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32 Management of AKI: Vasopressors 379
metabolic effects, including hyperglycemia, hyperlactatemia, acidosis, and
tachycardia [40].
There is limited information availab
renal blood flow (RBF). In hyperdynamic human sepsis, epinephrine was observed
to reduce RBF while not affecting creatinine clearance [33, 41]. However, its impact
on renal vascular resistance and urine output remains controversial [33, 41].
le regarding the effects of epinephrine on
Dopamine
Dopamine, a molecular precursor of epinephrine and norepinephrine, acts as an
alpha- and beta-agonist and also affects peripheral dopaminergic receptors. Initially,
dopamine was believed to have renal protective effects at “low doses” due to
selective vasodilation of afferent arterioles and increased RBF. However, studies
have demonstrated selective vasodilation only in healthy volunteers [
direct diuretic effect on proximal tubules increases the sodium and oxygen consumption of tubular cells [
dopamine, and dopamine is indicated primarily for severely bradycardic patients
[8]. Intraoperative use of dopamine is associated with an increased risk of postoperative AKI and the need for continuous renal replacement therapy (CRRT) in open
abdominal aneurysm repair [43]. In patients with AKI, dopamine appears to increase
renal resistive index compared to the addition of norepinephrine or norepinephrine
alone [44]. The effect on dopaminergic receptors is suspected to reduce RPP [45].
Moreover, in the SOAP study, a multicenter observational study involving 1058
patients with shock, dopamine administration was identified as an independent risk
factor for ICU mortality [46]. Finally, the SOAP II trial, which assigned 1679
patients with shock to receive either dopamine or norepinephrine as first-line vasopressor therapy, did not provide evidence of any benefit of dopamine in terms of
renal function, the need for CRRT, or mortality, while leading to a greater number of
adverse events [47].
42]. In septic shock, norepinephrine is preferred over
27], and the
Vasopressin
Vasopressin, produced in the hypothalamus and released by the posterior pituitary
gland, plays a crucial role in tonicity homeostasis. Acting on arginine vasopressin
receptors 1 and 2 (V1 and V2), vasopressin exerts two main effects: water osmotic
reabsorption mediated by the expression of aquaporin-2 channels on the distal tubule
cell membrane and vasoconstriction secondary to its effect on vascular smooth
muscle cells [48]. Additionally, vasopressi n is involved in the protective mechanism
of tubulo-glomerular feedback, where the vasoconstriction of afferent and efferent
arterioles reduces filtration, sodium load, and oxygen consumption in the renal
380 P. Persona and T. Pettenuzzo
medulla [49]. Stimulation of V2 receptors leads to the release of nitric oxide and an
increase in medullary blood flow, acting in opposition to V1 stimulation. Prolonged
stimulation of V1 and V2 receptors results in the dominance of nitric oxide release in
the outer medulla [
The clinical use
paign when the dosage of norepinephrine is increased over 0.25 mcg/kg/min due to
the decline in vasopressin blood concentration after 24–48 h from the onset of septic
shock [8]. In the VANISH study, a randomized controlled trial involving 409 adult
patients with septic shock, vasopressin administration did not improve the number of
kidney failure-free days compared to norepinephrine, although it was associated
with lower levels of serum creatinine and higher urine output [51]. Importantly,
vasopressin use reduced the need for CRRT compared to norepinephrine alone, even
though the starting criteria for CRRT were not defined a priori [52]. This finding
contrasts with that of the VASST trial, which randomized 779 patients with septic
shock already receiving norepinephrine to either vasopressin or norepinephrine in
addition to open-label vasopressors. In the VANCS trial, which included 300 patients
with post-cardiac surgery with vasoplegic shock, a lower incidence of a composite
outcome of mortality or severe complications, including AKI, was observed with
vasopressin compared to norepinephrine administration [53 ]. A subsequent metaanalysis, including 4 randomized controlled trials and 1453 patients, suggested that
vasopressin was associated with a lower risk of CRRT in patients with septic shock
compared to other vasopressors, although this finding was not robust to sensitivity
analyses [54]. Interestingly, when considering genetic AKI sub-phenotypes based on
markers of endothelial dysfunction and inflammation, the mortality benefit of vasopressin compared to norepinephrine was significant [55].
50].
of vasopressin is recommended by the Surviving Sepsis Cam-
Terlipressin
Terlipressin, a glycine vasopressin analog, is a modified version of the vasopressin
molecule with a longer half-life. Terlipressin exerts pronounced vasoconstrictive
effects on the efferent arterioles, while minimally affecting the afferent arterioles
[56]. Its primary use is in the treatment of AKI secondary to hepatorenal syndrome.
Terlipressin has been shown to improve renal function in this context by reducing
splanchnic vasodilation, increasing central circulating blood volume, and reducing
33].
endogenous renal vasoconstriction [
not been shown to increase RBF. In a prospective randomized controlled study
involving 20 adult patients with hyperdynamic septic shock who were randomized to
receive either norepinephrine or terlipressin, both drugs were associated with
increased urine flow and creatinine clearance [
appropriate blinding and randomization, a meta-analysis published in 2006, which
included 6 randomized controlled trials and 51 patients, demonstrated that
terlipressin therapy was associated with a significant improvement in creatinine
clearance, an increase in urine output, and a decrease in short-term mortality [
Despite increasing MAP, terlipressin has
57]. Although only 1 trial had
58].
