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444 A. Fioccola and G. Villa
Fig. 38.1 The role of both non-pharmacological and pharmacological strategies in increasing
treatment efficiency. The non-pharmacological strategies aim to reduce the filtration fraction, thus
decreasing the protein concentration into the hemodiafilter. This mainly inhibits clogging phenomena. The pharmacological strategies, blocking coagulation factors and/or platelets activation,
mainly inhibit clotting phenomena
protamine [13]. All these methods hinder coagulation factors and/or platelets into the
hemodiafilter, thus inhibiting clotting phenomena.
Unfractionated Heparin (UFH) Systemic Anticoagulation
Systemic anticoagulation with unfractionated heparin is one of the most frequently
employed techniques in patients undergoing CRRT. The unfractionated heparin
inhibits the IIa and the Xa factors via a potentiation of the activity of the antithrombin (AT) factor [14], with an anticoagulant effect directly measurable with the
activated partial thromboplastin time (aPTT) prolongation [11] or with the activated
clotting time (ACT) [15]. When compared with the LMWH, the UFH has lower
costs, shorter half- life, and less pharmacokinetic dependance on kidney function
[14]. These features give the UFH a higher popularity for anticoagulation in EBPs.
Systemic heparin anticoagulation apparently has reduced costs also if compared with
RCA. Nonetheless, including in the analysis the higher risk of bleeding (requiring
blood transfusion or even surgical hemostatic procedures), the AT replacement
required during heparin administration (to maintain a physiologic 70% level of
activity), or costs associated with heparin induced thrombocytopenia (HIT), systemic anticoagulation with UFH has much higher costs than RCA. For instance, HIT
occurs more frequently than LMWH [16] and especially in female subjects and
postsurgical patients [16] or when using higher doses of heparin [17]. Systemic
anticoagulation with UFH seems being preferred when multiple extracorporeal
treatments (e.g., extracorporeal membrane oxygenation, ECMO) are applied in the
same patients. Nonetheless, even if the patient already requires UFH for systemic
anticoagulation, RCA can be applied to CRRT to further prevent membrane fouling
into the hemodiafilter. This strategy has a strong rationale (considering the different
blood flows in the ECMO and CRRT circuits), and it seems more efficacious than
UFH alone in reducing membrane fouling.
Different
with unfractionated heparin. In one of the most known and employed [
protocols can be applied when performing a systemic anticoagulation
18], a heparin
38 Anticoagulation Strategies in Continuous Renal Replacement Therapy 445
Table 38.1 Common anticoagulant dosages in continuous renal replacement therapy
Anticoagulant
Heparin (UFH) 5–15 IU/
Regional heparin with
protamine
Enoxaparin
(LMWH)
Argatroban 0.1 mg/
Bivalirudin N/A 2 mg/h Target: aPTT 1.5–2 times baseline.
Regional citrate
anticoagulation
Adapted from: Legrand and Tolwani [11]
Loading
dose Maintenance Monitoring
kg
N/A Heparin prefilter: 1000–
0.15 mg/
kg
kg
N/A Infused to achieve a citrate
5–10 UI/kg/h Target: aPTT in the circuit 45–60 s or
1500 UI/h. Protamine postfilter: 10–12 mg/h
0.05 mg/kg/h Target: anti Xa 0.25–0.35 IU/mL.
0.05–0.2 mg/kg/min Target: aPTT 1.5–2 times baseline.
blood concentration of 3–
4 mmol/L
anti-Xa activity 0.3–0.6 IU/mL. Fre-
quency: every 6 h after starting
treatment or changing dose; then
every 12 h if
needed
Target: patient aPTT <45 s and circuit aPTT 50–80 s. Frequency: 4–
15 min after dose and then every 2–
8h
Frequency: every 6–12 h
Frequency: every 2–4 h until aPTT
values are therapeutic for two readings. Frequency can then be
decreased to every 12 h
Frequency: every 2–4 h until aPTT
values are therapeutic for two readings. Frequency can then be
decreased to every 12 h
Target: post-filter iCa < 0.35 mmol/
L
Measurement frequency: circuit and
systemic iCa levels every 6–8h
no further
changes
bolus of 10 UI/kg is administered, followed by a 10–15 UI/kg/h continuous intra-
venous infusion. Anticoagulation tests (aPTT/ACT) are checked every 6 h, with the
aim to keep APTT at 1.2–1.5 times the normal values and ACT between 160 and
180, changing the drug infusion speed accordingly (Table
38.1).
