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- •Contents
- •Outcome Evaluation
- •Introduction
- •Clinical Presentation of Muscular Weakness in the Critical Patients
- •Critical Illness Polyneuropathy (CIP) and Critical Illness Myopathy (CIM)
- •Ventilator-Induced Diaphragmatic Dysfunction (VIDD)
- •Dysphagia, Swallowing, and Effective Cough
- •The Pathophysiology of Acute Skeletal Muscle Wasting
- •Risk Factors
- •Short-Term and Long-Term Outcome
- •Conclusions
- •References
- •Introduction
- •The Neuroendocrine Response
- •Pathophysiology of Stress Response
- •The Hypothalamus-Pituitary-Adrenal (HPA) Axis
- •GH Axis
- •Pituitary-Thyroid Axis
- •Pituitary-Adrenal Axis
- •Mitochondrial Dysfunction
- •Metabolic Aspects of Stress Response
- •Conclusion
- •References
- •Introduction
- •Disorders of Fluid Balance
- •Dysionemias
- •Dysnatremias
- •Dyskalemias
- •Other Electrolyte Derangements (Calcium, Magnesium, Phosphorus)
- •Alterations of Acid Base Balance
- •Acid-Base Disturbances
- •Metabolic Acidosis
- •Respiratory Acidosis
- •Metabolic Alkalosis
- •Respiratory Alkalosis
- •Conclusion
- •References
- •Introduction
- •Epidemiology and Risk Factors
- •Diagnosis
- •Differential Diagnosis
- •Treatment
- •Prognosis
- •Future Perspectives
- •References
- •Introduction
- •Gut Microbiome
- •Gut-Organ Axis
- •Gut-Lung Axis
- •ICU Dysbiosis
- •Gut Changes
- •Microbial Therapy in ICU
- •Antimicrobial Stewardship
- •Nutrition as a Key Factor for Gut Microbiome Homeostasis
- •Probiotics, Prebiotics, and Synbiotics
- •Fecal Microbiota Transplantation
- •Conclusion
- •References
- •Introduction
- •Validation Process
- •Screening Tools Overview
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Fight-and-Flight Reaction
- •Calorimetry and Total Energy Expenditure
- •Role of Mitochondria in the Various Stages of Intensive Care Recovery
- •REE in Different Clinical Scenarios
- •Conclusions
- •References
- •Introduction
- •Nutrition in ICU: Evidence from RCTs
- •Inclusion of Too Many Patients Considered at Low Nutritional Risk
- •Unfavorable Energy to Protein Doses
- •Absence of Indirect Calorimetry-Guided Energy Dosing
- •Anabolic Resistance
- •Suppression of Fasting-Induced Recovery Pathways
- •Future Perspectives
- •Development and Validation of Tools to Guide Individualized Nutritional Support
- •Implications for Clinical Practice
- •Conclusion
- •References
- •Introduction
- •Protein Metabolism in Critical Illness
- •Protein Requirements and Current Evidence
- •Timing of Introduction
- •Early mobilization, Exercise, and Adjuvant Therapies
- •Conclusion
- •References
- •Introduction
- •Computed Tomography Scan
- •Bioelectrical Impedance Analysis
- •Musculoskeletal Ultrasound
- •Respiratory Muscle Ultrasound
- •Limb Muscles
- •Conclusions
- •References
- •Functional Principles
- •Hydration Status Evaluations in Critically Ill Patients
- •Body Composition and Nutrition in ICU
- •Limits of BIVA in Critically Ill Patients
- •Conclusions
- •References
- •Introduction
- •Introduction
- •Historical Perspective
- •Enteral Versus Parenteral Nutrition Nowadays
- •Conclusions
- •References
- •Enteral Nutrition
- •Components of Enteral Mixtures
- •Choice of the Enteral Mixture
- •Special Composition Formulas
- •Conclusions
- •References
- •Introduction
- •Complications Related to Enteral Feeding Tubes
- •Aspiration
- •Gastrointestinal Intolerance
- •Diarrhea
- •New Horizons
- •New Technologies to Prevent Enteral Nutrition Complications
- •Advanced Tube Feedings
- •smART Platform
- •Conclusions
- •References
- •Introduction
- •Composition of PN Admixtures
- •Energetic Substrates
- •Carbohydrates
- •Lipid Emulsions
- •Proteins
- •Micronutrients: Electrolytes, Vitamins, and Trace Elements
- •Types of Parenteral Nutrition
- •Compatibility and Stability of the Parenteral Nutrition
- •References
- •Introduction
- •Metabolic Complications
- •Hyperglycemia
- •Hypertriglyceridemia
- •Liver Disease: Steatosis, Cholestatic Disease, and Gallbladder Stones
- •Refeeding Syndrome
- •Mechanical Complications
- •Infectious Complications
- •Conclusions
- •References
- •Introduction
- •Macronutrients
- •Glutamine
- •Arginine
- •Leucine
- •ω-3 Fatty Acids
- •Micronutrients
- •Antioxidant Vitamins
- •Antioxidant Trace Elements
- •Probiotics, Prebiotics or Symbiotics
- •Use of Probiotics in Clinical Practice?
