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454 W. R. Clark et al.
surrogate [8]. In this randomized controlled trial (RCT), Ronco and colleagues in
Vicenza, Italy, reported significantly higher survival in patients treated with an
effluent-based CRRT dose of 35 or 45 mL/kg/h vs. 20 mL/kg/h, the latter being a
conventional dose prior to the study. No clinically validated dose metric for CRRT
existed before this trial, and the results led to the rapid adoption of effluent-based
dosing in clin ical practice. A series of additional RCTs along with a system
review/meta-analysis also assessed the relationship between effluent-based CRRT
dose and patient outcome [
center trials [12, 13] and two trials focused on the septic AKI population
14, 15]. These studies utilized a wide spectrum of CRRT modalities and yielded
[
inconsistent results, some corroborating the Vicenza trial with others showing no
benefit for a dose higher than 20–25 mL/kg/h. Based on the trials published before
2012 [8–13], the KDIGO Clinical Practice Guideline recommended a delivered
CRRT dose of 20–25 mL/kg/h [
As the widespread
practice has occurred over the past several years, attention has turned to its practical
implementation. A particular focus has been the difference between prescribed and
delivered CRRT dose along with the responsible factors. In turn, another area of
recent interest has been the use of delivered CRRT dose, being a major component of
the overall care provided to many critically ill AKI patients, as a clinical quality
criterion. After an analysis of the major CRRT dose/outcome trials (from the
perspective of the operating parameters employed), this chapter addresses these
more recently identified clinical considerations. This chapter will not address modalities beyond CRRT.
9–16]—included among these studies were two multi-
1].
incorporation of effluent-based CRRT dosing into clinical
atic
CRRT Dose/Outcome Studies: Consideration of Solute Kinetics
One important feature of the effluent-based CRRT dose parameter established by the
Vicenza trial is the need to understand that actual solute clearance as a function of
effluent volume is therapy-specific. In post-dilution CVVH, the modality utilized in
the Ronco et al. trial, there is generally a direct relationship between effluent rate and
solute clearance as long as filter function is preserved—this is the major benefit of
this therapy [5, 17]. Specifically, small solute (urea) clearance and effluent rate are
essentially assumed to be equivalent for this approach. However, due to
hemoconcentration, filter performance may degrade over time, based on surrogate
parameters such filtration fraction, sieving coefficient, and extracorporeal circuit
pressures [
on plasma flow rate and hematocrit [19 , 20]:
Based on the classical equation, filtration fraction (FF) is dependent
18].
39 Dose Prescription in Renal Replacement Therapy 455
where Q
FF = QUF=Q
QP = QB · 1–Hematocrit
is ultrafiltration rate, QB is blood flow rate, and QP is plasma flow rate.
UF
ðÞ
P
Thus, the progressive hematocrit increase that occurs along the length of the filter
used for a convective CRRT modality may need to be mitigated by increasing blood
flow rate to preserve filtration fraction at an acceptable value (less than 0.2).
As noted above, the dose/outcome trials performed subsequent to the Vicenza
study
employed a broad spectrum of CRRT approaches. Several of the studies
involved the pre-dilution delivery of replacement fluid. For pre-dilution therapies,
the interrelationship between blood flow rate and ultrafiltration/replacement fluid
rate also needs to be considered [21]. For example, to achieve urea clearances in
pre-dilution CVVH equivalent to 35 mL/kg/h in post-dilution CVVH, the degree to
which blood dilution occurs (with concomitant reduction of solute concentrations)
must be considered. Pre-dilution can never achieve the 1:1 relationship between
effluent rate and urea clearance characteristic of post-dilution therapies (when
operated with the appropriate blood flow rate), so prescription of pre-dilution
therapies should be done from the perspective of achieving desired depuration
(i.e., solute clearance) with acceptable volumes of replacement fluid.
Blood flow rate is also an important determinant of solute clearance in
pre-dilution modalities. The combination of a relatively low blood flow rate
(<150 mL/min) and relatively high replacement fluid (in an attempt to achieve
effluent doses frequently desired in clinical practice of 25 mL/kg/h or more) results
in a marked diminution of blood urea concentration due to pre-dilution. The only
way to interrupt this vicious cycle of hemodilution leadi ng to low urea clearance is to
prescribe a higher blood flow rate. The minimum blood flow for adequate solute
depuration in pre-dilution is 200 mL/min (the same approximate value for postdilution CVVH to avoid excessive hemoconcentration). When traditional CRRT
blood flow rates in the range of 125–150 mL/min are used, Troyanov et al. have
demonstrated that the decrease in solute clearances for pre-dilution (relative to postdilution) CVVH can be as high as 30–40% [22].
