AKI

ACUTE KIDNEY INJURY

Definition of Acute Kidney Injury (AKI)

Acute Kidney Injury (AKI) is defined as the sudden loss of kidney function, which generally occurs over a timeframe of hours to days. This condition results in the retention of metabolic waste products and the dysregulation of fluid, electrolyte, and acid-base homeostasis. According to the National Kidney Foundation - Kidney Disease Outcomes Quality Initiative (NKF-KDOQI), this encompasses the abrupt decline in the kidneys' ability to filter blood, leading to detrimental physiological imbalances.

Risk Factors for Acute Kidney Injury

The risk factors for AKI are categorized into two groups: Nonmodifiable and Modifiable.

Nonmodifiable Risk Factors

  • AIDS

  • Chronic kidney disease

  • Chronic liver disease

  • Congestive heart failure

  • Diabetes mellitus

  • Older age (specifically, 65 years or older)

  • Peripheral vascular disease

  • Prior kidney surgery

  • Renal artery stenosis
    This information is sourced from references 3-6.

Modifiable Risk Factors

  • Anemia

  • Hypercholesterolemia

  • Hypertension

  • Hypoalbuminemia

  • Hyponatremia

  • Mechanical ventilation

  • Nephrotoxic drug use

  • Rhabdomyolysis

  • Sepsis

KDIGO 2012-based Definition of Acute Kidney Injury

Diagnostic Criteria for AKI

  1. Increase in serum creatinine by ≥0.3 mg/dL (26.5 μmol/L) within 48 hours; or

  2. Increase in serum creatinine to ≥1.5 times baseline, which is known or presumed to have occurred within the past 7 days; or

  3. Urine volume <0.5 mL/kg/h for 6 hours.

AKI Staging

  • AKI Stage I:

    • Increase ≥0.3 mg/dL (26.5 μmol/L); or

    • Increase to 1.5-1.9 times from baseline; or

    • Urine volume <0.5 mL/kg/h for 6-12 hours.

  • AKI Stage II:

    • Increase to 2.0-2.9 times from baseline; or

    • Urine volume <0.5 mL/kg/h for ≥12 hours.

  • AKI Stage III:

    • Increase to ≥3.0 times from baseline; or

    • Serum creatinine ≥4.0 mg/dL (≥354 μmol/L); or

    • Initiation of renal replacement therapy; or

    • Decrease in eGFR to <35 mL/min/1.73m² in patients <18 years; or

    • Urine volume <0.3 mL/kg/h for ≥24 hours; or

    • Anuria for ≥12 hours.

Etiologies of AKI

There are three primary types of AKI based on causative factors:

  1. Prerenal

  2. Intrinsic renal

  3. Postrenal

Causes of Acute Kidney Injury
Pre-Renal Causes:

  • Impaired perfusion due to:

    • Cardiac failure

    • Sepsis

    • Blood loss

    • Dehydration

    • Vascular occlusion

Renal Causes:

  • Glomerulonephritis

  • Small-vessel vasculitis

  • Acute tubular necrosis

  • Drugs (including nephrotoxic agents)

  • Toxins

  • Prolonged hypotension

  • Interstitial nephritis due to drugs, toxins, inflammatory disease, or infection

Post-Renal Causes:

  • Urinary calculi

  • Retroperitoneal fibrosis

  • Benign prostatic enlargement

  • Prostate cancer

  • Cervical cancer

  • Urethral stricture/valves

  • Meatal stenosis/phimosis

History and Physical Exam

History Taking

The clinician should assess for:

  • Systemic illness that may affect renal function.

  • Use of nephrotoxic medications contributing to impaired renal function.

Physical Examination

Physical examination should focus on:

  • Intravascular volume status

  • Presence of skin rashes which can indicate underlying conditions related to renal impairment.

Diagnostic Evaluation

To evaluate AKI, the following diagnostic measures should be employed:

  • Serum Creatinine Levels

  • Urine Output

  • Creatinine Clearance

  • Urinalysis and Urine Microscopy

  • Renal Ultrasound

Treatment Goals

The primary objectives in managing AKI are:

  • To prevent further damage to the kidneys.

  • To promote recovery of renal function.

Management of AKI

When managing confirmed AKI, follow these steps:

  1. Obtain a focused history and physical examination.

  2. Assess volume status.

  3. Monitor:

    • Blood urea nitrogen,

    • Creatinine,

    • Electrolyte levels;

    • Assess hemodynamic stability.

  4. Conduct urine testing including dipstick, microscopy, and chemistries.

  5. Discontinue potential nephrotoxins.

  6. Review and adjust medications as needed.

  7. Use guideline-based care bundles when available.

  8. Determine the etiology of AKI:

    • Prerenal disease,

    • Intrinsic renal disease,

    • Postrenal disease.

  9. Administer fluid resuscitation with isotonic crystalloid.

  10. Administer diuretics if volume overload is present.

  11. Consider vasopressor support as necessary.

  12. Consider a renal biopsy depending on the clinical scenario.

  13. Engage in Nephrology consultation as indicated.

  14. Conduct renal ultrasonography when urinary tract obstruction is suspected and relieve any obstruction.

  15. Provide supportive management, monitor volume status, acid-base status, and electrolyte levels.

  16. Aim for clinical improvement in renal function.

  17. Consider renal replacement therapy if indicated (see Table 7).

Nephrology Consultation

Nephrology consultation is beneficial under the following circumstances:

  • Within 48 hours if initiating renal replacement therapy.

  • Inadequate response to treatment.

  • Unknown or unclear cause of AKI.

  • If AKI is classified as Stage 3 or higher.

  • In cases of Stage 4 or higher Chronic Kidney Disease (CKD).

Follow-Up Care

Follow-up assessments are essential especially if renal function is recovered. Recommendations include:

  • Follow-up within 3 months if renal function recovers by 90% or greater from baseline at the time of hospital discharge.

  • Schedule follow-up at 3 weeks for patients with slower recovery from baseline.

  • During follow-up, assess blood pressure, weight, serum creatinine, and GFR at each appointment.

  • Refer for nephrology consultation if GFR remains less than 60 mL per minute.