- •References
- •Introduction
- •Pathophysiological Mechanisms, Risk Factors, and Clinical Implications
- •Pathophysiological Mechanisms of ICUAW
- •Risk Factors Associated with Physical and Functional Recovery in Critically Ill Patients
- •Clinical Impact of Poor Physical and Functional Recovery in Critical Illnesses
- •How to Assess Physical and Functional Recovery in Critical Illnesses
- •Management and Therapies
- •Nutritional Therapy
- •Other Supportive Therapies
- •Patient- and Family-centered ICU Environment
- •Conclusions
- •References
- •Bioethics in Clinical Practices
- •Ethical Consideration on Nutrition
- •Conclusion
- •References
- •Introduction
- •Nutrition in ARDS
- •Caloric Goals
- •Diet Composition
- •Immunonutrition
- •Oral Versus Enteral Versus Parenteral Nutrition
- •Nutrition in COVID-19 Respiratory Failure
- •Nutrition in ECMO Support
- •Enteral Nutrition
- •Parenteral Nutrition
- •Nutritional Goals
- •Conclusions
- •References
- •Introduction
- •Timing and Route of Nutritional Support
- •Initial Assessment of the Burn Patient
- •Estimation of Energy Expenditure
- •Macronutrients and Micronutrients
- •Proteins
- •Carbohydrates
- •Immunonutrients
- •Arginine
- •Nucleotides
- •ω3 Fatty Acids
- •Glutamine
- •Monitoring of Nutritional Support
- •Nutritional Support for Trauma Patients
- •Route of Feeding: Digestive Tract (Enteral Nutrition) Versus Intravenous (Parenteral Nutrition)
- •Standard or Immune-Enhancing Enteral Nutrition
- •Estimation or Measurement of Energy Requirements
- •Macronutrients
- •Conclusions
- •References
- •Introduction
- •General Considerations
- •Assessment of Nutritional Needs
- •Metabolic Changes Induced by Sepsis, AKI, and CRRT
- •Protein Metabolism
- •Lipid Metabolism
- •Vitamins and Trace Elements
- •Phosphates
- •Approaches to Nutrition
- •Enteral
- •Parenteral
- •Timing
- •Recommendations
- •Conclusion
- •References
- •Introduction
- •Acute Liver Failure
- •Nutrition in ALF
- •Acute Pancreatitis
- •IAP Management
- •Conclusions
- •References
- •Introduction
- •Nutritional Considerations in Major Surgery
- •Nutritional Requirements During and After Major Surgery
- •Challenges in Meeting Nutritional Needs Post-Surgery
- •Strategies for Enhancing Nutritional Intake and Absorption
- •Intestinal Failure: Nutritional Challenges and Management
- •Impact of Intestinal Failure on Nutritional Status
- •Nutritional Management Strategies for Patients with Intestinal Failure
- •Role of Parenteral Nutrition and Enteral Nutrition in Intestinal Failure Cases
- •Open Abdomen: Nutritional Support and Wound Healing
- •Nutritional Requirements for Patients with Open Abdomen Wounds
- •Challenges in Providing Nutritional Support to Patients with Open Abdomen
- •Clinical Protocols and Guidelines for Nutritional Support
- •Conclusions
- •References
- •Introduction
- •Nutrition Therapy
- •Determination of Energy Expenditure
- •Route and Timing of Enteral Nutrition
- •Intolerance to Enteral Nutrition
- •Brain Energy Metabolism and Energy Dysfunction Following Acute Brain Injury
- •In Vivo Brain Energy and Glucose Monitoring
- •Alternative Energy Substrates
- •Lactate
- •Ketone Bodies
- •Immunonutrition and Micronutrients
- •Conclusions and Future Directions
- •References
- •Introduction
- •AKI and Cardiac Surgery
- •AKI and Vascular Surgery
- •AKI and Sepsis
- •AKI and Surgery
- •Trauma
- •Burn
- •AKI and COVID-19
- •Conclusion
- •References
- •Introduction
- •AKI Etiology
- •Subclinical AKI and AKI Biomarkers
- •Subphenotyping AKI
- •Conclusions
- •References
- •Introduction
- •What Are Biomarkers?