32 Management of AKI: Vasopressors 381
In a pilot study involving 22 septic shock ICU patients randomized to receive
either terlipressin or standard care, no significant difference in urinary output at 24 h
was found. However, terlipressin was found to be more effective than placebo in
treating patients with hepatorenal syndrome type 1 [
According to the results of another randomized controlled trial involving
120 patients diagnosed with acute-on-chronic liver failure and hepatorenal syndrome
and randomized to receive either terlipressin or noradrenaline, terlipressin may
provide earlier and more profound reversal of AKI, potentially leading to a mortality
benefit in this patient population [60].
59].
Angiotensin II
Angiotensin II is an active peptide derived from the cleavage of angiotensin I by the
angiotensin-converting enzyme. It is a crucial component of the renin-angiotensinaldosterone system, which plays a pivotal role in regulating blood volume, electrolyte balance, and systemic vascular resistance. Angiotensin II serves as a first-line
endogenous response to restore blood pressure in septic shock [
pressor activity affects both arterial and venous vessels [64].
he k
In t
proximal tubule cells, promoting sodium and bicarbonate reabsorption and facilitating sodium retention [
levels of angiotensin II, desensitization of AT1 and AT2 receptors, and
overexpression of angiotensin II cleavage enzymes [62, 66, 67].
The ATH
vasopressor in 321 patients with vasodilatory shock and norepinephrine dosages
higher than 0.2 mcg/kg/min. Patients receiving angiotensin II achieved the MAP
target earlier and showed an improvement in SOFA score at 48 h. A post-hoc
analysis of 105 patients receiving CRRT for AKI at the initiation of angiotensin II
or placebo revealed better 28-day survival, higher MAP, and a greater liberation rate
from CRRT in the angiotensin II group [
regarding the risk of multiorgan ischemic events due to angiotensin II’s potent
vasopressor activity [70]. Nevertheless, a systematic review including 31,281
patients supported angiotensin II’s acceptable safety profile [71]. The optimal
dosage of angiotensin II remains unclear, and some studies have suggested that the
infusion rate could be reduced after treatment initiation, potentially limiting the
occurrence of adverse events [
idney, angiotensin II acts on AT1 and AT2 receptors expressed in
65]. Patients with septic shock often exhibit reduced plasmatic
]
compared angiotensin II with placebo as a second-line
However, concerns have been raised
69].
19, 72].
61–63]. Its vaso-
382 P. Persona and T. Pettenuzzo
Conclusions
The use of vasopressors and inotropic agents in patients with AKI necessitates
attention to several considerations. Firstly, it is crucial to assess and optimize the
intravascular volume status before initiating these medications. Vasopressors in
patients with hemorrhagic or hypovolemic shock can further reduce tissue blood
flow if fluid resuscitation is inadequate [17, 19]. Secondly, the choice of the initial
agent should align with the suspected underlying etiology of shock associated with
AKI, such as sepsis, hepatorenal syndrome, cardiac failure, or anaphylaxis
[73]. Thirdly, clinical and instrumental monitoring of end-organ perfusion is essential for balancing the risks and benefits of vasopressor support. Vasopressors can
lead to significant complications, including hypoperfusion, myocardial ischemia,
dysrhythmias, skin necrosis, hyperglycemia, and drug interactions. One major
limitation is the absence of reliable bedside techniques to assess and monitor the
microcirculation, although sublingual microcirculation [74] and Doppler analysis of
RBF [75] are increasingly being investigated. Current clinical evidence is insufficient to determine whether one vasoactive agent is superior to another in preventing
or treating AKI. However, vasopressors should not be withheld from patients with
shock and AKI due to concerns about kidney perfusion. Indeed, appropriate vasopressor use can improve renal perfusion pressure in volume-resuscitated patients
with vasomotor shock. Norepinephrine, vasopressin, and angiotensin II are the
current therapeutic options for patients with septic shock, although additional therapies are under investigation. Finally, the identification of specific sub-phenotypes in
patients with septic shock may enable tailored efforts to mitigate AKI in individual
patients in the future.
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Chapter 33
AKI Management: Diuretics
Céline Monard and Antoine Schneider
Introduction
Diuretics form a class of drugs that induce a net loss of sodium and water from the
body by direct action on the kidney. Diuretics are among the most commonly
prescribed drugs in intensive care units and are administered to almost 50% of
patients [1]. Nevertheless, there remain many uncertainties and misconceptions
ing their use in ICU, particularly in the context of acute kidney injury (AKI)
regard
[2]. This chapter will review diuretics’ pharmacology and indications and provide
pract
ical guidance to use them wisely in critically ill patients with AKI.
Pharmacology of Diuretics
Overall, diuretics act by blocking sodium reabsorption within renal tubules, inducing
natriuresis and subsequent loss of water. They are typically classified according to
their site of action along the renal tubule as this location determines their respective
natriuretic potency and side effect profile. As a general rule, the more distal the site
of action of the diuretic, the lower the natriuretic efficacy (Fig. 33.1).
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-66541-7_33.
C. Monard · A. Schneider (
Adult Intensive Care Unit, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne,
Switzerland
e-mail: celine.monard@chuv.ch; antoine.schneider@chuv.ch
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
A.
Cotoia et al. (eds.), Nutrition, Metabolism and Kidney Support,
https://doi.org/10.1007/978-3-031-66541-7_33
✉)
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