• 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 (∼ 60% of cases)

Any condition leading to decreased renal perfusion

Avoid co-administering 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 (∼ 35% of cases)

Any disease causing severe direct kidney damage

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

Postrenal (∼ 5% of cases)

Postrenal causes include any condition that results in 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 nephronnecrosis or apoptosis of tubular cells → decreased reabsorption capacity of electrolytes, water, and/or urea (depending on the location of injury along the tubular system)
    • Na+; has multiple reabsorption sites, so its reabsorption is often impaired, which leads to increased Na+ in the urine and increased urine osmolality.
  • Acute tubular necrosis: necrotic debris obstructs tubules → decreased GFR → sequence of pathophysiological events similar to prerenal failure

Postrenal

  • Renal obstruction (e.g., stones, BPH, neoplasia, congenital anomalies) → increased retrograde hydrostatic pressure within tubuli → decreased GFR and compression of the renal vasculature → acidosis, fluid overload, and increased BUN, Na+, and K+.
  • A normal GFR can be maintained if the other kidney's function is normal.

Phases of AKI

Phase

Characteristic features

Duration

Kidney injury

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

Hours to days

Oliguric or anuric phase

Generally < 2 weeks

Polyuric phase

∼ 3 weeks

Recovery phase

Up to 2 years

References:[4][2][1]

Clinical features

  • May be asymptomatic.
  • Oliguria or anuria
  • Signs of volume depletion (in prerenal AKI caused by volume loss)
    • Orthostatic or frank hypotension and tachycardia
    • Reduced skin turgor
  • Signs of fluid overload
  • Signs of renal obstruction (in postrenal AKI)
  • Fatigue, confusion, and lethargy
  • In severe cases: seizures or coma
  • Affected individuals have a higher risk of secondary infection throughout all phases (most common reason for fatalities).

Subtypes and variants

Acute tubular 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 (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 or
  • Initiation of renal replacement therapy or
  • Patients < 18 years: decrease in eGFR to < 35mL/min/1.73m2
  • < 0.3 mL/kg/h for ≥ 24 h or
  • Anuria for ≥ 1

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


References:[1][13]

Treatment

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

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

References:[12][11]