- •Novel Biomarkers: How Can They be Implemented?
- •Biomarkers for the Prediction of AKI and Detection of Subclinical Stages
- •Postoperative Biomarker-Guided Prevention of AKI in Patients at High Risk
- •Biomarkers for Other Indications
- •Conclusion
- •References
- •Introduction
- •The Machine Learning Arena
- •The Challenges of Timely Prediction of Acute Kidney Injury
- •Early Machine Learning Models for AKI Prediction
- •New Techniques for AKI Prediction Using Deep Learning ML Models
- •Clinical Decision Support Systems
- •The Translational Research Gap and the Value of Data Sharing: A Plea for Data Sharing
- •Limitations of Machine Learning Models
- •Conclusions
- •References
- •Introduction
- •Doppler Assesses Vascular Congestion
- •Arterial Renal Doppler Ultrasound in AKI
- •Integration of Renal Resistive Index and Intrarenal Venous Flow
- •Contrast-Enhanced Ultrasound for Assessing Renal Perfusion
- •Conclusions
- •References
- •Introduction
- •Renal Perfusion and Goals of Fluids in AKI
- •Clinical Evaluation of a Patient with AKI in ICU
- •Studies Which Investigated the Association of Fluid Therapy and AKI
- •Volume of Fluid
- •Type of Fluid
- •Crystalloids
- •Colloids
- •Starches
- •Gelatins
- •Conclusion
- •References
- •Introduction
- •Pathophysiology of Renal Perfusion
- •Acute Kidney Injury
- •Norepinephrine
- •Epinephrine
- •Dopamine
- •Vasopressin
- •Terlipressin
- •Angiotensin II
- •Conclusions
- •References
- •Introduction
- •Pharmacology of Diuretics
- •Loop Diuretics
- •Other Classes of Diuretics
- •Indications for Diuretics in AKI
- •Control of Fluid Overload
- •AKI Prognostication
- •Situations in Which Diuretics Are Not Indicated
- •AKI Recovery
- •How to Use Diuretics in the ICU
- •Class and Dose Selection
- •Modality of Loop Diuretic Administration
- •Conclusions
- •References
- •Introduction
- •What Is Acute Kidney Disease?
