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Continuous Renal
Replacement Therapy
Pittsburgh Critical Care Medicine

Published and Forthcoming Books in

the Pittsburgh Critical Care Medicine series

ICU Care of Abdominal Organ Transplant Patients

Ali Al-​Khafaji
Renal and Metabolic Disorders
John A. Kellum and Jorge Cerda
Mechanical Ventilation
John W. Kreit
Infection and Sepsis in the ICU
Peter Linden and Karin E. Byers
Neurocritical Care
Lori Shutter and Bradley Molyneaux
Cardiac Problems in the ICU
Thomas C. Smitherman
Trauma Intensive Care
Samuel A. Tisherman and Raquel M. Forsythe
Pediatric Intensive Care
Scott Watson and Ann Thompson
Emergency Department Critical Care
Donald M. Yealy and Clifton Callaway
Continuous Renal
Replacement
Therapy
Second Edition
Edited by

John A. Kellum, MD, MCCM

Professor of Critical Care Medicine, Bioengineering and Clinical
Translational Science
Director, Center for Critical Care Nephrology
Vice Chair for Research, Department of Critical Care Medicine
University of Pittsburgh School of Medicine
Pittsburgh, Pennsylvania

Rinaldo Bellomo, MBBS, MD, FRACP, FCICM

Director of Intensive Care Research
Department of Intensive Care
Austin Hospital
Victoria, Australia

Claudio Ronco, MD
Director, Department Nephrology Dialysis and Transplantation
Director of International Renal Research Institute (IRRIV)
San Bortolo Hospital
Vicenza, Italy

1
1
Oxford University Press is a department of the University of Oxford. It furthers
the University’s objective of excellence in research, scholarship, and education
by publishing worldwide.Oxford is a registered trade mark of Oxford University
Press in the UK and certain other countries.
Published in the United States of America by Oxford University Press
198 Madison Avenue, New York, NY 10016, United States of America.
© Oxford University Press 2016
First Edition published in 2010
Second Edition published in 2016
All rights reserved. No part of this publication may be reproduced, stored in
a retrieval system, or transmitted, in any form or by any means, without the
prior permission in writing of Oxford University Press, or as expressly permitted
by law, by license, or under terms agreed with the appropriate reproduction
rights organization. Inquiries concerning reproduction outside the scope of the
above should be sent to the Rights Department, Oxford University Press, at the
address above.
You must not circulate this work in any other form
and you must impose this same condition on any acquirer.
Library of Congress Cataloging-​in-​Publication Data
Continuous renal replacement therapy/​edited by John A. Kellum, Rinaldo Bellomo,
and Claudio Ronco. —​2nd edition.
p. ; cm.
Includes bibliographical references and index.
ISBN 978–​0–​19–​022553–​7 (alk. paper)
I. Kellum, John A., editor. II. Bellomo, R. (Rinaldo), 1956–​, editor.
III. Ronco, C. (Claudio), 1951–​, editor.
[DNLM: 1. Acute Kidney Injury—​therapy. 2. Hemodialysis Solutions.
3. Kidney—​injuries. 4. Renal Replacement Therapy—​methods. WJ 342]
RC901.7.H45
617.4′61059—​dc23
2015022091
9 8 7 6 5 4 3 2 1
Printed by Webcom, Canada
This material is not intended to be, and should not be considered, a substitute for medical
or other professional advice. Treatment for the conditions described in this material is highly
dependent on the individual circumstances. And, while this material is designed to offer
accurate information with respect to the subject matter covered and to be current as of the
time it was written, research and knowledge about medical and health issues is constantly
evolving and dose schedules for medications are being revised continually, with new side
effects recognized and accounted for regularly. Readers must therefore always check the
product information and clinical procedures with the most up-​to-​date published product
information and data sheets provided by the manufacturers and the most recent codes
of conduct and safety regulation. The publisher and the authors make no representations
or warranties to readers, express or implied, as to the accuracy or completeness of
this material. Without limiting the foregoing, the publisher and the authors make no
representations or warranties as to the accuracy or efficacy of the drug dosages mentioned
in the material. The authors and the publisher do not accept, and expressly disclaim, any
responsibility for any liability, loss or risk that may be claimed or incurred as a consequence
of the use and/​or application of any of the contents of this material.
We dedicate this edition to the nursing professionals who deliver continuous renal
replacement therapy. Without their hard work and dedication, this therapy would
not exist. This volume is also dedicated to patients and their families in the hope
that we make a positive difference in their lives.
 Preface

