50: Acute Kidney Injury


CHAPTER 50
Acute Kidney Injury


Angela M. Love1, Adam Rothman2, and Alfredo Astua2


1 Hunter Holmes McGuire VA Medical Center, Richmond, VA, USA


2 Icahn School of Medicine at Mount Sinai, New York, NY, USA


Background


Definition of disease



  • AKI is defined as an abrupt decline in kidney function, either reversible or irreversible, associated with retention of metabolic waste products.
  • AKI is defined as:

    • Increase in serum creatinine over 48 hours of ≥0.3 mg/dL from baseline, or
    • Increase in serum creatinine of >50%, or
    • Urine output <0.5 mL/kg/h for more than 6 hours.

  • There are two further refined definitions for AKI. The RIFLE and Acute Kidney Injury Network (AKIN) criteria are supported by the Kidney Disease Improving Global Outcomes clinical practice guidelines.

Disease classification



  • The RIFLE criteria consist of three grading levels defined as risk, injury, or failure, and two clinical outcomes defined as loss of kidney function and end‐stage kidney disease.
  • The AKIN criteria are a modification of the RIFLE criteria and include a staging system (Table 50.1).

Incidence/prevalence



  • The exact prevalence of AKI in the ICU is limited by varying definitions of AKI and under‐reporting based on this limitation. Studies have reported an overall incidence of 20–50%.
  • Patients with sepsis have been reported to have a higher incidence of AKI.

Table 50.1 AKIN and RIFLE criteria for acute kidney injury.








































AKIN RIFLE Both
Stage Serum creatinine or GFR Class Serum creatinine or GFR Urine output
1 Increase of ≥0.3 mg/dL or 1.5–2× baseline Risk Creatinine >1.5× baseline or GFR decrease >25% <0.5 mL/kg/h for at least 6 hours
2 Increase of 2–3× baseline Injury Creatinine >2× baseline or GFR decrease >50% <0.5 mL/kg/h for at least 12 hours
3 Increase >3× baseline or ≥4 mg/dL with an acute increase of at least 0.5 mg/dL or newly required renal replacement therapy Failure Creatinine >3× baseline or >4 mg/dL with an acute increase of at least 0.5 mg/dL or GFR decrease >75% <0.3 mL/kg/h for at least 24 hours or anuria for at least 12 hours


Loss Persistent loss of kidney function for >4 weeks


End‐stage renal disease (ESRD) ESRD >3 months

Etiology



  • AKI has multiple etiologies, further defined based on location of injury as pre‐renal, intrinsic, or post‐renal.








Pre‐renal: due to transient renal hypoperfusion

  • Hypotension
  • Hypovolemia
  • Congestive heart failure with reduced ejection fraction
  • Hepatic cirrhosis
  • Abdominal compartment syndrome
  • Non‐steroidal anti‐inflammatory drug use
Intrinsic renal

  • Tubular: ischemic acute tubular necrosis (ATN), toxic ATN (medication, contrast)
  • Vascular/glomerular: thrombotic microangiopathy (hemolytic uremic syndrome, thrombotic thrombocytopenia purpura), glomerulonephritis, atheroembolic, malignant hypertension
  • Interstitial: acute interstitial nephritis, pyelonephritis.
Post‐renal: obstruction of collecting system

  • Urinary tract obstruction: urethral (such as benign prostatic hyperplasia), ureteral

Pathology/pathogenesis



  • Pre‐renal injury occurs secondary to underperfusion of an otherwise healthy kidney.
  • Intrinsic renal injury is caused by disease of the renal parenchyma:

    • Acute tubular necrosis (ATN) is the most common intrinsic cause, and can develop from renal ischemia or injury from endogenous and exogenous substances.
    • Acute interstitial nephritis (AIN) is frequently secondary to one of five etiologies: drug hypersensitivity reaction (most common), infection, immune‐mediated, glomerular disease, or idiopathic.

  • Post‐renal injury occurs in the setting of urinary tract obstruction. Causes of the obstruction can be within the urinary tract itself (clots, stones) or outside the tract (enlarged prostate, tumors, increased surrounding pressures). The increased pressure in the urinary tract alters the pressure gradient at the glomerular capillaries with a resultant decrease in glomerular filtration rate (GFR) and signs and symptoms of AKI.

Prevention


Recognition of high risk patients is key to prevention of AKI. Hospitalized patients, in particular, should have their renal function assessed before any surgical procedures, imaging studies requiring contrast, or administration of any nephrotoxic agents. These patients should also be monitored for any change in urine output from baseline.


Risk factors for acute kidney injury



  • Acute on chronic kidney disease (CKD).
  • Heart failure.
  • Liver disease.
  • Diabetes.
  • Prior history of AKI.
  • Oliguria (<0.5 mL/kg/h).
  • Neurologic impairment.
  • Hypovolemia.
  • Nephrotoxic agent exposure.
  • Use of iodinated contrast.
  • Symptoms or history of obstruction.
  • Age over 65 years.
  • Recent chemotherapy.

Primary prevention



  • Primary prevention is focused on understanding and responding to the associated risk factor.
  • Key components include:

    • Maintaining renal perfusion by correcting for hypovolemia, decreased cardiac output, and sepsis‐related vasodilation.
    • Avoiding nephrotoxic agents.
    • Limiting iodinated contrast (especially in diabetic and CKD patients).
    • Ensuring adequate urine output in rhabdomyolysis (>0.5 mL/kg/h).
    • Alkalinizing urine in hyperuricemia.