CRRT Dose as a Quality Criterion
Prescribed Versus
The KDIGO consensus statement specifies a range (20–25 mL/kg/h) for delivered
CRRT dose [1] but includes a caveat that prescribed dose should be higher than the
livered dose target in general clinical practice. Of note, this potential mismatch
de
between prescribed and delivered effluent volumes should be differentiated from
dimunitions in the effective dose (i.e., solute clearance), the latter of which may
result in unexpectedly low rates of depuration. Pre-dilution, membrane degradation,
Delivered CRRT Dose
456 W. R. Clark et al.
and unrecognized severe fluid overload (the latter of which resulting in expanded
solute distribution volumes from which clearance is occurring) are primarily responsible for reduced effective dose [17].
In the CRRT dose/outcome
80% of the prescribed dose. To achieve this, however, interventions atypical of
general clinical practice occurred frequently in order to preserve dose delivery. In the
Vicenza trial, when shortfalls in treatment delivery occurred on a particular day,
compensatory dose increases could be made the following day [8]. Furthermore,
concerns about potential decreases in filter membrane permeability resulted in
routine filter changes every 24 h accordi ng to institutional practice.
Data from observational trials indicate that shortfalls in delivery of the prescribed
CRRT dose are more common in routine clinical practice. Based on 115 CRRT
patients treated during 1999–2000 [23] (prior to publication of the Ronco et al. dose
trial), Venkataraman et al. reported a mean daily treatment duration of only
16.1 ± 3.5 (mean ± SD) hours, corresponding to a mean e ffluent flow rate (averaged
over 24 h) of 1.4 ± 0.3 L/h and delivery o f only 68% of the prescribed dose. Clotting
of the extracorporeal circuit was the most common cause of downtime. Vesconi et al.
observed significant variability in delivered dose among patients and even within the
same patient on different days [24]. Approximately 20% of patients received “intensive CRRT,” defined by a prescribed dose ≥35 mL/kg/h. These investigators
reported an approximately 20% difference between median prescribed and delivered
dose (34.3 and 27.1 mL/kg/h, respectively), with circuit clotting contributing to 74%
of downtime incidents.
In a series of 52 patients treated with pre-dilution CVVHDF, Claure et al.
assessed prescribed vs. delivered CRRT dose [25]. Filter clotting was the single
leading cause of therapy downtime, even though citrate anticoagulation was prescribed in all patients. Based on standard urea-based CRRT clearance equations
(accounting for pre-dilution), delivered dose was reported to be only 73% of the
prescribed effluent dose. Thus, with prescribed effluent volume as the reference, a
27% decrease in delivered urea clearance on average was reported.
RCTs, most studies achieved delivery of greater than
CRRT Dose in the Context of Therapy Quality
These analyses of shortfalls in CRRT delivery have led to the belief that CRRT dose
can be viewed as a quality indicator ([26–31]; Fig. 39.1
explored this possibility. In a single-center trial involving a total of 247 patients,
Griffin et al. assessed clinician adherence to an institutional delivered dose target of
20–25 mL/kg/h as part of a quality improvement (QI) initiative. Prior to implementation of the QI program, only 33% of 837 treatments fell in this range, with nearly
50% of treatments consisting of a delivered dose greater than 25 mL/kg/h. The QI
interventions included education of prescribing clinicians and adaptations in the
electronic medical record to allow greater access to dosing data. After these interventions, 66% of 952 treatments achieved compliance with the target dose range.
and recent studies have
),
39 Dose Prescription in Renal Replacement Therapy 457
Systematic and sustainable
monitoring of the CRRT
metric customized to the
logistical setting at the
institution
PURPOSE
Why?
How?
What?
Standardization of CRRT
practice to improve
patient care and resource
utilization
CRRT metric selection
based on local problem
and current evidence
Fig. 39.1 Considerations for the use of CRRT dose as a treatment quality criterion. (Reprinted with
permission from [27])
Conclusions
This chapter provides an update on CRRT dose, incorporating recent information
about this parameter as a treatment quality criterion. Two concluding points are
worth making. First, CRRT dosing is not a static phenomenon as dose needs to be
adapted in response to the constantly changing clinical status of a critically ill AKI
patient, in accordance with the concept of “precision CRRT” [32, 33]. Second, as
recently summarized by Karkar and Ronco [34], dose is just one CRRT parameter
that contributes to overall therapy delivery.