Systemic Anticoagulation with Low Molecular Weight Heparin (LMWH)
Systemic anticoagulation can also be performed with a low-molecular-weight heparin. However, this alternative is less frequently implemented for different reasons.
Firstly, LMWH has a longer half-life when compared to UFH, with a response to
reversal by protamine that might be less efficient [
dependent from renal elimination, possibly having very long half-lives if administrated without dose adjustment [20, 21] in patients with impaired renal function, with
14, 19]. Secondly, they are more
446 A. Fioccola and G. Villa
an increased risk of unexpected bleeding [22]. Finally, LMWH effect has to be
monitored using anti-Xa assays, keeping it between 0.25 and 0.35 UI/mL [23–
25]. These assays have higher costs when compared to aPTTs, the routine laboratory
test used to monitor UFH activity. Dosing of LMWH for anticoagulation in RRT is
reported in Table 38.1.
Regional Citrate Anticoagulation (RCA)
Regional citrate anticoagulation (RCA) has been introduced in the clinical practice
more than 30 years ago [ 26]. The KDIGO guidelines released in 2012 by the Kidney
Disease Improving Global Outcomes [27] identify the RCA as the first line for
CRRT circuit anticoagulation, in patients without contraindications (shock, hypoxia,
acute liver failure, metabolic disturbances) [
arin, the main advantages of citrate are a lower incidence of intraprocedural bleeding, reduced transfusion needs, and an increased filter patency [
patients undergoing an RRT with RCA have failed to show a decreased mortality
when compared to UFH systemic anticoagulation [
into the prefilter circuit, it forms complexes with the ionized calcium, an essential
cofactor of the coagulation cascade, thus avoiding or diminishing clotting phenomena. Some of the calcium-citrate complexes are eliminated in the effluent (30–60%)
],
[31
while the remaining reach the systemic circulation. The citr ate-calcium complexes reinfused to the patient through the outflow line (citrate load) are then
metabolized by the liver, the muscles, and the kidney toward the Krebs cycle,
releasing citrate, sodium bicarbonate, and ionized calcium. The most frequent
complications in patients without any impairment in citric acid metabolism are
hypocalcemia and metabolic alkalosis: the first can result from an insufficient
calcium replacement to the patient, while the latter is the consequence of bicarbonate
production after the endogenous citrate metabolism if an excess in citrate load is
administered. The buffer provided to the patient as citrate load (thus, metabolized to
sodium bicarbonate) is the reason why replacement and dialysate solutions used
during RCA have a lower bicarbonate concentration than the standard solutions used
for CRRT. On the other hand, in patients with inadequate or compromised citrate
metabolism (e.g., during decreased tissue oxygen delivery, mitochondrial dysfunction, or acute liver failure), citrate can accumulate in the organism, causing an
increased anion-gap metabolic acidosis. In this context, metabolic acidosis occurs
mainly for the lack of bicarbonate provided to the patients as unmetabolized citrate
load. Clinical signs of citrate intoxication and their common causes are synthetized
in Table 38.2 . It is important to underline that the presence of one or more of these
signs has always to be critically interpreted, because the underlining causes can be
different at the same time. Finally, it must be considered that the citrate is an energy
source for the organism. With an hourly citrate delivery of 11–20 mmol/h [32], as
provided by typical CRRT protocols, it provides an energy load of 150–280 kcal/
24 h [11].