- •Clinical Course of AKD Within the ICU
- •Management of AKD in Critical Care and Beyond
- •Conclusions and Future Directions
- •References
- •Introduction
- •Renal Functional Reserve
- •Renal Functional Reserve and Renal Recovery After Acute Kidney Injury
- •Conclusion
- •References
- •Background
- •Membrane and Filter Characteristics
- •Geometric Characteristics
- •Performance Characteristics
- •Mechanisms of Fluid and Solute Transport
- •Treatment Modalities
- •Treatment Dose
- •Nomenclature of Renal Replacement Therapies
- •Continuous Therapies
- •Intermittent Therapies
- •Hybrid Therapies
- •Conclusion
- •References
- •Introduction
- •Dialysis Catheters: Technical Aspects
- •Selection of the Site for Dialysis
- •Catheter Insertion Technique
- •Dialysis Catheter Complications
- •Dialysis Catheter Maintenance
- •Conclusions
- •References
- •Introduction
- •Non-pharmacological Strategies to Reduce Membrane Fouling
- •Pharmacological Strategies to Reduce Membrane Clotting
- •Unfractionated Heparin (UFH) Systemic Anticoagulation
- •Systemic Anticoagulation with Low Molecular Weight Heparin (LMWH)
- •Regional Citrate Anticoagulation (RCA)
- •Systemic Anticoagulation with Direct Thrombin Antagonists
- •Nafamostat
- •Conclusions
- •References
- •Introduction
- •CRRT Dose/Outcome Studies: Consideration of Solute Kinetics
- •CRRT Dose as a Quality Criterion
- •CRRT Dose in the Context of Therapy Quality
- •Conclusions
- •References
- •Introduction
- •Patient Selection and Indications for Starting RRT
- •Strategies to Identify Need for RRT
- •Rationale for an Early Strategy to Starting RRT
- •Rationale for a Conservative Strategy to Starting RRT
- •RRT Replacement Therapy and Clinical Outcomes
- •Current Clinical Practice Guideline Recommendations
- •Clinical Trial Evidence on Timing of Starting RRT
- •Implications for Practice
- •Existing Knowledge Gaps and Future Research
- •Conclusions
- •References
- •Introduction
- •Early ICU Phase before KRT
- •Nutrition Care
- •Monitoring
- •ICU Phase with KRT
- •Gains and Losses During CRRT
- •Electrolyte Loss in CRRT
- •Macronutrient Loss in CRRT
- •Macronutrient Gain in CRRT
- •Micronutrients and Vitamin Loss in CRRT
- •Management of Losses During CRRT
- •Monitoring During CRRT
- •Indirect Calorimetry During CRRT
- •ICU Phase After CRRT
- •EN and PN Product Selection
- •Conclusions
- •References
- •Introduction
- •Nomenclature
- •Continuous Therapies
- •Intermittent Renal Replacement Therapies (IRRTs)
- •Hybrid Therapies
- •Technical Aspects of RRT Techniques
- •Hemodynamic Stability
- •Solute Clearance
- •Fluid Balance
- •Vascular Access
- •Anticoagulation
- •Drug Dosing
- •Patient Mobilization
- •The Process of RRT Prescription and Administration
- •Indications of RRT
- •Timing
- •Prescription Parameters
- •Dosing
- •Membrane Choice
- •Dialysate and Reinfusion Solutions
- •Limitations of RRT in Critical Care
- •Patient Safety During RRT in Critical Care
- •Introduction
- •Steps in RRT Management and Protocol Application

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https://doi.

Part IV
Acute Kidney Injury

Chapter 26
Global Epidemiology and Outcomes
of Acute Kidney Injury
Vincenzo Pota and Max Bell
Introduction
Acute kidney injury (AKI) is a severe complication of critically ill patients, often
associated with high morbidity and mortality both in the short and long term. AKI is
defined as an abrupt decrease in kidney function. In most critically ill patients, AKI
is a complication of severe systemic illness (sepsis, shock, trauma); however, only in
a small minority of patients, it is driven by a specific kidney disease (vasculitis,
glomerulonephritis, or interstitial nephritis). In the following chapter, the epidemiology in different critical care settings will be described.
Classification and Global Epidemiology
Before discussing epidemiology, it is fundamental to examine the problem of the
different definitions used in earlier studies to analyze AKI incidence and prevalence
[1]. Serum urea and creatinine are markers of decreased urinary waste secretion used
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-66541-7_26.
