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390 C. Monard and A. Schneider
Fig. 33.1 Main diuretics and their site of action with associated sodium reabsorption potency
Loop Diuretics
Loop diuretics are undoubtedly the most commonly prescribed diuretics in the ICU
[1]. They inhibit the sodium potassium chloride cotransporter located in the apical
membrane of epithelial cells of the thick ascending limb of the loop of Henle. Since
this cotransporter is responsible for the reabsorption of 25% of the filtered sodium,
loop diuretics are extremely powerful. Administered orally, their bioavailability is
highly variable, from 50% (furosemide) to 80% (torasemide). Their half-life is 2 h,
and their peak of action occurs, respectively, within 30–60 min and 60–120 min after
intravenous and oral administrations. The main adverse effects of loop diuretics
include ototoxicity in case of rapid administration (>4 mg/min) and electrolyte
disturbances (hypernatremia, metabolic alkalosis, hypokalemia, hypochloremia,
and hypomagnesemia) as a direct consequence of their mechanisms of action
[3]. Most of these adverse effects can be avoided or minimized with adequate
prescription and monitoring.
Other Classes of Diuretics
Thiazide diuretics include hydrochlorothiazide, chlortalidone, and metolazone. This
class of drugs is commonly used in the outpatient setting, particularly for chronic
hypertension, but less frequently in the ICU. They remain of importance, though, as
they might be required in case of resistance to loop diuretics or to minimize their
toxicity. Thiazides block the sodium chloride cotransporter located in epithelial cells
of the proximal part of the distal convoluted tubule. Since this site accounts for only
33 AKI Management: Diuretics 391
5–10% of sodium reabsorption, thiazides’ natriuretic effect is low compared with
loop diuretics. On the other hand, they are also associated with fewer side effects,
particularly less hypokalemia.
Aldosterone antagonists such as spir
epithelial cells located at the end of the distal convoluted tubule. This area of the
nephron accounts for only 2% of the sodium reabsorption; hence, the natriuretic
effect of this class of drug is very limited. However, they are mainly used for their
potassium-sparing properties.
Acetazolamide inhibits carbonic anhydrase in epithelial cells of the proximal
tubule. This enzyme facilitates sodium and bicarbonate reabsorption. Its inhibition
leads to metabolic acidosis by increasing urinary excretion of sodium without
chloride [4]. Acetazolamide is used in some situations of severe metabolic alkalosis
but rarely for its diuretic properties only.
onolactone target aldosterone receptors of
Indications for Diuretics in AKI
There are limited indications for diuretics in critically ill patients with AKI. The main
and arguably only real indication is fluid overload. Additional indications for
diuretics include prognostication and correction of some electrolyte abnormalities
(dyscalcemia, metabolic alkalosis).
Control of Fluid Overload
Diuretics represent the first-line treatment in the management of acute pulmonary
edema as well as edematous syndromes such as cardiorenal syndrome or ascites.
They also play a key role in the management of fluid overload in less acute
situations. Fluid overload is largely associated with AKI and may represent either
a cause or a consequence of the syndrome, both being intertwined in a vicious circle
[5].
Indeed, in patients admitted to ICU, anuria and oliguria are likely to rapidly lead
to fluid overload. On the other hand, fluid accumulation through an increase in
central venous pressure and capillary leakage leads to renal congestion and
intracapsular edema. The modification of intrarenal hemodynamics will lead to
AKI with loss of function and tissue damage. The association between fluid overload
and AKI incidence and severity was demonstrated in a large prospective multicenter
6].
study [
death [
limitation of fluid overload have become a major objective in critical care. Recent
studies have tested the feasibility and efficacy of protocols aiming to prevent or
minimize fluid overload. These protocols included diuretics alone or in combination
with fluid restrictive strategies. Studies conducted in sepsis or ARDS but also in
general ICU populations have suggested the safety of such approaches.