28]. When compared to systemic hep-
29].
Nevertheless,
30]. Once the citrate is introduced
38 Anticoagulation Strategies in Continuous Renal Replacement Therapy 447
Table 38.2 Clinical signs suggesting citrate accumulation when performing a regional citrate
anticoagulation
Clinical sign Underlying mechanism
Metabolic alkalosis Bicarbonate production and/or increased plasmatic sodium
Hypocalcemia Inadequate calcium replacement in the post-filter line
Increased total calcium (Ca
Low ionized to total calcium ratio
2+
/Ca
(Ca
Metabolic acidosis with increased
anion gap
tot
< 2.5)
tot
(when hypertonic solutions are employed)
) High rates of calcium replacement in the post-filter line
Impaired citrate metabolism (hypoxia, liver failure)
Impaired citrate metabolism (hypoxia, liver failure)
The citrate infusion speed in the inflow line (prefilter) is set accordingly to the
blood flow rate in order to obtain a citrate concentration of 3–4 mmol/L (citrate dose)
into the filter (corresponding to a ionized calcium (
[11]. The citrate dose is continuously readjusted according to the
2+
Ca
) of 0.25–0.4 mmol/L)
i
i
Ca
2+
concentration
in the circuit (dynamic prescription). The higher the citrate dose, and the higher the
blood flow prescribed, the higher the citrate load. For this reason, the blood flow rate
during RCA is usually set to values lower than 150 mL/min [11, 33].
It
must be
considered that, in a subject with a normal citrate metabolism, a safe and tolerable
citrate load is 11–20 mmol/h [32].
Citrate solutions are usually provided as high concentrated (hypertonic) or low
concentrated (isotonic) formulations . The former have higher citrate concentration
(about 140 mmol/L) and require slow infusion rate to maintain citrate dose. For this
reason, they can be used in both diffusive and convective modalities (CVVHD,
CVVH, CVVHDF). The hypertonic solutions have an over-physiological sodium
concentration. In the sodium citrate 4%, the [Na
+
] is equal to 406 mmol/L, almost
three times the physiological one. For this reason, hypertonic solutions may cause
hypernatremia and increase the strong ion difference (SID), with an increased
tendency to cause metabolic alkalosis. They are normally infused in a syringe
pump, coupled with hyponatremic dialysate or hyponatremic post-filter replacement
solutions (Fig.
38.2, panel a and b). Differently, in isotonic preparations, the citrate
concentration is ten times lower (about 15–20 mmol/L). For this reason, they need
high infusion speeds to reach the target citrate concentration into the filter
(3–4 mmol/L), and they can only be used in convective modalities (CVVHDF,
CVVH), being normally administrated as a pre-replacement fluid (Fig. 38.2, panel
c and d) and thus determining the presence of an ultrafiltration.
In purely
diffusive or in mixed modalities (CVVHD, CVVHDF), a dialysate
calcium-free solution is normally used, in order to minimize the amount of free
ionized calcium into the filter, using the lowest possible quantity of citrate.
448 A. Fioccola and G. Villa
a
c
Fig. 38.2 Different CRRT circuit with RCA anticoagulation. In panel a, a continuous veno-venous
hemodialysis (CVVHD) is performed with a prefilter hypertonic citrate solution. In this case, the
high concentrated citrate allows to have a low infusion speed, with a negligible ultrafiltration, thus
preserving the purely diffusive nature of the treatment. In panel b and c, a continuous veno-venous
hemodiafiltration (CVVHDF) is performed with a hypertonic (b) or an isotonic (c) citrate solution.
