Written and peer-reviewed by physicians—but use at your own risk. Read our disclaimer.

banner image

amboss

Trusted medical answers—in seconds.

Get access to 1,000+ medical articles with instant search
and clinical tools.

Try free for 5 days

Acute kidney injury

Last updated: November 30, 2020

Summarytoggle arrow icon

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.

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]

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:[1][2][4]

Acute tubular necrosis

Renal cortical necrosis

Contrast-induced nephropathy


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

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]

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

References:[11][12]

Interested in the newest medical research, distilled down to just one minute? Sign up for the One-Minute Telegram in “Tips and links” below.

  1. Kumar V, Abbas AK, Aster JC. Robbins & Cotran Pathologic Basis of Disease. Elsevier Saunders ; 2015
  2. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. McGraw-Hill Education ; 2015
  3. Le T, Bhushan V,‎ Sochat M, Chavda Y, Zureick A. First Aid for the USMLE Step 1 2018. McGraw-Hill Medical ; 2017
  4. Basile DP, Anderson MD, Sutton TA. Pathophysiology of acute kidney injury. Compr Physiol. 2012; 2 (2): p.1303-53. doi: 10.1002/cphy.c110041 . | Open in Read by QxMD
  5. Goldman L, Schafer AI. Goldman-Cecil Medicine, 25th Edition. Elsevier ; 2016
  6. Erdbruegger U, Okusa MD. Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury (acute renal failure). In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/etiology-and-diagnosis-of-prerenal-disease-and-acute-tubular-necrosis-in-acute-kidney-injury-acute-renal-failure.Last updated: April 1, 2016. Accessed: April 17, 2017.
  7. Rudnick MR. Prevention of contrast-induced nephropathy. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. http://www.uptodate.com/contents/prevention-of-contrast-induced-nephropathy.Last updated: April 5, 2017. Accessed: April 17, 2017.
  8. Rudnick MR. Prevention of contrast nephropathy associated with angiography. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/prevention-of-contrast-nephropathy-associated-with-angiography.Last updated: June 15, 2017. Accessed: October 4, 2017.
  9. Rosner MH, Okusa MD, Palevsky PM, Sheridan AM. Pathogenesis and Etiology of Ischemic Acute Tubular Necrosis. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/pathogenesis-and-etiology-of-ischemic-acute-tubular-necrosis.Last updated: May 10, 2017. Accessed: June 21, 2018.
  10. Erdbruegger U, Okusa MD. Etiology and Diagnosis of Prerenal Disease and Acute Tubular Necrosis in Acute Kidney Injury in Adults. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/etiology-and-diagnosis-of-prerenal-disease-and-acute-tubular-necrosis-in-acute-kidney-injury-in-adults.Last updated: May 9, 2018. Accessed: October 25, 2018.
  11. Rahman M, Shad F, Smith MC. Acute kidney injury: a guide to diagnosis and management.. Am Fam Physician. 2012; 86 (7): p.631-9.
  12. Moore PK, Hsu RK, Liu KD. Management of Acute Kidney Injury: Core Curriculum 2018. American Journal of Kidney Diseases. 2018; 72 (1): p.136-148. doi: 10.1053/j.ajkd.2017.11.021 . | Open in Read by QxMD
  13. Nguyen MT, Maynard SE, Kimmel PL. Misapplications of commonly used kidney equations: renal physiology in practice. Clin J Am Soc Nephrol. 2009; 4 (3): p.528-34. doi: 10.2215/CJN.05731108 . | Open in Read by QxMD