It is also well established that fluid overload increases the relative risk of
7], particularly among patients with AKI [8]. Altogether, avoidance and
392 C. Monard and A. Schneider
Unfortunately, most of them were insufficiently powered to demonstrate effects on
major outcomes [9, 10]. In non-hypovolemic patients with AKI, a fluid restrictive
strategy including diuretics was found to be safe and to reduce RRT requirements
[11]. Very recently, a large retrospective study highlighted that a beneficial effect of
diuretics to limit AKI progression was observed only in the group of patients with
high central venous pressure (≥12 mmHg) [
management of fluid overload and reduction of kidney-related adverse events,
diuretics’ effect on mortality remains unclear to this day, even among AKI and
fluid-overloaded patients [13, 14].
12]. However, despite their benefit in the
AKI Prognostication
Furosemide is commonly used to assess tubular function in patients with AKI.
Indeed, an adequate response (diuresis induction) following furosemide administration implies the integrity of associated tubular functions: active secretion in the
proximal convoluted tubule and sodium cotransport blockage in the loop of Henle.
This practice has been standardized and is now referred to as the furosemide stress
test (FST) [
(or 1.5 mg/kg in case of previous exposition to diuretics) of furosemide. It is
considered positive if urine output in the next 2 h exceeds 200 ml. The FST has
been evaluated in prospective trials to predict AKI progression, AKI recovery, or the
need for RRT [16]. Currently, evaluations are ongoing to evaluate its ability to
predict liberation from RRT (NCT05612490). Recent results suggest an improved
performance if combined with biomarkers [17]. The FST could guide the management of patients with AKI, particularly regarding the decision to introduce RRT
[18]. Of note, FST should not be performed in hypovolemic patients, and urine
losses should be replaced if necessary.
15]. FST consists of the intr avenous administration of 1 mg/kg
Situations in Which Diuretics Are Not Indicated
AKI P
It has been suggested that diuretics could prevent AKI and provide nephroprotection
by decreasing tubular cells’ oxygen consumption and tubular obstruction through
increased urinary flow [19, 20
studies were not confirmed in clinical studies. Indeed, the ability of loop diuretics to
prevent AKI has been tested in different settings such as contrast administration,
surgery, or experimental rhabdomyolysis. Almost all these trials failed to demonstrate an association between diuretic use and reduction of AKI. A recent metaanalysis evaluated the benefits of furosemide after cardiac surgery and could not find
a reduction in AKI incidence [
revention
However, these results obtained in experimental
].
21]. The few positive results come from small studies
33 AKI Management: Diuretics 393
suggesting a reduction in contrast-associated AKI with coadministration of fluids
and loop diuretics before contrast injection [22]. Although encouraging, these results
still need to be confirmed in large multicenter trials. In the absence of benefits,
experts recommend against the use of diuretics for the sole purpose of AKI prevention, except for diuretic-responsive patients to control or avoid fluid overload
[23, 24].
AKI Recovery
Effects of loop diuretics on clinical outcomes of critically ill patients with AKI have
been examined in a meta-analysis including 62 studies and 555 patients. Diuretics
were not associated with improved mortality or renal recovery despite a shorter
duration of RRT, a shorter time to decline in serum creatinine, and a greater increase
in UO [
whether they are already weaned or still receiving RRT [
older studies suggested an association between diuretic use and mortality or absence
of recovery in patients with AKI [28, 29]. These results raised concerns regarding
potential nephrotoxicity associated with loop diuretics [30]. However, this hypothesis was not confirmed in further experimental studies [31]. Moreover, the association between diuretics and adverse outcomes observed previously was only
significant in the diuretic nonresponsive patients indicating that severity of AKI
was a major confounding factor. Altogether, furosemide is safe for the kidney if
properly used and avoided in hypovolemia. However, in the absence of fluid
overload, diuretics are unlikely to be beneficial in AKI and may lead to electrolytic
abnormalities [32]. Diuretics are therefore not recommended in overt AKI without
fluid overload, neither to accelerate recovery nor to limit disease progression.