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Pujol W, Grandoulier AS, Fleureau C, Jacobs R, Broux C, Floch H, Branchard O, Franck S,
Rozé H, Collin V, Boer W, Calderon J, Gauche B, Spapen HD, Janvier G, Ouattara A. Highvolume vs standard-volume haemofiltration for septic shock patients with acute kidney injury
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16. Fayad AI, Buamscha DG, Ciapponi A. Intensity of continuous renal replacement therapy for
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therapy in acute kidney injury: a reappraisal. Blood Purif. 2017;44:140–55.
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Kellum JA, Mehta R, Rosner MH. On behalf of the nomenclature standardization faculty:
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398–405.
21. Huang Z, Letteri JJ, Clark WR, Zhang W, Gao D, Ronco C. Ultrafiltration rate as dose surrogate
in pre-dilution hemofiltration. Int J Artif Organs. 2007;30:124–32.
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clearances during continuous venovenous haemofiltration at various ultrafiltration flow rates
using multiflow-100 and HF1000 filters. Nephrol Dial Transplant. 2003;18(5):961
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Vesconi S,
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Formica M, Marchesi M, René R, Livigni S, Ronco C. DOse REsponse Multicentre
Kellum JA,
Cruz DN, Fumagalli R, Kindgen-Milles
Palevsky P. Dosing patterns for continuous renal replacement
D, Monti G, Marinho A, Mariano F,
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EP, Mehta RL. Toward the optimal dose metric in continuous renal replacement therapy. Int J
Artif Organs. 2012;35(6):413–24.
26. Griffin BR, Thomson A, Yoder M, et al. Continuous renal replacement therapy dosing in
critically ill patients: a quality improvement initiative. Am J Kidney Dis. 2019;74:727–35.
27. Neyra JA, Tolwani A. A quality improvement initiative targeting CRRT delivered dose: the
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28. Neyra JA, Tolwani A. CRRT prescription and delivery of dose. Semin Dial. 2021;34:432–9.
29. Vásquez Jiménez E, Anumudu SJ, Neyra JA. Dose of continuous renal replacement therapy in
critically ill patients: a bona fide quality indicator. Nephron. 2021;145:91–8.
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Chapter 40
Indications and Timing of Renal
Replacement Therapy
Sean M. Bagsha w and Ron Wald
Introduction
Acute kidney injury (AKI) is a vexing challenge for nephrologists, intensivists, and
other healthcare profession als caring for critically ill patients [1]. Abundant evidence
has shown AKI portends a higher risk for a spectrum of adverse events, including
new or worsened chronic kidney disease (CKD), progression to end-stage kidney
disease (ESKD), cerebral and cardiovascular events [2, 3], new infections and sepsis
[4, 5], gastrointestinal bleeding [6], malignancy [ 7 ], fracture risk [8], and death
[9, 10].
Renal replacement therapy (RRT) is an essential organ support modality in the
practice of modern critical care. RRT can encompass a continuum of different
modalities, including continuous (CRRT), intermittent (IHD), hybrid systems and
acute peritoneal dialysis (PD). A significant proportion of critically ill patients with
severe AKI, particularly in those who develop urgent indications characterized by
metabolic, toxic, or fluid-related complications attributed to AKI, are considered for
and receive RRT [11]. RRT is used in 10–12% of critically ill patients with severe
AKI, and while temporal trends have suggested growing utilization, this is contingent on resource availability [12, 13]. RRT can have an important role in effectively
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-66541-7_40.
S. M. Bagshaw (
Department of Critical Care Medicine, Faculty of Medicine and Dentistry, University of
Alberta, and Alberta Health Services, Edmonton, AB, Canada
e-mail: bagshaw@ualberta.ca
R. Wald
Division
Li Ka Shing Knowledge Institute of St Michael’s Hospital, Toronto, ON, Canada
e-mail: Ron.Wald@unityhealth.to
© 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_40
✉)
of Nephrology, St. Michael’s Hospital, Toronto, ON, Canada
461
462 S. M. Bagshaw and R. Wald
facilitating the removal of excess fluid, eliminating metabolic waste, correcting
electrolyte derangements, and restoring base buffer. RRT can also support additional
therapies that may be less tolerated in the setting of severe AKI (e.g., nutrition,
medications, transfusions). RRT does not, however, “replace” many of the neuroendocrine functions of the kidneys (e.g., production of erythropoietin, reabsorption
of amino acids, activation of vitamin D, regulat
rone system) [
14]. Whether
this loss of function is causally related to the burden of
ion of the renin-angiotensin-aldoste-
the short- and long-term adverse events associated with AKI in critical illness and
whether starting RRT can mitigate these events are uncertain.