In panel d, a schematic CVVH performed with an isotonic citrate preparation. Both in panel c and d,
the citrate is delivered as a pre-dilution (Q
allows to use higher flows. When hypertonic preparations with citrate are employed, hyponatremic
dialysate and/or replacement solutions are normally used, in order to decrease the possibility of
systemic hypernatremia. This latter side effect increases strong ion difference (SID), further
enhancing a tendency to metabolic alkalosis
b
d
), thanks to its low concentration in the solution that
r-pre
Regional Anticoagulation with Prefilter Unfractionated
Heparin and Post-filter Protamine
This technique allows to obtain a regional anticoagulation with lower costs when
compared to the RCA. The heparin is administered in the prefilter line and the
protamine in the post-filter. They are initially set with a ratio of 100(UI/h):1(mg/h),
with subsequent adjustments according to aPTT checked every 2–8 h [11]. For
le, for an UFH initially set at 1500 UI/H, the protamine speed infusion will
examp
be 15 mg/h. This technique can also be coupled with a prefilter anti-aggregation
strategy [13], in order to enhance filter
widespread technique, because it potentially exposes the patient to both side effects
of heparin and protamine: HIT, increased bleeding, pulmonary hypertension (with
possible right heart failure), and anaphylaxis. The KDIGO guidelines suggest
against the use of this technique that should not be used in clinical practice anymore.
patency. The heparin/protamine is not a
38 Anticoagulation Strategies in Continuous Renal Replacement Therapy 449
Systemic Anticoagulation with Direct Thrombin Antagonists
Direct thrombin antagonists (argatroban, bivalirudin) can be used for systemic
anticoagulation in patients that develop a heparin induced thrombocytopenia (HIT)
but still need an anticoagulation method to continue the EBP or do have clinical
indications for systemic anticoagulation (i.e., deep venous thrombosis, pulmonary
embolism, or cardiac valve implants). Argatroban is normally administrated as a
bolus of 0.1 mg/kg, with a subsequent continuous infusion of 0.1–0.2 mg/kg/h [
34–
36]. Bivalirudin is given at 2 mg/h, with the infusion speed corrected on the aPTT, to
be kept at 1.5–2.5 times the normal values [37] (Table 38.2).
Nafamostat
Nafamostat is a protease inhibitor, used for circuit anticoagulation in patients with
increased bleeding risk, thanks to its short half-life [
Korea, and its diffusion is mainly hampered by its possible side effects: agranulocytosis, anaphylaxis, and hyperkalemia.
38]. It is popular in Japan and
Conclusions
Pharmacological and non-pharmacological strategies should be always considered
during CRRT or any EBP applied to critically ill patients. In particular, a filtration
fraction as lower as possible should be applied to CRRT to prevent filter clotting and
clogging. Systemic anticoagulation with heparin and regional citrate anticoagulation
are the overall most employed pharmacological techniques to increase filter patency.
The 2012 KDIGO guidelines suggest RCA as first line in patients without contraindications [
27], although epidemiological data [5, 39] reveals that anticoagulation
with systemic heparin is still the most common performed technique.
References
1. Villa G, et al. Methods for dose quantification in continuous renal replacement therapy: toward
a more precise approach. Artif Organs. 2021;45(11):1300–7. https://doi.org/10.1111/aor.
13991.
2. Michel T, Ksouri H, Schneider AG. Continuous renal replacement therapy: understanding
circuit hemodynamics to improve therapy adequacy. Curr Opin Crit Care. 2018;24(6):
455–62. https://doi.org/10.1097/MCC.0000000000000545.
Neri M,
3.
principles. Crit Care. 2016;20(1):318. https://doi.org/10.1186/s13054-016-1489-9.
et al. Nomenclature for renal replacement therapy in acute kidney injury: basic
450 A. Fioccola and G. Villa
4. Honore PM, Spapen HD. What a clinician should know about a renal replacement membrane? J
Transl Int Med. 2018;6(2):62–5. https://doi.org/10.2478/jtim-2018-0016.
5. Uchino S, Fealy N, Baldwin I, Morimatsu H, Bellomo R. Continuous is not continuous: the
incidence and impact of circuit ‘down-time’ on uraemic control during continuous veno-venous
haemofiltration. Intensive Care Med. 2003;29(4):575–8. https://doi.org/10.1007/S00134-003-
1672-8.