25]. These results were consistent among AKI patients requiring RRT,
26, 27]. On the contrary,
How to Use Diuretics in the ICU
Clinicians prescribing diuretics should be familiar with their pharmacokinetic and
pharmacodynamic properties. The complexity of critically ill patients and their
altered body composition justifies following practical guidelines. Figure 33.2
shows our proposed algorithm to guide diuretic use in critically ill patients with AKI.
Class and Dose Selection
As already mentioned, furosemide is the first-line agent and the most potent natriuretic agent. Other classes (thiazides, acetazolamide) might be used, alone or in
combination, to mitigate complications associated with loop diuretics such as
394 C. Monard and A. Schneider
Fig. 33.2 Diuretic use in critically ill patients with AKI
hypokalemia or metabolic alkalosis (Fig. 33.2). Furosemide effect is dosedependent, and its dose-response relation follows a sigmoid curve [33]. The starting
dose must be above a certain threshold dose to induce natriuresis. This threshold
depends on the patient’s background and comorbidities. It is usually recommended
to start with a bolus of 20–40 mg (≈0.4 mg/kg) and to adjust subsequent doses
according to urine output response. The maximum dose, or ceiling dose, is the dose
above which no additional natriuretic effect is observed. The ceiling dose is 80 mg
for most patients. Beyond this dose, daily natriuresi
s and diuresis might be increased
by administering repeated doses to prolong diuretic effect over time. Diuretic
resistance is frequent among patients receiving prolonged treatment with loop
diuretics, particularly those with chronic kidney disease, heart failure, nephrotic
syndrome, or cirrhosis. Different mechanisms may be involved including neurohormonal activation (increase in renin-angiotensin, aldosterone, and antidiuretic hormones following vo
lume depletion), enhanced reabsorption in the proximal tubule,
and distal convoluted tubule hypertrophy [32]. To maintain diuresis, these patients
require higher doses of loop diuretics or diuretic combination, which was found to be
safe and effective [33]. Thus, furosemide starting dose in patients with chronic
kidney disease, heart failure, or nephrotic syndrome may be up to 40–80 mg, and
ceiling dose may reach 200 mg.
Modality of Loop Diuretic Administration
In critically ill patients, loop diuretics are mainly administered intravenously as their
oral bioavailability is rather unpredictable and the effect might be delayed.
33 AKI Management: Diuretics 395
Continuous intravenous administration of loop diuretics has been claimed to lead to
higher diuresis compared with bolus administration. However, data regarding outcomes are conflicting. A prospective randomized trial including patients with acute
decompensated heart failure found no difference between both strategies [
34]. On
the contrary, a meta-analysis including small studies conducted in the ICU found a
greater urine output when furosemide was administered continuously, but without an
impact on mortality, length of stay, renal function, or electrolyte disturbances
35]. More recently, a large retrospective study confirmed these results [36]. It has
[
also been suggested that continuous administration was associated with fewer
adverse events, particularly ototoxicity. To conclude, the available evidence does
not allow recommending one strategy over another, and the choice may depend on
local resources. Since furosemide is highly bound to albumin, the latter being
necessary for furosemide to reach its secretion site in the tubule, some authors
suggested using albumin in association with furosemide to ma
ximize its action.
Currently, there is no data to support its systematic use, but albumin
coadministration may improve diuretic response in patients with severe
hypoalbuminemia [
37]. As diuretics are affecting electrolytes and acid-base balance,
close monitoring is mandatory to avoid adverse effects. Particularly, when using
loop diuretics, hypokalemia and hypomagnesemia may occur leading to cardiac
arrhythmias.
Conclusions
Diuretics and loop diuretics in particular are among the most widely used drugs in
the ICU. Currently, their use in patients with or at-risk of AKI should be restricted to
confirmed indications such as control or prevention of fluid overload and
prognostication.