Significant advances have occurred in the care of patients with acute kidney
injury (AKI). Continuous renal replacement therapy (CRRT) has become stan-
dard of care for many critically ill patients with severe acute kidney injury, and
most major medical centers have developed the capability of providing CRRT.
However, many hospitals lack the capacity and many that have it, underuse it.
The goal of this CRRT handbook is to provide a concise but authoritative
guide in the use of CRRT. In a single, slim volume, we cover the basics of CRRT
management as well as some topics related more generally to AKI. The intent
of this book is to provide a quick reference for both novice and experienced
CRRT providers, to enrich existing expertise, and to help all involved in the
care of severe AKI achieve a better understanding of this powerful therapy.
As a result of the tremendous success of the first edition, we have updated
this second edition with new information on machines and biomarkers, and
on a nomenclature that has undergone much-​needed standardization dur-
ing the years the first edition was published. We hope that new readers and

vii
those already familiar with the handbook find it useful. Our ultimate goal is to
improve outcomes for patients with AKI through teamwork and education.

John A Kellum
Rinaldo Bellomo
Claudio Ronco
2015
 Contents

Contributors╇ xiii

Part 1: Theory

1 The Critically Ill Patient with Acute Kidney Injury

Aditya Uppalapati and John A. Kellum 3
2 History and Rationale for Continuous Renal
Replacement Therapy
Ilona Bobek and Claudio Ronco 13
3 Nomenclature for Renal Replacement Therapy
in Acute Kidney Injury
Mauro Neri, Jorge Cerdá, Francesco Garzotto,
Gianluca Villa, and Claudio Ronco 21
4 Basic Principles of Solute Transport
Zhongping Huang, Jeffrey J. Letteri, Claudio Ronco,
and William R. Clark 35
5 Principles of Fluid Management in the Intensive
Care Unit
Rinaldo Bellomo and Sean M. Bagshaw 43
6 Indications, Timing, and Patient Selection
John A. Kellum, Raghavan Murugan, and Mitra K. Nadim 47
7 Biomarkers for Initiation of Renal Replacement Therapy
Alexander Zarbock and Lakhmir S. Chawla 57
8 Extended Indications
Rinaldo Bellomo and Ian Baldwin 63
9 Dose Adequacy and Assessment
Zaccaria Ricci and Claudio Ronco 67
10 Acid–Base and Electrolyte Disorders
John A. Kellum 75

Part 2: Practice
11 Choosing a Renal Replacement Therapy
in Acute Kidney Injury
Jorge Cerdá and Claudio Ronco 93
12 Vascular Access for Continuous Renal
Replacement Therapy
Alexander Zarbock and Kai Singbartl 105
13 The Circuit and the Prescription
Rinaldo Bellomo and Ian Baldwin 111
14 The Membrane: Size and Material
Zhongping Huang, Jeffrey J. Letteri, Claudio Ronco,
and William R. Clark 117
15 Fluids for Continuous Renal Replacement Therapy
Paul M. Palevsky and John A. Kellum 125
16 Alarms and Troubleshooting
Zaccaria Ricci, Ian Baldwin, and Claudio Ronco 131
17 Nonanticoagulation Strategies to Optimize
Circuit Function in RRT
Ian Baldwin 139
18 Anticoagulation
Rinaldo Bellomo and Ian Baldwin 145
19 Regional Citrate Anticoagulation
Nigel Fealy 151
20 Drug Dosing in Continuous Renal Replacement Therapy
Adrian Wong, Sandra L. Kane-Gill, and John A. Kellum 157

Part 3: Special Situations

21 Renal Replacement Therapy in Children

Michael L. Moritz 169
22 Therapeutic Plasma Exchange in Critical Care Medicine
Joseph E. Kiss 179
23 MARS: Molecular Adsorbent Recirculating System
Nigel Fealy and Rinaldo Bellomo 187
24 Sorbents
Dehua Gong and Claudio Ronco 193
25 Hybrid Therapies
Claudio Ronco, Silvia De Rosa, and Sara Samoni 201