6. Fealy N,
continuous veno-venous haemofiltration. Crit Care Resusc. 2002;4(4):266–70.
7. Villa G, et al. A role of circuit clotting and strategies to prevent it during blood purification
therapy with oXiris membrane: an observational multicenter study. Blood Purif. 2022;51(6):
503–12. https://doi.org/10.1159/000524230.
8. Brandenburger T, Dimski T, Slowinski T, Kindgen-Milles D. Renal replacement therapy and
anticoagulation. Best Pract Res Clin Anaesthesiol. 2017;31(3):387 – 401. https://doi.org/10.
1016/J.BPA.2017.08.005.
9. Karkar A, Ronco C. Prescription of CRRT: a pathway to optimize therapy. Ann Intensive Care.
2020;10(1):32. https://doi.org/10.1186/S13613-020-0648-Y.
10. Li L, Bai M, Yu Y, Li Y, Zhao L, Sun S. Regional citrate anticoagulation vs no-anticoagulation
for CRRT in hyperlactatemia patients with increased bleeding risk: a retrospective cohort study.
Semin Dial. 2020;34(3):209–17. https://doi.org/10.1111/SDI.12923.
11. Legrand M, Tolwani A. Anticoagulation strategies in continuous renal replacement therapy.
Semin Dial. 2021;34(6):416–22. https://doi.org/10.1111/SDI.12959.
12. Singh S. Anticoagulation during renal replacement therapy. Indian J Crit Care Med. 2020;24
(Suppl 3):S112. https://doi.org/10.5005/JP-JOURNALS-10071-23412.
13. Fabbri LP, Nucera M, Al Malyan M, Becchi C. Regional anticoagulation and antiaggregation
for CVVH in critically ill patients: a prospective, randomized, controlled pilot study. Acta
Anaesthesiol Scand. 2010;54(1):92–7. https://doi.org/10.1111/J.1399-6576.2009.02031.X.
14. Alquwaizani M, Buckley L, Adams C, Fanikos J. Anticoagulants: a review of the pharmacology, dosing, and complications. Curr Emerg Hosp Med Rep. 2013;1(2):83–97. https://doi.org/
10.1007/s40138-013-0014-6.
15. Levy JH, McKee A. Bleeding, hemostasis, and transfusion medicine. In: Cardiothoracic critical
care. Philadelphia: Butterworth-Heinemann; 2007. p. 437–60. https://doi.org/10.1016/B978-
075067572-7.50033-3.
16. Martel N, Lee J, Wells PS. Risk for heparin-induced thrombocytopenia with unfractionated and
low-molecular-weight heparin thromboprophylaxis: a meta-analysis. Blood. 2005;106(8):
2710–5. https://doi.org/10.1182/BLOOD-2005-04-1546.
17. Smythe MA, Koerber JM, Mattson JC. The incidence of recognized heparin-induced thrombocytopenia in a large, tertiary care teaching hospital. Chest. 2007;131(6):1644–9. https://doi.org/
10.1378/CHEST.06-2109.
18. Ostermann M, Dickie H, Tovey L, Treacher D. Heparin algorithm for anticoagulation during
continuous renal replacement therapy. Crit Care. 2010;14(3):419. https://doi.org
cc9003.
19. Harenberg J, Gnasso A, de Vries JX, Zimmermann R, Augustin J. Inhibition of low molecular
weight heparin by protamine chloride in vivo. Thromb Res. 1985;38(1):11–20. https://doi.org/
10.1016/0049-3848(85)90003-9.
20. Lim W, Dentali F, Eikelboom JW, Crowther MA. Meta-analysis:
and bleeding in patients with severe renal insufficiency. Ann Intern Med. 2006;144(9):673–84.
https://doi.org/10.7326/0003-4819-144-9-200605020-00011.
