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40 Indications and Timing of Renal Replacement Therapy 475
Conclusions
The long-standing questions surrounding the optimal timing of RRT initiation in
critically ill patients with AKI appear to have been largely answered following
publication of STARRT-AKI [48]. Clinicians should now recognize that starting
RRT may be avoidable in many patients without an adverse impact on survival
[49]. In some cases, RRT may not be appropriate given a patient’s or family’s
preferences for care or due to the perception of being non-beneficial in the context
of the overall prognosis for a patient nearing the end-of-life, where RRT will clearly
not modify outcome [11]. For now, a conservative approach to starting RRT,
characterized by watchful waiting and initiating RRT when confronted with worsening, persistent, or medically refractory complications of AKI, is supported by
high-quality evidence and should be recommended in updated iterations of clinical
practice guidelines.
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Chapter 41
Nutrition in ICU Patients with Acute
Kidney Injury
Michael Hiesmayr and Arabella Fischer
Introduction
Acute kidney injury (AKI) disrupts the homeostasis of body fluids, electrolytes,
osmolality, and pH and reduces the excretion of waste products mainly from protein
metabolism; the production and activation of hormones, vitamins, and bioactive
substances; and the contribution to gluconeogenesis [1]. AKI affects distant organ
function,
Nutrition with high protein [2] or high additional glutamine has a negative effect on
AKI pati
to inte
replacement therapy (KRT) with hemofiltration or dialysis. In acutely ill patients,
many centers use continuous renal replacement therapy (CRRT) because it appears
easier to maintain hemodynamic stability. CRRT can replace the excretory function
of “waste” from protein metabolism and the volume regulatory function but none of
the metabolic, endocrine, and regulatory funct ions of the kidney. AKI is a severe
complication of critical illness, and when CRRT is necessary, hospital mortality is
more than doubled to 40–50% [4, 5]. Risk factors for AKI can be attributed to patient
factors,
modifiable, such as hypervolemia, hypovolemia, hypotension, hypoxia, intra-
increases the severity of illness, and is associated with poorer outcomes.
ents [3]. Acute kidney injury [AKI] is observed in 30% of patients admitted
nsive care units (ICU) and necessitates in 10% of ICU patients kidney
exposure to toxins, and the process of care. Some patient risk factors are
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-66541-7_41.
M. Hiesmayr (
Center of Medical Data Science, Medical University Vienna, Vienna, Austria
e-mail: michael.hiesmayr@meduniwien.ac.at
A. Fischer
Department of
University Vienna, Vienna, Austria
e-mail: arabella.fischer@meduniwien.ac.at
© 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_41
✉)
Cardiac Thoracic and Vascular Anesthesia and Intensive Care, Medical
481
482 M. Hiesmayr and A. Fischer
abdominal hypertension, and the use of nephrotoxic drugs, whereas acute and
chronic diseases such as infections, heart failure, liver failure, gastrointestinal
disease, chronic kidney disease (CKD), disease-related malnutrition, and older age
cannot be modified. One of the most frequent triggers of AKI in high-income
countries is sepsis [
The kidney is
6].
highly sensitive to hypotension and hypovolemia because the
kidney needs a large proportion of cardiac output [20%] but accounts for only 8%
of total oxygen consumption. Nevertheless, some parts of the kidney have extremely
low oxygen partial pressure of 20 mm Hg. The major substrate for energy production
in segments S1 and S2 of the proximal tubule is fatty acid oxidation, whereas
anaerobic glycolysis is only possible in the more distal parts of the nephron
[7]. The kidney contributes 40% to whole body gluconeogenesis, mainly from
lactate. High lactate, together with lower glucose levels, indicates overall a poorer
prognosis [
surgical trauma [
8]. The first signs of AKI appear often very early after disease onset or
9, 10 ]. The most frequently used signs are an increase in creatinine
and/or a decrease in urinary volume. AKI severity has be en recently clearly defined
with the KDIGO severity grading system into three grades based on an increase in
creatinine, a decrease in urinary volume, and the use of KRT. Many patients in
KDIGO Grade 3 need renal replacement therapy and have progressed from injury to
failure [11]. In the metabolic treatment of AKI patients, three elements must be
considered simultaneously: first, the critical illness and its treatment that have
triggered AKI; second, the missing complex function of the kidney; and, third, the
side effects of KRT mainly through the loss of nutrients, micronutrients, electrolytes,
and vitamins [
12]. The evolution of critical illness should be divided into three
phases [12]. The first phase is the “early ICU stay before KRT” and is characterized
by an escalating inflammatory response driven by the liberation of cytokines necessitating often fluid resuscitation, the use of vasoactive drugs, sedation, and ventilator
support. During this first phase, the degree of organ impairment becomes clear, and it
becomes clear whether AKI necessitates the use of KRT. Most patients recover from
AKI 1 within 7 days, but unfortunately, some residual susceptibility may subclinically persist [ 13].