Part 4: Organizational Issues

26 The ICU Environment

Ayan Sen 209
27 Patient Care Quality and Teamwork
Kimberly Whiteman and Frederick J. Tasota 221
28 Organizational Aspects: Developing Policies
and Procedures for Continuous Renal
Replacement Therapies
Jorge Cerdá 229
29 Documentation, Billing, and Reimbursement for
Continuous Renal Replacement Therapy
Kevin W. Finkel 239
30 Machines for Continuous Renal Replacement Therapy
Claudio Ronco 245
31 Quality Improvement for Continuous Renal
Replacement Therapies
Ian Baldwin and Rinaldo Bellomo 275
32 Educational Resources
Ian Baldwin and Kimberly Whiteman 279

Glossary ╇ 291

Index ╇ 303
 Contributors
Sean M. Bagshaw, MD
Faculty of Medicine and Dentistry
Division of Critical Care Medicine
University of Alberta
Edmonton, Canada
Ian Baldwin, RN, PhD
Adjunct Professor
Deakin and RMIT Universities
Austin Health
Melbourne, Australia
Ilona Bobek, PhD
Budapest, Hungary
Jorge Cerdá, MD, FACP, FASN
Clinical Professor of Medicine
Department of Medicine
Albany Medical College
Albany, New York
Lakhmir S. Chawla, MD
Associate Professor of Medicine
Department of Medicine
Veterans Affairs Medical Center
Washington, District of Columbia
William R. Clark, MD
Senior Medical Director
Renal Medical Affairs
Baxter Healthcare Corporation
Deerfield, Illinois
Silvia De Rosa
Nigel Fealy, RN, MN, ACCCN
Department of Intensive Care
Austin Hospital
Melbourne, Australia
Kevin W. Finkel, MD, FACP,
FASN, FCCM
Professor and Director of Renal
Diseases and Hypertension
University of Texas Health
Science Center
xiii
Houston Medical School
Houston, Texas
Francesco Garzotto, PhD
San Bortolo Hospital
Department of Nephrology
Dialysis and Transplantation
International Renal Research
Institute of Vicenza
Vicenza, Italy
Dehua Gong, MD
Research Institute of Nephrology
Jinling Hospital
Nanjing University
Nanjing, China
 Zhongping Huang, PhD
Contributors
Department of Mechanical
Engineering
Widener University
Chester, Pennsylvania
Sandra L. Kane-​Gill, PharmD,
FCCP, FCCM
Associate Professor of Pharmacy
and Therapeutics
Faculty, School of Pharmacy
Center for Critical Care Nephrology
University of Pittsburgh
University of Pittsburgh
Medical Center
Pittsburgh, Pennsylvania
Joseph E. Kiss, MD
Institute for Transfusion Medicine
University of Pittsburgh School of
xiv
Medicine
Pittsburgh, Pennsylvania
Jeffrey J. Letteri, BS
Director
Baxter Healthcare Renal Division
Nantucket, Massachusetts
Michael L. Moritz, MD
Division of Nephrology
Department of Pediatrics
Children’s Hospital of Pittsburgh
The University of Pittsburgh School
of Medicine
Pittsburgh, Pennsylvania
Raghavan Murugan,
MD, FRCP
Associate Professor of Critical
Care Medicine and Clinical and
Translational Science
Department of Critical Care
Medicine
University of Pittsburgh School
of Medicine
Pittsburgh, Pennsylvania
Mitra K. Nadim, MD
Department of Medicine
University of Southern California
Los Angeles, California
Mauro Neri
International Renal Research
Institute of Vicenza
San Bortolo Hospital
Vicenza, Italy
Paul M. Palevsky, MD
Chief of Renal Section
VA Pittsburgh Healthcare System
Professor of Medicine and Clinical
and Translational Science
University of Pittsburgh School of
Medicine
Pittsburgh, Pennsylvania
Zaccaria Ricci, MD
Pediatric Cardiac Intensive Care Unit
Department of Pediatric Cardiac
Surgery
Bambino Gesù Children’s
Hospital, IRCCS
Rome, Italy
Sara Samoni
Ayan Sen, MD, FACEP, FCCP
Consultant and Assistant Professor
of Critical Care and Emergency
Medicine
Mayo Clinic
Phoenix, Arizona
Kai Singbartl, MB, ChB, PhD,
FRCA, FFA(SA)
Department of Anesthesiology
Penn State College of Medicine
Hershey, Pennsylvania
Frederick J.Tasota, RN, MSN
UPMC Presbyterian
Pittsburgh, Pennsylvania
Aditya Uppalapati, MD
Department of Medicine
Saint Louis University
Saint Louis, Missouri
Gianluca Villa, MD
Contributors
International Renal Research
Institute of Vicenza
San Bortolo Hospital
Vicenza, Italy
Department of Health Sciences
Section of Anesthesiology
University of Florence
Florence, Italy
Kimberly Whiteman,
DNP, RN
Assistant Professor of Nursing
Co-​Director Graduate and
Professional Studies Nursing
Programs
Waynesburg University
Pittsburgh, Pennsylvania
Adrian Wong, PharmD
xv
Resident
University of Pittsburgh School of
Pharmacy
Pittsburgh, Pennsylvania
Alexander Zarbock, MD
Department of Anaesthesiology
Intensive Care and Pain Medicine
University Hospital Münster
Münster, Germany
Part 1