V. Pota (
Department of Women, Child, General and Specialty Surgery, L. Vanvitelli University of
Campania, Naples, Italy
e-mail: vincenzo.pota@unicampania.it
M. Bell
Department of Perioperative Medicine and Intensive Care, Karolinska University Hospital,
Stockholm, Sweden
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
e-mail: max.bell@regionstockholm.se
© 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_26
✉)
307

308 V. Pota and M. Bell
in diagnosing AKI before 2004, but varying cut-offs and levels were applied to
define what was then called acute renal failure (ARF). The fact that no consensus
existed made comparisons between studies difficult and hampered efforts for
benchmarking hospital or ICU performance. The Risk, Injury, Failure, Loss, and
End-stage (RIFLE) definition was proposed in 2004 to standardize the outcome of
AKI. The three severity grades are defined based on the worst change in serum
inine (sCr) or urine output. In 2007, the Acute Kidney Injury Network (AKIN)
t
crea
criteria were proposed based on the consideration that even minor increases in serum
creatinine in a shorter period are associated with adverse effects. Lastly, the current
definition made by Kidney Disease Improving Global Outcomes (KDIGO) is very
similar to the AKIN definition; the period examined was extended from 48 h to
7 days [
2]
.
A recent article analyz
ed the difference in AKI incidence using the three definitions and confirmed the difference in the relationship between AKI and its epidemiology [
1]. The authors considered all the patients admitted to their intensive care unit
in about 6 months (1376 patients were admitted with a total of 5734 observation
days). Using the RIFLE definition, the authors estimate an AKI incidence in 35% of
patients admitted to ICU and during their first week of ICU stay. The use of the
AKIN definition let the authors estimate an AKI incidence in 38% of the same
patients admitted to ICU and during their first week of ICU stay. Finally, using the
KDIGO definition let the authors estimate an AKI incidence in 38% of the same
patients admitted to ICU during their first week of ICU stay. The incidence of
different severity stages of AKI has also been demonstrated to change using one
of the three definitions. For the same group of patients, using the RIFLE scale , the
“risk” stage, the “injury” stage, and the failure stage have been detected in 17%,
10%, and 6.3% of cases, respectively. For the same group of patients, stage 1 has
been in 20% of cases using the AKIN scale, while stage 2 in 9.2% of cases and stage
3 in 7.9%. Finally, using the KDIGO definition, the incidence of the three different
severity stages was 20%, 8.6%, and 7.7%, respectively.
A review published in 2018 analyzed the global epidemiology of AKI and the
reasons behind the change in incidence and outcomes of this disease in different
regions of the world [3]. The countries have been classified based on gross national
income per capita (World Bank’s classification) [4]. The countries are categorized
into low-to-middle-income countries (LMICs), which include the low (<US$1005)
and lower-middle (US$1006–3955) ranges, and high-income countries, which
includes the upper-middle (US$3956–12,235) and high (>US$12,236) ranges.
In high-
income countries, the typical patient with AKI is 65 years old and has
several comorbidities like diabetes mellitus, chronic kidney disease, etc. The setting
of diagnosis and treatment is the hospital. AKI is usually a complication of severe
systemic illness, treatment of an illness (CT contrast), or in rare cases driven by a
specific kidney disease (vasculitis, glomerulonephritis, or interstitial nephritis). In
LMIC, AKI occurs mainly in the community setting as an acute illness. It is usually
triggered by diarrheal states and dehydration, infections like malaria, or toxins. The
epidemiology is also affected by public health issues and socioeconomic factors.

26 Global Epidemiology and Outcomes of Acute Kidney Injury 309
In high-income countries, the reported incidence of AKI among hospitalized
patients shows some variation. This is explained by differing use of the AKI criteria,
differences in case mix, or variations in the way relevant terms (such as baseline
creatinine) are defined. Two multicentric studies from China, conducted using data
from the same year (2013) and employing KDIGO criteria, reported notably different proportions of hospitalized patients who sustained AKI: 3.02% and 11.6%
[5, 6]. A recent meta-analysis has shown that the proportion of hospitalized adult
patients who developed AKI ranged from 3.0% to 18.3% [7]. However, even for
values at the lower limit of this range, it is abundantly clear that AKI affects many
hospitalized patients worldwide.
The epidemiology of AKI in LMICs has been reviewed in several papers.
