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What is
acute kidney injury (AKI)?

Acute kidney injury (AKI) is a clinical syndrome characterized by an abrupt decline in kidney function due to one or more of the following:

  • Lack of blood flow to the kidneys
  • Direct damage to the kidneys
  • Exposure to nephrotoxic agents
  • Inflammation in the kidneys
  • Blockage of urine from the kidneys

AKI can range from minor loss of kidney function to complete kidney failure. It develops rapidly – over a few hours or days. Early detection and treatment are critical to 1) promptly identify reversible conditions, and 2) prevent serious adverse outcomes. If not caught early, AKI will worsen existing illnesses, and can lead to an increased risk of chronic kidney disease (CKD), kidney failure, and death.

AKI is detected through laboratory test findings that show elevated serum creatinine (SCr) levels in the blood and/or low urine output.

AKI Clinical Markers (any of the following):
  • Increase in SCr by ≥ 0.3 mg/dl within 48 hours; or
  • Increase in SCr to ≥ 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or
  • Urine volume < 0.5 ml/kg/h for 6 hours.1

Previously referred to as Acute Renal Failure (ARF), the syndrome was renamed to reflect the range of the disease from minimal changes in clinical markers to more serious changes that may require renal replacement therapy (RRT).2 The reclassification recognizes that even small changes in kidney function are associated with worse short-and long-term outcomes, and demonstrates the need for early intervention.

What are the symptoms of AKI?

Just like CKD, there may not be any symptoms in the early stages of AKI. However, AKI can worsen very quickly. Anyone who is at increased risk should be evaluated promptly. Marked attention should be given to patients with existing kidney problems; those hospitalized for another illness or condition, such as congestive heart failure, infection, or urological obstruction; and patients who have had cardiac or other major surgery.

Warning signs include any of the following:

  • Decreased urine output
  • Fluid retention
  • Swelling in the arms and/or legs
  • Fatigue or drowsiness
  • Confusion
  • Nausea
  • Shortness of breath
  • High blood pressure
  • Irregular heart beat
  • Flank pain
  • Chest pain or pressure
  • Seizures or coma in severe cases

Who is at risk?

While AKI usually occurs in connection with another disease or condition, such as CKD, diabetes or heart disease, it can also occur in people with normally functioning kidneys. Everyone is at risk, but some are at increased risk. Causes are generally categorized as prerenal, intrinsic, and postrenal.

Prerenal AKI is caused by a sudden decrease in blood flow to the kidneys, resulting in loss of kidney function. This may result from exposures that harm the kidneys or systemic causes or traits making the patient more susceptible to injury. For example:

Exposure Susceptibility3
Sepsis Chronic kidney disease
Critical illness Diabetes
Circulatory shock Heart disease
Burns Other chronic diseases (lung, liver)
Trauma Cancer
Cardiac surgery Dehydration
Major non-cardiac surgery Anemia
Nephrotoxic drugs Advanced age
Iodine contrast agents Female gender
Poisonous plants and animals African American race

Intrinsic AKI is caused by an underlying condition within the kidneys that causes damage and leads to a sudden loss of kidney function. For example:

  • Glomerulonephritis
  • Lupus
  • Acute tubular necrosis
  • Vascular disease
  • Acute interstitial nephritis

Postrenal AKI occurs when there is a blockage in the urinary tract, causing fluids and wastes to build up in the kidneys. This can result from:

  • Kidney stones
  • Enlarged prostate
  • Blood clots in the urinary tract
  • Colon, prostate, or cervical cancer

Applying Clinical Guidelines: detecting AKI

✓ Test at-risk patients.

  • Two simple tests will detect AKI:
    1. Measurement of serum creatinine (SCr), and
    2. Measurement of urine output.
  • AKI is detected if:
    1. SCr has increased by ≥ 0.3 mg/dl within 48 hours; or
    2. SCR has increased to ≥ 1.5 times baseline*; or
    3. Urine volume is < 0.5 ml/kg/h for 6 hours.1

*In patient record or measured within last 7 days.

