• Clinical science

Acute kidney injury (AKI…)

Summary

Acute kidney injury is defined as 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 (intrinsic) or inadequate urine drainage (postrenal). The main symptom of acute kidney injury is oliguria or anuria; in some cases, however, polyuria may occur as a result of disturbed tubular reabsorption. In acute kidney injury (AKI), acid-base homeostasis as well as the fluid and electrolyte balance are disturbed, and the excretion of urinary waste substances, including drugs, is impaired. Patients with prerenal AKI typically present with dehydration and low blood pressure. A postrenal cause, on the other hand, may be diagnosed using ultrasound (renal tract obstruction). The causes of intrinsic AKI may be diverse, making it difficult to diagnose. Rapid evaluation, diagnosis, and treatment are crucial in order to prevent irreversible and permanent loss of renal function.

Etiology

Prerenal (∼ 60% of cases)

Any condition leading to decreased renal perfusion:

In patients with reduced renal perfusion (e.g., congestive heart failure, renal artery stenosis), co-administering ACE inhibitors and NSAIDs can significantly decrease GFR. ACE inhibitors inhibit the angiotensin II-mediated vasoconstriction of the efferent arterioles, reducing GFR, while NSAIDs constrict the afferent arteriole, reducing renal perfusion and further decreasing GFR.

Intrinsic (∼ 35% of cases)

Any disease causing severe direct kidney damage:

Prolonged prerenal failure also leads to intrinsic renal failure, as decreased renal perfusion causes tubular necrosis!

Postrenal (∼ 5% of cases)

Any condition causing obstruction to urinary flow:

Clinical features

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
  • Glomerular filtration returns to normal, thus increasing urine production (polyuria), while tubular reabsorption remains disturbed.
  • Complications: loss of electrolytes and water (dehydration, hyponatremia, and hypokalemia)

∼ 3 weeks

Recovery phase

Up to 2 years
  • Patients have a higher risk of secondary infection throughout all phases (most common reason for a fatal outcome).

Subtypes and variants

Acute tubular necrosis

Contrast-induced nephropathy

  • Definition: acute kidney injury after IV administration of iodinated contrast medium
  • Risk factors
  • Clinical features/diagnostics: See “Symptoms/clinical findings” above and “Diagnostics” below.
  • Course
    • Creatinine is highest after 3–5 days and usually falls back to the patient's baseline level within 1 week.
    • The course is usually mild (end-stage renal disease usually only occurs in patients with pre-existing CKD).
  • Prevention
    • Always evaluate kidney function before administering contrast agent.
    • Use low dose and concentration of contrast medium.
    • Discontinue nephrotoxic substances before administration.
    • Ensure hydration: isotonic NaCl before and after administration of contrast medium (isotonic bicarbonate can also be used
    • Acetylcysteine (no clear recommendations )


References:[1][2][3][4][5][6][7][8]

Diagnostics

Types of AKI Prerenal Intrinsic Postrenal
BUN/Cr ratio > 20:1 < 20:1 < 20:1

Fractional excretion of sodium

FENa= (V*UNa)/(GFR*PNa), using plasma and urine sodium concentrations (PNa and UNa), urine flow rate (V), and GFR.

or

FENa= (SCr*UNa)/(SNa*UCr), using serum sodium (SNa), urine sodium (UNa), serum creatinine (SCr), and urine creatinine (UCr).

 < 1% > 1%

Acute: Normal (< 1%)

Subacute: >1%
Urine sodium concentration < 10 mEq/L > 30 mEq/L 10–30 mEq/L
Urine osmolality > 500 mOsm/kg < 300 mOsm/kg 300–500 mOsm/kg


References:[9][10]

Treatment