Patient Selection and Indications for Starting RRT
An important consideration when starting RRT in a critically ill patient with severe
AKI is to clearly define the intent and objective. This has certainly represented a
long-standing dilemma for clinicians, particularly in the absence of conventional
“absolute” indications (Table 40.1). A KDIGO Controversies Conference on Acute
Kidney Injury revisited the issue of timing of RRT initiation and highlighted both the
clinical uncertainty and the variation in practice [15]. The consensus statement
proposed RRT to be considered when a patient’s metabolic and fluid “demands”
Table 40.1 Summary of potential indications and contraindications for starting renal replacement
therapy in the setting of acute kidney injury in the intensive care unit
Urgent indications
(in the absence of contraindications to RRT)
Relative indications
(in the absence of urgent
indications of AKI)
Relative contraindications Low l
Abbreviations: AKI acute kidney
KDIGO Kidney Disease: Improving Global Outcomes, RRT renal replacement therapy
Severe hyperkalemia (K
diac toxicity) refractory to medical therapy
Severe acidemia or metabolic acidosis (pH ≤ 7.2 or serum
[HCO
-] ≤ 12 mmol/L despite normal or low arterial pCO2)
3
refractory to medical therapy
Severe hypoxemia and perception of volume overload (diureticresistant pulmonary edema)
Uremic complications (bleeding, pericarditis, encephalopathy)
Intoxication with a dialyzable drug or toxin (salicylates, lithium,
toxic alcohols, metformin)
Persistent severe AKI (KDIGO stage 3 +/- prolonged
oligoanuria)
Severe non-kidney organ dysfunction exacerbated by AKI
Severe or worsening illness acuity and trajectory
Anticipated solute burden (tumor lysis syndrome, rhabdomyolysis, intravascular hemolysis)
Limited physiological reserve to tolerate the consequences of
AKI (i.e., demand-supply mismatch)
ikelihood f
Receiving palliative care and/or approaching end-of-life
High likelihood of non-recovery in patients who are not longterm dialysis candidates
injury, CKD chronic kidney disease, ICU intensive care unit,
+
≥ 6.0 mmol/L, rapidly rising, or car-
or benefit (futile prognosis)
40 Indications and Timing of Renal
Replacement Therapy 463
Ye s
Shared
decision-making
carer
• Multidisciplinary
care team
• Social/cultural
factors
Ye s
Medical evaluation for
RRT initiation
• Severity/duration • Patients/family/
• Demand/capacity
balance assessment
• Biomarkers
• Dynamic testing
(furosemide stress test)
• Risk of complications
• Potential for recovery
• Fluid status
• Effects of AKI on non renal organ function
No
Monitoring for
RRT indication
Withholding RRT
Start optimal RRT care
(shared decision-making
where possible)
• Modality • Recovery
• Dose
• Vascular access
• Anticoagulation
• Transition
• Drug dosing
• Combination with other forms
of extracorporeal life support
• Membrane
Stop RRT
(shared decision-making
where possible)
- Assessment of kidney
function
- Optimal follow-up care
• Transition of goal of care
toward comfort care
Fig. 40.1 Schematic diagram of RRT decisions in AKI. (Reproduced from [15])
exceed their kidney’s “capacity” in the setting of AKI, where complications are
predictable. The challenge has been to identify reliable, validated, and readily
available tools to quantify this kidney demand-supply relationship at the point-ofcare and augment clinical decision-making for when to start RRT [16].
In patients with complications attributed
to AKI that are refractory to medical
therapy (e.g., hyperkalemia, acidemia, fluid overload), starting RRT is appropriate.