The second phase is the “ICU phase with KRT.” In this phase,
KRT stabilizes waste removal and fluid homeostasis. During this phase, patients
experience the peak of the inflammatory response and a transition from resuscitation
to de-resuscitation with a focus on fluid removal, and the de-escalation of treatments
is necessary. The last phase is the “ICU phase after KRT.” A return to autonomy and
to reducing care requirements is the main objective to prepare for ICU discharge. In
this phase, variable care requirements help overcome residual organ damage, such as
ICU-acquired weakness, poor tolerance of physical effort, dyspnea, reduced kidney
function, poor appetite, and dysphagia, and should allow sufficient nutrition and
guided physical rehabilitation. CRRT needs to be switched to dialysis if KDIGO
3 persists (Fig.
41.1).
41 Nutrition in ICU Patients with Acute Kidney Injury 483
predilution
Citrate
hemodialyzer
CaCl
Blood flow
Fig. 41.1 Input and output during continuous renal replacement therapy in veno-venous
hemodiafiltration mode with predilution and citrate anticoagulation. * To determine any mass
transfer calculation, convert all flow to ml/hour and consider that the concentration in the effluent
of small molecules (glucose, citrate, lactate, urea) and ions (Na+, K+, Mg++, Ca++, PO
sieving coefficient near 1 is in equilibrium with the plasma concentration at the entry of the filter. **
Effluent flow = dialysate + predilution + postdilution + anticoagulation + anticoagulation reversal +
fluid removal
in
Effluent
dialysate
out
Blood flow
3-
) with a
4
Early ICU Phase before KRT
After ICU admission, all ICU patients, even when AKI has not been identified,
should receive the preventive “KDIGO” bundle (volume optimization, blood pressure support with vasopressors, avoidance of nephrotoxic drugs, prevention of
hyperglycemia) to prevent the occurrence and progression of AKI. In the early
phase, after disease onset or surgery, small changes in creatinine already indicate
AKI. Fluid administration needs to be closely monitored since the kidney is very
sensitive to hypotension and venous congestion. If volume status is already elevat ed
and abdominal congestion is suggested by elevated central venous pressure, further
fluid loading may be detrimental. The duration of this phase is typically short. In
10% of ICU patients, KRT is needed and established between ICU admission and
ICU day 4 in the vast majority.
Nutrition Care
Nutrition should be progressively given to AKI patients, many of them having
already malnutrition due to preexisting chronic conditions, such as CKD or chronic
heart failure. The evolution of urea and glucose in response to increased nutrition
needs to be integrated into the decision to progress with the amount of nutrition
given. High protein may increase the proportion of patients needing KRT and
shorten the time period until KRT starts [3, 14]. High glucose levels and the need
for higher-dose insulin have an unfavorable effect on the injured kidney. Current
recommendations suggest reaching the target energy of 20–25 Kcal/kg BW/day and
484 M. Hiesmayr and A. Fischer
the targe t protein of 1–1.3 g/kg BW/day by days 3–7[15, 16]. During the first week
of ICU stay, the recommended target is 70% of the estimated energy expenditure.
Many factors are modulating energy expenditure in critically ill patients, and thus,
the best estimate for energy expenditure can be obtained by indirect calorimetry. The
provided enteral nutrition (EN) or parenteral nutrition (PN) should always be below
the measured energy expenditure specifically during the early phase of critical illness
because large amounts of
as fat and glycogen or generated via gluconeogenesis from lactate and amino acids.