Causes of intrinsic renal disease










































Common causes of ATN Common causes of AIN
Ischemia (shock state) Beta‐lactam antibiotics
Rhabdomyolysis Rifampin
Cast nephropathy (myeloma light chains) Sulfonamides
Aminoglycosides Fluoroquinolones
Amphotericin B NSAIDs
Acyclovir IV Allopurinol
Cisplatin Proton pump inhibitors
Ethylene glycol Sarcoidosis
Methanol Diuretics
Tumor lysis Aspirin
IV iodinated contrast Bacterial pyelonephritis

Viruses (CMV, EBV, HIV, rubeola)

Diagnosis


Typical presentation


AKI generally presents as an increase in serum creatinine on surveillance blood work. This can be associated with a decrease in urine output. Many times, however, patients are asymptomatic, and may be diagnosed incidentally on routine blood work testing.


Clinical diagnosis


History



  • Key questions include pertinent prior history and details of the current illness.
  • Important past medical history includes prior history of renal dysfunction (acute or chronic), diabetes mellitus, and congestive heart failure.
  • Important current information includes NSAID use, decreased oral intake or decreased urine output, difficulty with urination, recent iodinated contrast, and severe volume loss.

Physical examination


The physician should conduct a physical exam directed at possible causes and consequences of AKI.



  • Physical exam findings for patients with AKI may include tachycardia, loss of skin turgor, or dry mucous membranes. One can also evaluate for bladder distension by checking for suprapubic tenderness. Flank tenderness could be suggestive of possible pyelonephritis.
  • Physical exam findings for sequelae of AKI include assessing volume overload manifested as peripheral edema, pulmonary crackles, and jugular venous distension. Also assess for uremia manifesting as altered mental status, pericardial rub in pericarditis, or distant cardiac sounds in uremic pericardial effusions.
  • More invasive exam techniques include measuring bladder pressure through an indwelling urinary catheter in order to assess for abdominal compartment syndrome. Ultrasound can also be used to evaluate for bladder distention.

Laboratory diagnosis


List of diagnostic tests



  • Initial blood work should include blood urea nitrogen (BUN) and serum creatinine.
  • Urine osmolality, urine sodium, urine creatinine, and urine urea are useful to calculate FeNa and FeUrea to help differentiate the location of the injury (pre‐renal, intrinsic/ATN) (see Algorithm 50.1).

    • FeNa is <1% in pre‐renal injury, reflecting increased reuptake of sodium at the renal tubules. FeNa utility is limited in patients with CKD, early intrinsic injury, and in the elderly.
    • FeUrea has improved sensitivity and specificity in patients taking loop diuretics. A value of <35% suggests pre‐renal injury due to renal hypoperfusion.

  • Urinalysis is also essential for differentiating between different intrinsic diagnoses and pre‐renal AKI.

    • Pre‐renal and post‐renal AKI: urine sediment is usually bland.
    • Glomerular injury: RBC casts, dysmorphic RBCs.
    • Vascular injury: RBC casts.
    • Tubular injury: muddy brown granular casts, tubular epithelial cells.
    • Interstitial injury: WBC casts (AIN, pyelonephritis), eosinophils (AIN).
    • Urinary tract infection: bacteria, elevated leukocyte esterase.

List of imaging techniques



  • A bedside renal and bladder ultrasound provides a safe and easy way to perform modality for detecting urinary obstruction.
  • Further imaging for AKI is often not necessary in the initial investigation but can be useful if the cause of the injury is not apparent.

    • A CT scan is helpful in diagnosing nephrolithiasis, renal mass, or abscess.

Diagnostic algorithm (Algorithm 50.1)

Schematic illustration of diagnostic algorithm for AKI. Abbreviations are available in prelims.

Algorithm 50.1 Diagnostic algorithm for AKI


Treatment


Treatment rationale



  • First line (initial) treatment is supportive care:

    • Adjust or discontinue nephrotoxic medications.
    • Optimize perfusion in patients at risk for kidney injury.

      • Isotonic crystalloids to provide fluid resuscitation in the absence of hemorrhagic shock.
      • Vasopressors as needed in conjunction with volume resuscitation to maintain renal perfusion pressure (i.e. MAP >65 mmHg).

    • Correct metabolic derangements.
    • Escalate management if the severity of AKI progresses from stage 1 to stage 3 (see Algorithm 50.2).

  • Dialysis is only indicated for certain conditions:

    • Fluid overload state refractory to diuretics.
    • Hyperkalemia that cannot be readily corrected.
    • Symptoms of uremia (pericarditis, uremic encephalopathy).
    • Severe metabolic acidosis (pH <7.1) refractory to treatment.

Table of treatment
















Treatment Comments
Conservative Avoid nephrotoxic agents, optimize fluid status, correct metabolic derangements
Medical Medical diuresis (i.e. loop diuretics) can be useful in fluid overloaded patients with non‐oliguric acute kidney injury
Surgical Foley catheters, ureteral stents, and nephrostomy tubes may be needed in cases of obstructive uropathy causing AKI

Management/treatment algorithm (Algorithm 50.2)

Schematic illustration of management or treatment algorithm of AKI.

Algorithm 50.2 Management/treatment algorithm of AKI

Nov 20, 2022 | Posted by in ANESTHESIA | Comments Off on 50: Acute Kidney Injury
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