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Acute kidney injury

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Updated 2024 ESPEN guidelines for nutritional support in hospitalized patients with acute kidney injury.

Background

Overview

Definition
AKI is a sudden decrease in kidney function resulting from structural or functional injury that is characterized by decreased GFR, increased serum creatinine, and oliguria.
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Pathophysiology
AKI has multiple possible causes, including renal hypoperfusion, intrinsic renal dysfunction (glomerulonephritis, vasculitis, tubular necrosis, interstitial nephritis), or obstruction to the emptying of the kidneys (post-renal AKI).
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Epidemiology
The incidence of AKI in the US is estimated at 179-317 cases per 100,000 person-years.
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Disease course
Hypoperfusion of the kidneys with resultant ischemic injury represents the most important group of etiologies, mediating AKI through cellular injury caused by a mismatch between oxygen and nutrient delivery to the nephrons.
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Prognosis and risk of recurrence
Approximately 40% of patients with AKI do not recover renal function by hospital discharge. In this group of patients, AKI is associated with 1-year age-adjusted mortality of approximately 60%, compared to approximately 10% in patients who recovered renal function within 7 days.
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Guidelines

Key sources

The following summarized guidelines for the evaluation and management of acute kidney injury are prepared by our editorial team based on guidelines from the European Society for Clinical Nutrition and Metabolism (ESPEN 2024), the European Society of Intensive Care Medicine (ESICM 2024,2010), the National Institutes of Health (NIH 2024), the American College of Radiology (ACR 2023,2021), the American Society for ...
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Screening and diagnosis

Diagnostic criteria: as per ERBP 2012 guidelines, diagnose and stage the severity of AKI as follows (meeting any of the criteria):
Situation
Guidance
Stage 1
Serum creatinine increase 1.5-1.9 times baseline
Serum creatinine increase > 0.3 mg/dL (26.5 mcmol/L)
Urinary output < 0.5 mL/kg/hour during a 6 hour block
Stage 2
Serum creatinine increase 2.0-2.9 times baseline
Urinary output < 0.5 mL/kg/hour during two 6 hour blocks
Stage 3
Serum creatinine increase > 3 times baseline
Serum creatinine increase > 4.0 mg/dL (353 mcmol/L)
Initiation of RRT
Urinary output < 0.3 mL/kg/hour during > 24 hours
Anuria for > 12 hours
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  • Definitions

  • Differential diagnosis

Classification and risk stratification

Risk assessment: as per ADQI 2020 guidelines, avoid using biomarkers of acute damage before a kidney injury for the assessment of AKI risk.
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Diagnostic investigations

Baseline renal function testing: as per JSBPCC/JSDT/JSICM/JSN/JSPN 2018 guidelines, assess the baseline renal function using multiple methods whenever possible.
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  • Urinalysis

  • Renal ultrasound

  • Novel biomarkers

  • Evaluation for etiology

  • Nutritional assessment (referral to a dietitian)

  • Nutritional assessment (clinical assessment)

  • Nutritional assessment (body composition assessment)

  • Nutritional assessment (calorimetry)

Medical management

General principles: as per UKKA 2019 guidelines, obtain relevant assessment in patients at risk of AKI exposed to a significant renal insult, to ensure that exposure is limited and further insults are avoided or minimized.
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  • Fluid management

  • Vasopressors

  • Management of hyperglycemia

  • Therapies with no evidence for benefit

Inpatient care

Renal function monitoring, patients at risk for AKI: as per UKKA 2019 guidelines, obtain close monitoring for AKI in adult inpatients deemed at high risk of AKI, particularly if there has been a new exposure. Monitor urine output and measure serum creatinine daily until at least 48 hours after the period of increased risk has elapsed.
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  • Renal function monitoring (patients with AKI)

  • Hemodynamic monitoring

Nonpharmacologic interventions

Nutritional support, timing: as per ESPEN 2024 guidelines, initiate early nutritional support (within 48 hours from hospital admission) in preference to later nutritional support in polymorbid medical inpatients to decrease sarcopenia and improve self-sufficiency.
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  • Nutritional support (route of administration)

  • Nutritional support (energy intake)

  • Nutritional support (protein intake)

  • Nutritional support (carbohydrate and lipid intake)

  • Nutritional support (electrolyte intake)

  • Nutritional support (glucose control)

  • Nutritional support (supplements with no evidence for benefit)

Therapeutic procedures

RRT, indications: as per UKKA 2019 guidelines, consider initiating acute RRT in patients with progressive or severe AKI unless a decision has been made not to escalate therapy.
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  • RRT (choice of modality)

  • RRT (dosing)

  • RRT (insertion of dialysis catheter)

  • RRT (periprocedural anticoagulation)

  • RRT (technical considerations)

  • RRT (evaluation of fistula malfunction)

  • RRT (management of fistula malfunction)

Specific circumstances

Pediatric patients, diagnosis and evaluation: as per JSBPCC/JSDT/JSICM/JSN/JSPN 2018 guidelines, consider using the KDIGO diagnostic criteria for AKI to predict the survival outcomes in pediatric patients ≥ 3 months of age.
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  • Pediatric patients (RRT)

  • Pediatric patients (monitoring)

  • Patients with COVID-19-associated AKI (evaluation)

  • Patients with COVID-19-associated AKI (general principles of management)

  • Patients with COVID-19-associated AKI (hemodynamic support)

  • Patients with COVID-19-associated AKI (RRT)

Preventative measures

Prevention of AKI in ICU, fluid therapy: as per ESICM 2010 guidelines, initiate controlled fluid resuscitation in true or suspected volume depletion.
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  • Prevention of AKI in ICU (vasopressors and inotropes)

  • Prevention of AKI in ICU (vasodilators)

  • Prevention of AKI in ICU (nutritional support)

  • Prevention of AKI in ICU (other measures)

  • Prevention of contrast-induced nephropathy (risk assessment)

  • Prevention of contrast-induced nephropathy (restriction of contrast medium use)

  • Prevention of contrast-induced nephropathy (discontinuation of medications)

  • Prevention of contrast-induced nephropathy (IV and oral fluids)

  • Prevention of contrast-induced nephropathy (N-acetylcysteine)

  • Prevention of contrast-induced nephropathy (other agents)

  • Prevention of contrast-induced nephropathy (RRT)

  • Prevention of contrast-induced nephropathy (creatinine monitoring)

  • Prevention of postoperative AKI

  • Prevention of rhabdomyolysis-induced AKI

  • Prevention of amphotericin B-induced nephrotoxicity

  • Prevention of aminoglycoside-induced nephrotoxicity

  • Prevention of cardiac surgery-associated AKI (preoperative care)

  • Prevention of cardiac surgery-associated AKI (intravascular volume maintenance)

  • Prevention of cardiac surgery-associated AKI (pharmacologic strategies)

  • Prevention of cardiac surgery-associated AKI (cardiopulmonary bypass strategies)

  • Prevention of cardiac surgery-associated AKI (minimally invasive extracorporeal circulation)

  • Prevention of cardiac surgery-associated AKI (postoperative care)

  • Measures with no evidence for benefit

Follow-up and surveillance

Discharge from hospital: as per UKKA 2019 guidelines, include a record in the discharge summary regarding AKI detected whilst in hospital, its maximum stage, etiology, the need for renal support (temporary/ongoing), and discharge renal function, if dialysis-independent.
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  • Follow-up