This endogenous liberation of macronutrients is only slowly downregulated when
external macronutrients are given to critically ill patients. This phenomenon contrasts with the reaction of healthy persons that immediately reduce internal liberation
upon refeeding after a short period of starvation. In critically ill patie
gluconeogenesis was observed even after 2 weeks. It is currently unknown how long
this phenomenon persists in patients with AKI KDIGO stages 2 and 3, where the
gluconeogenetic capacity of the kidneys may be greatly reduced. Actual weight in
critically ill patients with AKI may not represent metabolically active tissues since
fluid accumulation and removal may induce large changes in the actual body weight.
Therefore, the actual body weight before injur
BMI < 25. For patients with a BMI >25 adjusted body weight +25%– 30% of the
difference between adjusted and preinjury weight should be used [
body weight is simply derived from height as height-100 in men and (height-100) ×
0.9 in women, the BROCA Index proposed in 1871.
macronutrients are either liberated from body stores such
nts, substantial
y should be used for patients with
17]. Adjusted
Monitoring
In this early phase, without KRT, the careful monitoring of metabolic tolerance and
the accumulation of waste products and electrolytes is mandatory. Hyperglycemia
poorly controlled with insulin, high levels of triglycerides, and hypercapnia may
suggest overfeeding. Raising urea is a proxy for waste product accumulation or the
overfeeding of protein. Urea production rate (urea concentration in urine × 24 hour
urinary volum e) may indicate the maximum amount of protein that can be tolerated.
Metabolic acidosis and rising potassium and phosphate levels may indicate the loss
of function of the proximal tubules.
ICU Phase with KRT
With the start of KRT nutrition, needs to be readjusted because KRT on the one hand
eliminates waste products and fluid but on the other hand generates macronutrient
loss and facilitates the gain and loss of electrolytes, micronutrients, and vitamins. In
the early phase of critical illness, many centers prefer continuous KRT methods with
a filter run time of up to 3 days, whereas in the late phase of ICU stay or when
41 Nutrition in ICU Patients with Acute Kidney Injury 485
patients did not regain sufficient kidney function, intermittent dialysis is preferred.
Three main types of continuous KRT methods exist: continu ous veno-venous
hemofiltration (CVVH), continuous veno-venous hemodialysis (CVVHD), and continuous veno-venous hemodiafiltration (CVVHDF). The dialysis mode is based on
the diffusion of substances according to concentration gradients. The filtration mode
is based on the convection of substances along pressure gradi
ents. In the filtration
mode, a replacement solution is used to dilute the blood. The replacement solution
can be given either prefilter, postfilter, or both pre- and postfilter. In all modes, fluid
is eliminated via ultrafiltration to achieve a negative fluid balance.
Gains and Losses During CRRT
Gains and losses can be measured or approximated. Approximation has the advantage of allowing the anticipation of losses. All substances with a higher concentration in the plasma than in the dialysate or replacement fluid are lost, whereas
substances added by the replacement fluid, such as lactate, to be metabolized into
bicarbonate and to counteract metabolic acidosis or citrate for anticoagulation are
gained. These substrates even interfere with metabolic pathways. Lactate competes
with aerobic glycolysis and induces glucose increase during CRRT [
The measurement is easily performed by calculating ef fluent flow and effluent
concentration. The recommended dialysate + substitution flow is 20–25 ml/kg/h.
The concentration of glucose and electrolytes in the effluent can easily be measured,
but the concentration of amino acids, citrate, micronutrients, and vitamins is not
universally available because of the complex high-performance liquid chromatography (HPLC) and mass spectrometry methodology. An approximation can be done
by using arterial or venous measurem ents and estimating concentration in plasma
after dilution with anticoagulants and predilution. The concentration of electrolytes
entering the hemofilter/dialyzer is filtered into the effluent in pure hemofiltration or
equilibrates with the countercurrent of the dialysate. All electrolytes as well as
glucose and citrate have a sieving coefficient near 1, and thus, the concentration in
the effluent is about the same as the plasma concentration in the filter.
18].
Electrolyte Loss in CRRT
The example in Box 1 shows all the steps to calculate PO
twice as high as a typical PO
3-
need of 30–40 mmol/24 h. Thus, it is not surprising
4
that CRRT is one of the major risk factors for hypophosphatemia. ESPEN guidelines
recommend using replacement solutions containing electrolytes. Table 41.1 shows
that not all choices are available as they depend on the company providing the
equipment and the mode of anticoagul ation. The elimination of electrolytes remains
stable over the lifetime of the hemofilter [
19].
3-
loss. This loss is already
4