Theory
 Chapter 1

The Critically Ill Patient

with Acute Kidney Injury
Aditya Uppalapati and John A. Kellum

The terms acute kidney injury (AKI) and acute renal failure (ARF) are not syn-
onymous. Although the term renal failure is best reserved for patients who
have lost renal function to the point that life can no longer be sustained with-
out intervention, AKI is used to describe the milder as well as severe forms
of acute renal dysfunction in patients. Although the analogy is imperfect, the
AKI–╉ARF relationship can be thought of as being similar to the relationship
between acute coronary syndrome and ischemic heart failure. AKI is intended
to describe the entire spectrum of disease—╉from being relatively mild to
severe. In contrast, renal failure is defined as renal function inadequate to clear

3
the waste products of metabolism despite the absence of or correction of
hemodynamic or mechanical causes. Clinical manifestations of renal failure
(either acute or chronic) include the following:
• Uremic symptoms (drowsiness, nausea, hiccough, twitching)
• Hyperkalemia
• Hyponatremia
• Metabolic acidosis

Oliguria
Persistent oliguria may be a feature of AKI, but nonoliguric renal failure is not
uncommon. Patients may continue to make urine despite an inadequate glo-
merular filtration. Although prognosis is often better if urine output is main-
tained, use of diuretics to promote urine output does not seem to improve
outcome (and some studies even suggest harm). More important, azotemia
(increased serum creatinine [SCrt]) together with oliguria portends a worse
prognosis than either sign alone.

Classification
The Kidney Disease Improving Global Outcomes (KDIGO) work group
defines AKI as an increase in SCr by 0.3 mg/╉dL or more (≥26.5 mmol/╉L)
 Table 1.1 KDIGO criteria for staging severity of AKI
The Critically Ill Patient with AKI

Stage Serum Creatinine Level Urine Output

1 1.5–​1.9 times baseline or (0.3 mg/​dL ((26.5 mmol/​L) <0.5 mL/​kg/​h for
increase 6–​12 h
2 2.0–​2.9 times baseline <0.5 mL/​kg/​h for
(12 h
3 3.0 times baseline or increase in serum creatinine to <0.3 mL/​kg/​h for
(4.0 mg/​dL ((353.6 mmol/​L) or initiation of renal ≥24 h or anuria for
replacement therapy or, in patients <18 years, decrease ≥12 h
in estimated glomerular filtration rate to <35 mL/​min
per 1.73 m2
Source: Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group.
KDIGO clinical practice guideline for acute kidney injury. Kidney Int. 2012;2(suppl):1–​138.
Chapter 1

within 48 hours, an increase in SCr to 1.5 times baseline or more, which is

known or presumed to have occurred within the prior 7 days, or urine vol-
ume less than 0.5 mL/​kg/​h for 6 hours. AKI is staged for severity as shown in
Table 1.1.