21. Garcia DA, Baglin TP, Weitz JI, Samama MM. Parenteral anticoagulants: antithrombotic
therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians
Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2 Suppl):e24S–43S. https://
doi.org/10.1378/CHEST.11-2291.
Baldwin I, Bellomo R. The effect of circuit ‘down-time’ on uraemic control during
/10.1186/
low-molecular-weight heparin
38 Anticoagulation Strategies in Continuous Renal Replacement Therapy 451
22. Farooq V, et al. Serious adverse incidents with the usage of low molecular weight heparins in
patients with chronic kidney disease. Am J Kidney Dis. 2003;43:531. https://doi.org/10.1053/j.
ajkd.2003.11.012.
23. Reeves JH, Cumming AR, Gallagher L, O’Brien JL, Santamaria JD. A controlled trial of low-
molecular-weight heparin (dalteparin) versus unfractionated heparin
continuous venovenous hemodialysis with filtration. Crit Care Med. 1999;27(10):2224–8.
https://doi.org/10.1097/00003246-199910000-00026.
24. De Pont ACJM, Oudemans-van Straaten HM, Roozendaal KJ, Zandstra DF. Nadroparin versus
dalteparin anticoagulation in high-volume, continuous venovenous hemofiltration: a doubleblind, randomized, crossover study. Crit Care Med. 2000;28(2):421–5. https://doi.org/10.1097/
00003246-200002000-00022.
25. Joannidis M, et al. Enoxaparin vs. unfractionated heparin for anticoagulation during continuous
veno-venous hemofiltration: a randomized controlled crossover study. Intensive Care Med.
2007;33(9):1571–9. https://doi.org/10.1007/S00134-007-0719-7.
26. Mehta RL, McDonald BR, Aguilar MM, Ward DM. Regional citrate anticoagulation for
continuous arteriovenous hemodialysis in critically ill patients. Kidney Int. 1990;38(5):
976–81. https://doi.org/10.1038/KI.1990.300.
27. Khwaja A. KDIGO clinical practice guidelines for acute kidney injury. Nephron Clin Pract.
2012;120(4):c179. https://doi.org/10.1159/000339789.
28. Davenport A, Tolwani A. Citrate anticoagulation for continuous renal replacement therapy
(CRRT) in patients with acute kidney injury admitted to the intensive care unit. NDT Plus.
2009;2(6):439. https://doi.org/10.1093/NDTPLUS/SFP136.
29. Monchi M, Berghmans D, Ledoux D, Canivet JL, Dubois B, Damas P. Citrate vs. heparin for
anticoagulation in continuous venovenous hemofiltration: a prospective randomized study.
Intensive Care Med. 2004;30(2):260–5. https://doi.org/10.1007/S00134-003-2047-X.
30. Zarbock A, et al. Effect of regional citrate anticoagulation vs systemic heparin anticoagulation
during continuous kidney replacement therapy on dialysis filter life span and mortality among
critically ill patients with acute kidney injury: a randomized clinical trial. JAMA. 2020;324(16):
1629–39. https://doi.org/10.1001/JAMA.2020.18618.
31. Pistolesi V, et al. Regional citrate anticoagulation (RCA) in critically ill patients undergoing
renal replacement therapy (RRT): expert opinion from the SIAARTI-SIN joint commission. J
Anesth Analg Crit Care. 2023;3(1):1–14. https://doi.org/10.1186/S44158-023-00091-W.
32. Fiaccadori E, et al. Regional citrate anticoagulation for renal replacement therapies in patients
with acute kidney injury: a position statement of the work group ‘renal replacement therapies in
critically ill patients’ of the Italian Society of Nephrology. J Nephrol. 2015;28(2):151–64.
https://doi.org/10.1007/S40620-014-0160-2/FIGURES/1.
33. Morabito S, Pistolesi V, Tritapepe L, Fiaccadori E. Regional citrate anticoagulation for RRTs in
critically ill patients with AKI. Clin J Am Soc Nephrol. 2014;9(12):2173–88. https://doi.org/10.