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Chapter 34
Acute Kidney Disease
G. Azzopardi and J. Prowle
Introduction
Acute kidney injury compl icates up to 20% of hospital admission and around 50% of
ICU admissions [1]. The development of a consensus definition of AKI in 2004
revolutionized the recogni tion, clinical management, and research priority of the
immediate management of kidney injury complicating acute illness. However, in
addition to being strongly associated with short term risk of death, AKI is also
associated with increased risk of development and/or progression of chronic kidney
disease [CKD] by almost threefold [2]. CKD is a growing global health priority,
ated with eventual need for dialysis or kidney transplantation, reduced quality
associ
of life, and an increased risk of cardiovascular disease, hospitalization, and mortality
[3, 4]. Despite this, the follow-up and management of kidney health after critical
illness
and AKI are underdeveloped [5, 6]. Partially this disconnect may have arisen
from a lack of standardization in classifying the outcomes of AKI and a disconnect
between the current definition of AKI made over a 7-day period and that of CKD
which requires evidence of sustained kidney dysfunction over more than 3 months
[7]. To address this challenge and enhance patient care, the Acute Di sease Qual ity
ive developed and defined the acute kidney disease (AKD) to represent an
Initiat
intermediate period of kidney dysfunction and complete our ability to describe any
patient’s kidney health at any time point [8]. However, several challenges remain in
the
marrying of these definitions and mapping a patient’s kidney health journey, a
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-66541-7_34.
G. Azzopardi · J. Prowle (
Adult Critical Care Unit, The Royal London Hospital, Barts Health NHS Trust, London, UK
William Harvey Research Institute, Queen Mary University of London, London, UK
e-mail: g.azzopardi@qmul.ac.uk; j.prowle@qmul.ac.uk
© 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_34
✉)
399
400 G. Azzopardi and J. Prowle
number of which have been highlighted in a recent KDIGO consensus conference on
harmonizing acute and chronic kidney disease definition and classification [9]. An
important difference between the definitions that makes harmonizing them difficult
is that AKI diagnosis using serum creatinine is largely defined as an acute change in
kidney function relative to a prior baseline, whereas CKD is defined by the absolute
level of kidney function and/or indication of chronic glomerular or tubular disease
10]
by the presence of proteinuria [
.
What Is Acute Kidney Disease?
Acute kidney disease [AKD] is a term developed to complete the spectrum of kidney
disease, bridging the gap between acute kidney injury [AKI] and chronic kidney
disease [CKD]. The Acute Disease Quality Initiative ADQI 16 workgroup proposed
a classification system for AKD, reflective of AKI staging, which allows for both
progression and recovery (Table 34.1). Within this original scheme, AKD is defined
as the continued fulfilment of AKI creatinine diagnostic criteria beyond 7 days after
injury, so that the presence of AKD was defined by persistence of a 1.5-fold rise in
creatinine above baseline. A number of issues arise with operationalizing this
definition, however. Firstly, the dependence on knowledge of a baseline creatinine
for diagnosis and staging of AKD, which may be unknown and is potentially less
relevant than the absolute level of kidney function as the patient emerges from the
acute episode; in recognition of this, a stage 0 for AKD was suggested to represent
apparently recovered AKI where there might still be underlying kidney damage;
however, this is a somewhat ill-defined and ill-understood concept with only
research suggestions for its quantification. Secondly, many possible trajectories of
AKD might be followed over the 90-day period (Fig. 34.1); representing recurrent
AKI, slow recovery, or progressive deterioration in kidney function, importantly
Table 34.1 Proposed ADQI-16 classification of AKD mapping to AKI staging
AKI KDIGO stage
(0–7 days) AKD stage (7–30 days)
Ongoing RRT Ongoing RRT
3: 3× serum creatinine/
RRT
2: 2× serum creatinine 2: 2× serum creatinine
1: 1.5× serum
creatinine
Subacute
Table reproduced
Disease Quality Initiative (ADQI) [9]
AKI acute kidney injury, AKD acute kidney disease, RRT renal replacement therapy
AKI
3: 3× serum creatinine/RRT
1: 1.5× serum creatinine
ubacute AKD (subtype A
0: S
loss of renal reserve indicating injury; C, creatinine not back to
baseline)
from Acute kidney disease and renal recovery: consensus report of the Acute
, no evidence of injury; B, biomarkers or