Incidence and Etiology of AKI

4

RIFLE (risk, injury, failure, loss, end-​stage kidney disease [ESRD]) criteria
developed by the acute dialysis quality initiative and acute kidney injury net-
work (AKIN) criteria developed by an international network of AKI research-
ers were used to define AKI and its severity. They were based on SCrt level
and urine output. Both of these criteria have been well validated in various
patient populations. With increasing severity or stage, AKI was associated with
increasing mortality. These criteria were adopted by the KDIGO in its AKI
clinical practice guideline (Figure 1.1).

Incidence and Progression

AKI occurs in 35% to 65% of intensive care unit (ICU) admissions and 5% to
20% of general hospital admissions. Mortality rates increase significantly with
AKI, and most studies show a three-​to fivefold increase in the risk of death
among patients with AKI compared with patients without AKI. Furthermore,
increases in severity of AKI are associated with a stepwise increase in risk of
death and need for renal replacement therapy (RRT).
Individuals who survive an AKI hospitalization have a greater likelihood of a
recurrent hospital admission compared with those with no evidence of kidney
disease (AKI or chronic kidney disease) and are at an increased risk of devel-
oping ESRD. Risk factors for developing AKI as defined by KDIGO criteria are
presented in Table 1.2.
 Creatinine criteria Urine output criteria

The Critically Ill Patient with AKI

Increased creatinine UO < 0.5 mL/kg/h
x 1.5* x6h High
Risk sensitivity

Increased creatinine x 2 UO < 0.5 mL/kg/h

Injury x 12 h

Increased creatinine x 3 UO < 0.3 mL/kg/h

ria
or creatinine ≥ 4mg/dL x 24 h or High

Oligu
Failure (acute rise of anuria x 12 h specificity
≥0.5 mg/dL)

Loss Persistent ARF = complete loss of

renal function > 4 weeks

Chapter 1
End-stage renal disease
ESRD

Figure 1.1 The RIFLE cCriteria for diagnosis and staging of acute kidney injury AKI—​used
to describe three levels of renal impairment (Risk, Injury, Failure) and two clinical outcomes
(Loss and End-​stage kidney disease). ARF, acute renal failure; UO, urine output. *An alterna-
tive proposal is to define “risk” to include any increase in serum creatinine of at least
0.3 mg/​dL over 48 hours or less, even if less than a 50% increase.

5
Source: Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P. Acute renal failure: definition, outcome
measures, animal models, fluid therapy and information technology needs: the Second International
Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. 2004;8:R204–​
R212. Used with permission.

Table 1.2 Risk factors for developing AKI as defined

by KDIGO criteria
Increasing age, especially older than Surgical admissions more likely than
65 years medical admissions*
Female gender Cardiac surgery
Black race* Sepsis
Dehydration or volume depletion Radio contrast media
Hypoalbuminemia Shock
Preexisting chronic kidney disease Cancer
Diabetes mellitus Genetic factors/​polymorphisms*
Cardiac dysfunction (CAD, Drugs: NSAIDs, ACE-​I,* diuretics,
LVEF <35%) cyclosporine, tacrolimus, penicillin,
Chronic obstructive pulmonary aminoglycosides
disease*
Mechanical ventilation
Chronic liver disease
Critical illness, trauma
ACE-​I, angiotensin-​converting enzyme inhibitor; CAD, coronary artery disease; LVEF, left
ventricular ejection fraction; NSAIDs, nonsteroidal anti-​inflammatory drugs.
*Evidence is inconclusive.
 Etiology of AKI
The Critically Ill Patient with AKI

Clinical features may suggest the cause of AKI and dictate further investigation.
AKI is common in the critically ill, especially in patients with sepsis and other
forms of systemic inflammation (e.g., major surgery, trauma, burns), but other
causes must be considered.
Volume-​Responsive AKI
It is estimated that as many as 50% of cases of AKI are “fluid responsive,” and
the first step in managing any case of AKI is to ensure appropriate fluid resus-
citation. However, volume overload is a key factor contributing to the mortal-
ity attributable to AKI, so ongoing fluid administration to nonfluid-​responsive
patients is discouraged.
Chapter 1