Reliable information on the incidence of AKI in LMICs was slowly collected due
to limitations in the amount and availability of local and regional data, the use of
obsolete AKI classification systems, and barriers to the publication of LMIC data in
scientific journals. A meta-analysis published in 2015 showed increasing use of
KDIGO or KDIGO-equivalent definitions of AKI in LMICs, making their data
comparable to those from other regions of the world [
incidence in LMIC regions is increasingly close to that of developed countries, in
contrast to previous reports [
Finally, it can be concluded that AKI occurs in about 13.3 million people
annually, and 85% live in the developing world [8].
8].
7]. Thus, the aggregate
AKI and Cardiac Surgery
Acute kidney injury (AKI) is a common occurrence during the perioperative period
of cardiac surgery and is associated with significant morbidity and mortality [9].
Patients who meet the Kidney Disease Improving Global Outcomes (KDIGO)
criteria for AKI and have undergone cardiac surgery within the previous week are
considered to have cardiac surgery-associated AKI (CSA-AKI). CSA-AKI can be
further categorized into an early form, which occurs within 7 days of cardiac surgery
and is likely induced by various perioperative factors such as surgical trauma,
cardiopulmonary bypass, and postoperative care, and a late form known as cardiac
surgery-associated acute kidney disease (CSA-AKD), which manifests between
7 and 30 days after cardiac surgery [
Applicat
Failure, Loss, and End-stage (RIFLE) criteria for diagnosing CSA-AKI has led to
underestimation of the event. Additionally, the RIFLE criteria classify all patients
undergoing renal replacement therapy (RRT) as “failing,” yet the criteria for initiating RRT in the cardiac surgery setting lack standardization and can vary significantly
among different centers [11].
The pathophysi
includes hypoperfusion, ischemia-reperfusion injury, neurohumoral activation,
inflammation, oxidative stress, nephrotoxins, and mechanical factors.
f the Acute Kidney Injury Network (AKIN) and Risk, Injury,
ion o
ology of AKI following cardiac surgery is multifactorial and
10].

310 V. Pota and M. Bell
Globally, over two million cardiac surgeries are performed annually, with the
incidence of CSA-AKI ranging from 5% to 42% [12]. A systematic review and
meta-analysis aimed at estimating the global incidence and outcomes of AKI after
cardiac surgery in adults revealed pooled rates of CSA-AKI of 13.6%, 3.8%, and
2.7% for stages 1, 2, and 3 of AKI, respectively. The rate of renal replacement
therapy requirement was 2.3%. Lower pooled AKI incidence rates were observed in
studies using RIFLE criteria compared to those using AKIN and KDIGO criteria.
Mortality rates associated wi th AKI were reported as 10.7% in the short term and
30.0% in the long term, with higher mortality associated with more advanced stages
of AKI. Renal recovery rates were reported as 67% for complete recovery, 30.7% for
partial recovery, and 1.3% for no recover y [13].
Specific reports exist for minimally invasive procedures such as transcatheter
aortic valve replacement (TAVI) and MitraClip. A recent meta-analysis of 31 TAVI
studies indicated an AKI incidence of 14.4% within 30 days post-procedure
[14]. Recent data suggest that the incidence of post-TAVI AKI decreases as patient
comorbidities decrease [15]. In the largest multicenter registry available, the overall
incidence of CSA-AKI (using the AKIN scale and only measuring AKIN 2 and 3)
was observed in 6.0% of patients [16].
AKI and Vascular Surgery
Patients undergoing vascular surgery are often predisposed to acute kidney injury
(AKI) due to the close pathophysiological connection between renal and vascular
diseases [
sclerotic disease, higher vascular calcification loads, and an increased incidence of
cardiovascular events and mortality.
patients undergoing vascular surgery. Databases such as the American College of
Surgeons National Surgical Quality Improvement Program, the Society of Thoracic
Surgeons National Database, and the Society for Vascular Surgery Vascular Quality
Initiative (VQI) report AKI incidences. In a cohort of all vascular surgery patients,
the incidence of vascular surgery-associated AKI has been reported to reach up to
49%, varying significantly based on the procedure type [18].
