• Clinical science

Acute kidney injury (Acute renal failure)

Summary

Acute kidney injury (AKI) is a sudden loss of renal function with a consecutive rise in creatinine and blood urea nitrogen (BUN). It is most frequently caused by decreased renal perfusion (prerenal) but may also be due to direct damage to the kidneys (intrarenal or intrinsic) or inadequate urine drainage (postrenal). In AKI, acid-base homeostasis, as well as the fluid and electrolyte balance, is disturbed, and the excretion of substances, including drugs, within the urine is impaired. The main symptom of AKI is oliguria or anuria; in some cases, polyuria may occur as a result of disturbed tubular reabsorption. Diagnosis of AKI requires an increase in serum creatinine concentration and/or decrease in urine output. Specific investigations are guided by the suspected cause. Rapid evaluation, diagnosis, and treatment are necessary to prevent irreversible loss of renal function.

Etiology

Prerenal acute kidney injury (∼ 60% of cases)

Prerenal causes include any condition leading to decreased renal perfusion.

Avoid coadministering ACE inhibitors and NSAIDs in patients with reduced renal perfusion (e.g., congestive heart failure, renal artery stenosis) because doing so can significantly decrease the glomerular filtration rate (GFR)!

Intrinsic acute kidney injury (∼ 35% of cases)

Intrinsic causes include any disease that leads to severe direct kidney damage.

Prolonged prerenal failure leads to intrinsic failure because decreased renal perfusion causes tubular necrosis!

Postrenal acute kidney injury (∼ 5% of cases)

Postrenal causes include any condition that results in bilateral obstruction of urinary flow from the renal pelvis to the urethra.

As long as the contralateral kidney remains intact, patients with unilateral ureteral obstruction typically maintain normal serum creatinine levels.

References:[1][2][3]

Pathophysiology

Prerenal

Intrinsic

  • Damage to a vascular or tubular component of the nephron necrosis or apoptosis of tubular cells → decreased reabsorption capacity of electrolytes (e.g., Na+), water, and/or urea; (depending on the location of injury along the tubular system) → increased Na+ and H2O in the urine → decreased urine osmolality

Postrenal

Four phases of AKI (some patients may not undergo all phases)

Phase

Characteristic features

Duration

Initiating event (kidney injury)

  • Symptoms of the underlying illness causing AKI may be present.
  • Hours to days

Oliguric or anuric phase (maintenance phase)

  • 1–3 weeks

Polyuric/diuretic phase

  • ∼ 2 weeks

Recovery phase

  • Months to years

References:[4][2][1]

Clinical features

Subtypes and variants

Acute tubular necrosis

Renal cortical necrosis

Contrast-induced nephropathy


References:[2][5][6][7][8][9][3][10]

Diagnostics

Approach [11][12]

  • The diagnosis of AKI requires an acute increase in serum creatinine and/or decrease in urine output (see the criteria for different stages in the table below); therefore, renal function tests should be done in every patient with suspected AKI
  • Additional laboratory investigations and imaging should be guided by the suspected cause.
Stages of AKI by Kidney Disease Improving Global Outcomes (KDIGO, 2012)
Stage Serum creatinine Urine output
1
  • Increase of 0.3 mg/dL (26.5 μmol/L) within 48 h or
  • 1.5–1.9 times baseline within 7 days
  • < 0.5 mL/kg/h for 6–12 h
2
  • 2–2.9 times baseline
  • < 0.5 ml/kg/h for ≥12 h
3
  • ≥ 3 times baseline or
  • Increase to ≥ 4 mg/dL (354 μmol/L) or
  • Initiation of renal replacement therapy or
  • Patients < 18 years: decrease in eGFR to < 35 mL/min/1.73 m2
  • < 0.3 mL/kg/h for ≥ 24 h or
  • Anuria for ≥ 12 h

Prerenal

Intrinsic

Postrenal

Comparison of diagnostic findings in different types of AKI

Prerenal Intrinsic Postrenal
BUN/Cr ratio
  • > 20:1
  • < 15:1
  • Varies

Fractional excretion of sodium

  • < 1%
  • > 2%
Urine sodium concentration (mEq/L)
  • < 20
  • > 40
Urine osmolality (mOsm/kg)
  • > 500
  • < 350
  • < 350
Urine sediments
  • Absent

Consequences of acute and chronic renal failure (MAD HUNGER): Metabolic Acidosis, Dyslipidemia, High potassium, Uremia, Na+/H2O retention, Growth retardation, Erythropoietin failure (anemia), Renal osteodystrophy.


References:[1][13]

Treatment

The longer the underlying cause, the greater the chance that AKI progresses to chronic renal failure. Treat early!

References:[12][11]