Sepsis-​Induced AKI
Sepsis is a primary cause or contributing factor in more than 50% of cases of
AKI, which includes cases severe enough to require RRT. Patients with sepsis,
including those outside the ICU, develop AKI at rates as high as 40%. Incidence
increases with the severity of sepsis. Sepsis-​induced AKI can develop in
patients with normal, decreased, as well as increased renal blood flow. In sep-
sis, the kidney often has a normal histological appearance.
6

Hypotension
Hypotension is an important risk factor for AKI, and many patients with AKI
have sustained at least one episode of hypotension. Treating fluid-​responsive
AKI with fluid resuscitation is clearly an important step, but many patients also
require vasoactive therapy (e.g., norepinephrine) to maintain arterial blood
pressure. Despite a common belief among many practitioners, norepineph-
rine does not increase the risk of AKI compared with dopamine, and renal
blood flow actually increases with norepinephrine in animal models of sepsis.
Postoperative AKI
Risk factors of postoperative AKI include hypovolemia, hypotension, major
abdominal surgery, and sepsis. Surgical procedures (particularly gynecological)
may be complicated by damage to the lower urinary tract with an obstruc-
tive nephropathy. Abdominal aortic aneurysm surgery may be associated with
renal arterial disruption. Cardiac surgery may be associated with atheroembo-
lism, hemolysis, and sustained periods of reduced arterial pressure as well as
systemic inflammation.

Other Causes
• Nephrotoxins: May cause renal failure via direct tubular injury, interstitial
nephritis, or renal tubular obstruction. In patients with AKI, all potential
nephrotoxins should be withdrawn.
• Rhabdomyolysis: Suggested by myoglobinuria and increased creatine

The Critically Ill Patient with AKI

kinase levels in patients who have experienced a crush injury, coma, or
seizures. Often, elevated liver transaminases—​aspartate aminotransfer-
ase > alanine aminotransferase—​are also noted as a result of muscular
injury.
• Glomerular disease: Red cell casts, hematuria, proteinuria, and systemic fea-
tures (e.g., hypertension, purpura, arthralgia, vasculitis) are all suggestive of
glomerular disease. Renal biopsy or specific blood tests (e.g., Goodpasture’s
syndrome, vasculitis) are required to confirm diagnosis and guide appropri-
ate treatment.
• Hemolytic uremic syndrome: Suggested by hemolysis, uremia, thrombocyto-
penia, and neurological abnormalities
• Crystal nephropathy: Suggested by the presence of crystals in the urinary
sediment. Microscopic examination of the crystals confirms the diagnosis

Chapter 1
(e.g., urate, oxalate). Release of purines and urate are responsible for ARF
in tumor lysis syndrome.
• Renovascular disorders: Loss of vascular supply may be diagnosed by
renography. Complete loss of arterial supply may occur in abdominal
trauma or aortic disease (particularly dissection). More commonly, the
arterial supply is compromised in part (e.g., renal artery stenosis) and
blood flow is further reduced by hemodynamic instability or locally via

7
drug therapy (e.g., nonsteroidal anti-​inflammatory drugs [NSAIDs],
angiotensin-​converting enzyme inhibitors). Renal vein obstruction may
be a result of thrombosis or external compression (e.g., raised intra-​
abdominal pressure).
• Abdominal compartment syndrome: Suggested by oliguria, a firm abdomen
on physical examination, and increased airway pressures (secondary to
upward pressure on the diaphragms). Diagnosis is likely when sustained,
increased intra-​abdominal pressures (bladder pressure measured at end
expiration in the supine position) exceed 25 mmHg. However, abdominal
compartment syndrome may occur with intra-​abdominal pressures as low
as 10 mmHg.

Nephrotoxins
Box 1.1 lists some medications that can be nephrotoxic. In addition, aminogly-
cosides, NSAIDs, allopurinol, furosemide, sulfonamides, thiazides, pentami-
dine, amphotericin, organic solvents, Paraquat, herbal medicines, and heavy
metals are also nephrotoxic.