In the absence of absolute indications, RRT is generally started in response to
“relative” indications. These can vary by setting and case-mix and generally should
consider dynamic trends in illness acuity, and non-kidney organ dysfunction, along
with the perception of benefit by clinicians [11]. For example, there is no highquality evidence to guide starting RRT in patients receiving extracorporeal life
support (ECLS); however, these patients may have different thresholds (e.g., fluid
accumulation) for triggering RRT when compared to those not receiving ECLS
[17, 18]. An added consideration that should guide the decision for starting RRT is
engagement with patients and families in a shared process that routinely integrates
the overall prognosis, the potential for kidney recovery, the patient-specific risks of
RRT, and an understanding of patients’ preferences [15] (Fig. 40.1).
Further, it is critical to recognize that RRT is an invasive organ support technology with the potential for a fixed risk of complications. These can be related to
dialysis catheter insertion and maintenance (e.g., bloodstream infection) or therapyspecific events (e.g., anticoagulation, intradialytic hemodynamic instability, arrhythmias, electrolyte abnormalities, delayed or non-recovery) (Table 40.2).
Strategies to Identify Need for RRT
The development of tools to guide clinicians in identifying when to ideally start RRT
in critically ill patients with AKI is urgently needed. Prior studies and clinical trials
employed a wide spectrum of definitions for “early,” “delayed,” or “late” RRT
initiation [19, 20]. These definitions have often used common physiological
464 S. M. Bagshaw and R. Wald
Table 40.2 Summary of the potential benefits and risks for starting renal replacement therapy in
the setting of acute kidney injury in the intensive care unit
Benefits Drawbacks
Avoid or mitigate volume accumulation Complications with the dialysis catheter (bleeding,
Avoid and/or mitigate acid-base
derangement
Avoid
and/or mitigate metabolic
derangement
Avoid
unnecessary or adverse diuretic
exposure
Immunomodulation and clearance of
inflammatory mediators
Avoid or mitigate non-kidney organ
effects (heart, lungs, liver, brain)
Abbreviations: AKI acute
kidney injury, RRT renal
pneumothorax, bloodstream infection)
Complications with anticoagulation
Iatrogenic hemodynamic instability (exacerbate AKI
and delay
Excess loss of unmeasured micronutrients and trace
elements
Excess clearance or suboptimal dosing of drugs
(antimicrobials, antiepileptics)
Increased bedside workload for healthcare processional, resource use and direct health costs
kidney recovery)
replacement therapy
parameters (e.g., urine output, fluid overload) and laboratory parameters (e.g., serum
creatinine, urea, pH, serum potassium). Many have also used measures of time (e.g.,
hours, days) from AKI onset, duration from hospital or ICU admission or duration
from the detection of an AKI-related complication, or absolute indication [10, 19–
22]. These proposed thresholds for starting RRT are prone to bias and can be
challenging to operationalize.
Several
for
critically
risk
prediction scores
p
atients with AKI [ 23]; however, few have focused on predicting the
ill
have
been
propos
ed
to
estimate the
risk of
mortality
receipt of RRT. Pannu et al. derived and validated a clinical risk index comprised of
eight routinely available clinical factors to predict postoperative RRT within 14 days
among patients undergo ing cardiac surgery (baseline eGFR, diabetes mellitus,
proteinuria, heart failure, CCS angina score ≥ 3, serum hemoglobin, type of surgery,
and emergency surgery) [24]. The discrimination in the validation cohort was
excellent (AUC 0.83, 95% CI, 0.79–0.86). In a similar risk prediction index focused
on receipt of RRT within 14 days of noncardiac surgery, Wilson et al. described nine
routinely captured perioperative variables (age; male sex; baseline eGFR; albuminuria; prior myocardial infarction; liver disease; surgery type; serum hemoglobin) and
reported excellent discrimination in the validation model (sensitivity 21%; specificity 99.9%; AUC 0.95, 95 CI, 0.95–0.96) [25]
. R
isk prediction indices have also been
described for cardiogenic shock [CALL-K score) [26] and in a secondary analysis of
a pooled dataset from the AKIKI and IDEAL-ICU trials; however, neither have been
externally validated [27]. Numerous studies have applied machine learning/artificial
intelligence techniques to derive risk prediction models for the development of AKI
and prognosis among those with AKI receiving RRT; howe ver, none have focused
specifically on probability of receiving RRT [28–3
Novel
biomarkers of kidney injury or damage (e.g., neutrophil gelatinase-
0].
associated lipocalin [NGAL], urinary tissue inhibitor of metalloproteinase-2 and
insulin growth factor binding protein-7 [TIMP-2]•[IGFBP-7], urinary CC-motif