for inguinal leg bypass to 19% for emergency revascularization for critical limb
ischemia. Thoracic and abdominal aortic procedures typically have higher AKI rates
than peripheral vascular surgery. Elective endovascular aneurysm repair of
infrarenal abdominal aortic aneurysms (AAAs) presents AKI incidences between
5.5% and 18%, while more complex AAA repairs may lead to higher AKI rates, up
to 32% for juxtarenal AAAs. Thoracic endovascular aortic repair for thoracic aortic
aneurysms exhibits a wide range of AKI incidences, ranging from 9.7% to 30% [ 17]
endovascular surgery. Elective open aortic repairs demonstrate AKI rates of 26%,
17]. Chronic kidney disease (CKD) patients exhibit accelerated athero-
A recent review has focused on the epidemiology and outcomes of AKI in
ral v
Periphe
Open aortic
ascular procedures generally show lower AKI rates, rangi ng from 4%
procedures have notably higher AKI incidences compared to
.

26 Global Epidemiology and Outcomes of Acute Kidney Injury 311
47%, and 68% in infrarenal AAAs, juxtarenal, and suprarenal aneurysms, respectively. Open thoracic repairs also show high AKI rates, ranging from 34% for
elective thoracic aortic aneurysms to 48% for aortic arch replacement [17].
In cardiovascular surgery, contrast-induced acute
significant concern. The KDIGO initiative provides the latest definition of CI-AKI,
which includes criteria such as a low-grade but steady increase in serum creatinine
over several days and a sudden increase in serum creatinine within 48 h after contrast
medium exposure. CI-AKI incidence varies widely depending on the procedure
during which the contrast medium was administered [19].
For instance, in the NEPHRIC trial, CI-AKI was observed in 15% of patients
undergoing coronary or aortofemoral angiography. More recent data from the
National Cardiovascular Disease Registry (NCDR) CathPCI Registry reported an
overall CI-AKI incidence of 7.1%, with 0.3% of cases requiring initiation of dialysis
[20, 21].
kidney injury (C I-AKI) is a
AKI and Sepsis
The epidemiology of septic acute kidney injury (S-AKI) rema ins relatively
underexplored, highlighting the need for coordinated efforts between sepsis and
AKI researchers to better understand this syndrome.
S-AKI is characterized by acute renal impairment occurring in the context of
sepsis, with outcomes dependent on the severity of the acute lesion relative to
preexisting organ reserve. While renal dysfunction may be reversible, the duration
of impairment and available renal resources can limit recovery. A new global
consensus definition of sepsis defines it as lif e-threatening organ dysfunction
resulting from a dysregulated host response to infection [22].
The simultaneous presence of sepsis-3 and KDIGO criteria defines S-AKI. The
SOAP study, involving 3147 ICU-admitted patients, found that 37% had sepsis, with
AKI occurring in 51% of septic patients and S-AKI associated with a 41% ICU
mortality [
patients requiring renal replacement therapy [24].
outcomes. Among critically ill AKI patients, those with S-AKI experience higher
23]. In the recent VANISH trial, AKI incidence was 45%, with 30% of
Consistent with SOAP study findings, S-AKI is strongly linked to adverse clinical
from other causes [25].
005, a l
In 2
acute renal failure (47.5%) [26]. A subsequent multicenter trial in 2018 reported
sepsis as the primary etiology for AKI (40.7%) [27].
A recent
tality, and 90-day mortality rates of patients with S-AKI at 45.99%, 49.84%,
36.67%, and 64.66%, respectively [28]. Patients who recover from S-AKI show
improved survival rates [29].
arge prospective study identified septic shock as the leading cause of
meta-analysis reported ICU mortality, hospital mortality, 28-day mor-

312 V. Pota and M. Bell
A noteworthy finding from a recent analysis of ICU patients with moderate to
severe AKI is that 32% experience a relapse with a new episode of AKI during
hospitalization following initial S-AKI reversal [30]. This underscores the complexity and variability of AKI outcomes and emphasizes the need for ongoing monitoring
and management throughout the hospital course.