Evaluation of AKI
Evaluation of AKI is based on clinical history, physical examination, labora-
tory results, and assessment of hemodynamics and volume status. Newer
The Critically Ill Patient with AKI

Box 1.1 Common Nephrotoxic Drugs

• Antibiotics (penicillins, cephalosporins, sulfa, rifampin, quinolones)
• Diuretics (furosemide, bumetanide, thiazides)
• NSAIDS (including selective COX-​2 inhibitors)
• Allopurinol
• Cimetidine (rarely other H2 blockers)
• Proton pump inhibitors (omeprazole, lansoprazole)
• Indinavir
• 5-​Aminosalicylates

Table 1.3 Evaluation of AKI

Chapter 1

Clinical history and examination

Conduct an ultrasound of the bladder and kidneys if suspected retention, obstruction,
hydronephrosis.
Insert Foley catheter if needed and check for patency; flush catheter.
If abdomen is distended and tense, check bladder pressure.
Clinical Assessment Urine Analysis
Hemodynamics Prerenal Intrinsic Renal
8

• Mean arterial Osmolality >500 <350

pressure, heart rate (mOsm/​L)
• Volume status Sodium <20 >40
and central (mmol/​L)
venous pressure,
examination, chest Fractional <1 >2
radiograph excretion
• Echocardiogram, right sodium (%)
ventricular and left Urea (%) <35 >35
ventricular function Microscopy Hyaline Muddy brown: ARF trial
Fluid responsiveness casts network (ATN)
• Passive leg raise Bacteria, white blood
test, stroke volume cells: pyelonephritis
variation, pulse Eosinophils: interstitial nephritis
pressure variation,
Red blood cell casts: evaluate for
velocity time
vasculitis, glomerulonephritis
integral variability,
inferior vena cava Red blood cells: consider renal
distensibility index artery or vein occlusion
Biomarkers Urinary [TIMP-​2]•[IGFBP7]: >0.3, high risk; >2.0, very high
(40%–​50%) chance of developing stage 2/​3 acute kidney
infection in the next 12–​24 h; plasma/​urine NGAL, interleukin
18, KIM-​1, L-​FABP
biomarkers are also gaining strength in the early detection and evaluation

The Critically Ill Patient with AKI

of AKI. Urine analysis can be suggestive but not diagnostic of AKI etiology
(Table 1.3).

Management of AKI
Identification and correction of reversible causes of AKI is critical. All cases
require careful attention to fluid management and nutritional support.

Urinary Tract Obstruction

Lower tract obstruction requires the insertion of a catheter (suprapubic if

Chapter 1
there is a urethral disruption) to allow decompression. Ureteric obstruction
requires urinary tract decompression by nephrostomy or stent. A massive
diuresis is common after decompression, so it is important to ensure adequate
circulating volume to prevent secondary AKI.

Hemodynamic Management

9
Fluid-​responsive AKI may be reversible in its early stage. However, volume
overload is a key factor contributing to the mortality attributable to AKI, so
ongoing fluid administration to nonfluid-​responsive patients is discouraged. In
severe cases, fluid resuscitation may be guided by functional hemodynamic
monitoring, and parameters such as stroke volume variation, pulse pressure
variation, velocity time integral variability, inferior vena cava distensibility
index, and the passive leg raise test can help guide fluid responsiveness. After
assessing fluid status and volume responsiveness, necessary inotrope or vaso-
pressor support should be started to ensure tissue perfusion.

Glomerular Disease
Specific therapy in the form of immunosuppressive drugs may be useful after
diagnosis has been confirmed.