2215/CJN.01280214.
34. Reddy BV, Grossman EJ, Trevino SA, Hursting MJ, Murray PT. Argatroban anticoagulation in
patients with heparin-induced thrombocytopenia requiring renal replacement therapy. Ann
Pharmacother. 2005;39(10):1601–5. https://doi.org/10.1345/APH.1G033.
35. Link A, Girndt M, Selejan S, Mathes A, Böhm M, Rensing H. Argatroban for anticoagulation in
continuous renal replacement therapy. Crit Care Med. 2009;37(1):105–10. https://doi.org/10.
1097/CCM.0B013E3181932394.
36.
Tang IY, et al. Argatroban and renal replacement therapy in patients with heparin-induced
thrombocytopenia. Ann Pharmacother. 2005;39(2):23
1E480.
37.
Kiser TH,
heparin for prevention of hemofilter occlusion during continuous renal replacement therapy.
Pharmacotherapy. 2010;30(11):1117–26. https://doi.org/10.1592/PHCO.30.11.1117.
MacLaren R, Fish DN, Hassell KL, Teitelbaum I. Bivalirudin versus unfractionated
1–6. https://doi.org/10.1345/APH.
as anticoagulant during
452 A. Fioccola and G. Villa
38. Choi J-Y, et al. Nafamostat mesilate as an anticoagulant during continuous renal replacement
therapy in patients with high bleeding risk a randomized clinical trial. Medicine (Baltimore).
2015;94(52):e2392.
https://doi.org/10.1097/MD.0000000000002392.
39. Palevsky PM, O’Connor TZ, Chertow GM, Crowley ST, Zhang JH, Kellum JA. Intensity of
renal replacement therapy in acute kidney injury: perspective from within the acute renal failure
trial network study. Crit Care. 2009;13(4):310. https://doi.org/10.1186/CC7901.
Chapter 39
Dose Prescription in Renal Replacement
Therapy
William R. Clark, Danielle Soranno, Anna Lorenzin, and Claudio Ronco
Introduction
The assessment of prescribed and delivered dose of continuous renal replacement
therapy (CRRT) for critically ill patients with acute kidney injury (AKI) is now part
of routine clinical practice [1]. The concept of dialysis dose was first established for
chroni
c hemodialysis (HD) more than 40 years ago with the introduction of urea
Kt/V, which remains the standard for quantifying dose in end-stage renal disease
[2]. For the treatment of critically ill AKI patients, adaptations of urea kinetic
ds demonstrated superior urea clearance, and azotemia control can be
metho
achieved with continuous renal replacement therapy (CRRT) relative to conventional HD [3, 4]. Additional studies indicated CRRT has a similar advantage in the
removal of solutes substantially larger in molecular size than urea [5, 6].
While the studies demonstrating CRRT’s superiority over conventional HD with
respec
t to solute removal were based on kinetic modeling techniques, they helped
establish CRRT as the preferred treatment modality for AKI in many intensive care
units [7]. The concept of dose in AKI was adapted and broadened by a landmark trial
which normalized effluent volume rather than a specific solute acted as the dose
in
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-66541-7_39.
W. R. Clark (
Davidson School of Chemical Engineering, Purdue University, West Lafayette, IN, USA
e-mail: clarkw@purdue.edu
D. Soranno
Riley
e-mail: dsoranno@iu.edu
A. Lorenzin · C. Ronco
International
e-mail: cronco@goldnet.it
© The
A. Cotoia et al. (eds.), Nutrition, Metabolism and Kidney Support,
https://doi.org/10.1007/978-3-031-66541-7_39
✉)
Hospital for Children, Nephrology, Indianapolis, IN, USA
Renal Research Institute of Vicenza, Vicenza, Italy
Author(s), under exclusive license to Springer Nature Switzerland AG 2024
453