neu- Ethical Approval/Informed Consent
Not applicable.
rocritical care team so as not to hinder them with inter-
ventions aimed at improving renal outcomes.
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in pub‑
lished maps and institutional affiliations.
Conclusions
Received: 30 June 2021 Accepted: 30 August 2021
Acute kidney injury is a frequent complication in neu-
rocritical patients that involves different pathologies,
such as TBI, SAH, and stroke. Its presence in these
patients is associated with worse clinical outcomes that
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