Interstitial Nephritis
Acute interstitial nephritis most often results from drug therapy. However,
other causes include autoimmune disease and infection (e.g., Legionella,
leptospirosis, Streptococcus, cytomegalovirus). Numerous drugs have
been implicated, but the most common ones are as listed in Box 1.1.
 Table 1.4 Clinical consequences of AKI
The Critically Ill Patient with AKI

System Mechanisms Complications

Electrolyte • Hyponatremia • Central nervous system
disturbances • Hyperkalemia (see Nervous System)
• Malignant arrhythmias
Acid–​base • Downregulation of beta • Decreased cardiac output,
(decreased receptors, increased inducible blood pressure
chloride excretion, nitric oxide synthase • Lung, intestinal injury,
accumulation of • Hyperchloremia decreased gut barrier
organic anions such • Impairment of insulin function
as PO4, decreased resistance • Hyperglycemia, increased
albumin, buffering) protein breakdown
• Innate immunity
• See below
Cardiovascular • Volume overload • Congestive heart failure
Chapter 1

• Secondary hypertension
Pulmonary • Volume overload, decreased • Pulmonary edema, pleural
oncotic pressure effusions
• Infiltration and activation of • Acute lung injury
lung neutrophils by cytokines • Pulmonary hemorrhage
• Uremia
Gastrointestinal • Volume overload • Abdominal compartment
syndrome
10

• Gut ischemia and reperfusion

• injury
Immune • Decreased clearance of
oxidant stress
• Tissue edema
• White cell dysfunction
Hematological • Decreased synthesis of RBCs,
increased destruction of RBCs,
blood loss
• Decreased production of
erythropoietin, von Willebrand
factor
Nervous system • Secondary hepatic failure,
malnutrition, altered drug
metabolism
• Hyponatremia, acidosis
• Uremia
Pharmacokinetics and • Increased volume of
dynamics distribution
• Decreased availability, albumin
binding, elimination
RBC, red blood cell.
• Acute gastric and duodenal
ulcer bleeding, impaired
nutrient absorption
• Increased risk of infection
• Delayed wound healing
• Anemia
• Bleeding
• Altered mental status
• Seizures, impaired
consciousness, coma
• Myopathy,
neuropathy: prolonged
length on mechanical
ventilation
• Drug toxicity or underdosing
Urine sediment may reveal white cells, red cells, and white cell casts.

The Critically Ill Patient with AKI

Eosinophiluria is present in about two-​thirds of cases, and specificity for
interstitial nephritis is only about 80%. Other causes of AKI in which eosin-
ophiluria is relatively common are rapidly progressive glomerulonephritis
and renal atheroemboli. Discontinuation of the potential causative agent is
a mainstay of therapy.

Abdominal Compartment Syndrome

Baseline blood pressure and abdominal wall compliance influence the
amount of intra-​abdominal pressure that can be tolerated. Enteral decom-
pression with nasogastric or rectal tubes, percutaneous drainage to remove
intra-​abdominal fluid, and a brief trial of neuromuscular blockade might

Chapter 1
help as a temporizing method. However, surgical decompression is the only
definitive therapy and should be undertaken before irreversible end-​organ
damage occurs.

Renal Replacement Therapy

11
CRRT forms the mainstay of replacement therapy in critically ill patients who
often cannot tolerate standard hemodialysis because of hemodynamic insta-
bility. Hybrid techniques (discussed in Chapter 25) may be reasonable alterna-
tives in settings in which CRRT cannot be accomplished, but outcome data are
limited. Peritoneal dialysis is not usually sufficient. Mortality in the setting of
ARF in the critically ill is high (40%–​60%). Recent studies suggest that sustained
renal failure or incomplete renal recovery is more common than previously
thought (as many as 50% of survivors do not return to baseline renal function
after an episode of ARF).

Clinical Consequences of AKI

Until recently, it was assumed that patients with AKI died, not because of
AKI itself, but because of their underlying disease. Several studies, however,
have documented a substantial mortality attributable to AKI after controlling
for other variables, including chronic illness and severity of underlying acute
illness. Table 1.4 lists some of the more important clinical consequences
of AKI.
 Key References
The Critically Ill Patient with AKI

Kellum JA. Acute kidney injury. Crit Care Med. 2008;36:S141–​S145.

1. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work
Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int.er.,
Suppl. 2012;2(suppl):1–​138.
2. Kellum JA. Acute Kidney Injury. Crit Care Med. 2008;36:S141–​S145.
3. Uchino S, Kellum JA, Bellomo R, et al. Acute renal failure in critically ill patients: a
multinational, multicenter study. JAMA. 2005;294:813–​818.
12 Chapter 1
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