AKI and Surgery
Surgery represents a significant contributor to acute kidney injury (AKI) among
hospitalized patients, accounting for 40% of AKI cases in hospital settings. Postoperative AKI is associated with an elevated risk of developing chronic kidney disease
(CKD) and increased short- and long-term mortality [
A recent observational cohort study investigating AKI following major surgery
revealed considerable heterogeneity in postoperative AKI rates. The reported incidence ranged from 3.1% to 35.3%, with the majority of patients classified in the less
severe stages of AKI (Risk or Stage 1). The variability in incidence reflects differences in surgical settings and AKI definitions used, with the highest rates observed
following cardiac (18.7%), general (13.2%), and thoracic (12.0%) surgeries [29].
Furthermore, a systematic review focused on AKI in various postoperative
settings, including major abdominal, hepatobiliary, gynecological, upper gastrointestinal, and colorectal surgeries. The pooled incidence of AKI across all studies was
found to be 13.4%. Among AKI cases, 72% were categorized as Stage 1 or RIFLER, 17% as Stage 2 or RIFLE-I, and 11% as Stage 3 or RIFLE-F. In terms of
outcomes, patients with AKI had a relative risk for hospital mortality and 30-day
mortality of 12.6% compared to patients without AKI [30].
29].
Trauma
Patients admitted to the intensive care unit (ICU) following trauma are at risk of
developing acute kidney injury (AKI). However, the reported incidence of posttraumatic AKI can vary widely based on the definition of AKI and the characteristics
of the patient population under study.
A s
revealed an overall incidence of post-traumatic AKI of 24%. The authors also
provided insights into the severity of AKI in trauma patients, reporting that 13%,
5%, and 4% experienced mild, moderate, and severe AKI, respectively, based on the
RIFLE and AKIN definitions [31].
In terms
mortality risk compared to those without AKI. The absolute mortality rate among
traumatized patients with AKI, reported at any time point, was 27%. The increased
matic review and meta-analysis focused on AKI in trauma patients
yste
of outcomes, traumatized patients with AKI faced a significantly higher

26 Global Epidemiology and Outcomes of Acute Kidney Injury 313
mortality risk in these pati ents is attributed to various factors, including the extent of
trauma and the severity of resulting organ failure(s).
Burn
Burn patients are at risk of developing acute kidney injury (AKI), with several risk
factors identified including older age, chronic hypertension, diabetes mellitus, the
percentage of total body area surface burnt, high Abbreviated Burn Severi ty Index
(ABSI) score, inhalation injury, rhabdomyolysis, surgery, high APACHE II score,
high SOFA score, sepsis, and mechanical ventilation.
In a recent systematic review and meta-analysis, the overall incidence of AKI in
burned patients was found to be 38%. The mean time from burn injury to AKI
diagnosis varied from 1 to 17 days. Additionally, the authors reported the incidence
rates of AKI severity among burned patients, with 10%, 8%, and 13% experiencing
mild, moderate, and severe AKI, respectively [32].
In terms of outcomes, the mortality rate among burned patients with AKI was
reported to be 43%. This underscores the serious nature of AKI in the context of burn
injuries and highlights the importance of timely diagnosis and management in
improving patient outcomes.
AKI and COVID-19
The rates of acute kidney injury (AKI) complicating COVID-19 have shown variation throughout the pandemic. Early reports from China indicated an AKI incidence
of 10% or less among hospitalized patients with COVID-19. However, subsequent
studies in Chinese cohorts revealed higher rates of kidney involvement [
In c
COVID-19 wave in the United States were substantially higher, ranging from 32%
to 57%. Additionally, 9–20% of hospitalized COVID-19 patients with AKI required
renal replacement therapy (RRT) [35]. Similar rates of AKI have been reported in
European cohorts, with one retrospective study finding an AKI rate of approximately
26% among hospi talized COVID-19 patients [36].
Some resear
waves of the pandemic, possibly due to modifications in patient demographic
characteristics and improvements in the management of COVID-19. A recent
international meta-analysis reported a pooled prevalence of AKI in 28% of hospitalized patients and 45% in ICU patients. The reported rate of RRT use was 9%
among all hospitalized patients and 19% among ICU patients [37].
st, the rates of AKI among patients hospitalized during the initial
ontra
chers have suggested that AKI rates decreased during successive
33, 34].
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