✓ Once AKI is identified, further evaluation is needed to establish etiology.

Applying Clinical Guidelines: diagnosing AKI.

✓ Evaluate promptly to determine cause, which may be reversible or treatable. Initial evaluation should include:

  • Thorough patient history to identify use of nephrotoxic drugs, exposure to contrast media, or systemic illness.
  • Thorough physical examination to identify signs of congestive heart failure or infection.
  • Blood urea nitrogen.
  • Electrolytes.
  • Complete blood count and differential.
  • Assessment of renal function by eGFR.
  • Urinary sediment and urinary diagnostic indices.
  • Ultrasound to rule out obstruction.
  • Possible kidney biopsy.

✓ Use team-based approach to prevent, diagnose, and treat aggressively. Make rapid referral to nephrologist and other specialists as indicated.4

✓ Treatment plan will focus on treating the underlying illness or injury, preventing cardiovascular collapse and death,5 and managing complications of AKI.

Applying Clinical Guidelines: treating AKI.

✓ Treat underlying cause.

  • If patient has CKD, manage according to KDOQI CKD Guidelines.
  • If patient does not have CKD, consider patient at risk.

✓ Treat complications of AKI.6

Complication Treatment
Dehydration Intravenous (IV) fluids
Edema Diuretics/other medicines to reduce fluid buildup
Obstruction Remove blockage in urinary tract
Hyperkalemia Calcium, glucose or sodium polystyrene sulfonate
Hypocalcemia Calcium; possibly infusion of calcium
Metabolic acidosis Sodium bicarbonate
Low blood pressure Inotropes to improve cardiac output
Nephrotoxic Temporary dialysis
Chronic kidney disease Manage according to KDOQI CKD Guidelines
No CKD Consider patient at risk

✓ Monitor patient by measuring SCr and urine output to stage severity.

✓ Evaluate patient 3 months post-AKI for resolution, new onset, or worsening of pre-existing CKD.

✓ Long-term close follow-up of a patient’s kidney function is strongly recommended after even one episode of AKI, and even if no prior CKD was present.

AKI is a serious public health problem.

AKI is increasingly prevalent and associated with severe morbidity and mortality. It affects 13 million people annually worldwide,7 and is responsible for 2 million deaths per year.8 AKI is largely seen among hospitalized patients, where 45 percent of patients admitted to the ICU and 20 percent of hospitalized patients are affected.9 Whether a result of pre-existing kidney problems, sepsis, surgery, or exposure to contrast iodine or nephrotoxic agents, AKI is serious and can be fatal. Remember:

  • Early detection
  • Prompt treatment
  • Rapid referral to specialist(s)
  • Management through multidisciplinary care

1 Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guidelines for Acute Kidney Injury. Kidney Inter., Suppl. 2012; 2:1-138. Accessed from http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdf (PDF, 1.7MB).

2 Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care 2007; 11:R31. Accessed from http://www.ccforum.com/content/11/2/r31.

3 Kellum JA, Lamiere N, KDIGO AKI Guideline Work Group. Diagnosis, evaluation, and management of acute kidney injury: a KIDGO summary. Crit Care 2013, 17:204. Accessed from http://www.ccforum.com/content/17/1/204.

4 Rahman M, Shad F, Smith MC. Acute Kidney Injury: A Guide to Diagnosis and Management. Am Fam Physician, Oct 1, 2012, 1:86(7):631-639. Accessed from http://www.aafp.org/afp/2012/1001/p631.html.

5 Palevsky PM, Zhang JH, O'Connor TZ, Chertow GM, Crowley ST, Choudhury D, Finkel K, Kellum JA, Paganini E, Schein RM, Smith MW, Swanson KM, Thompson BT, Vijayan A, Watnick S, Star RA, Peduzzi P. "Intensity of renal support in critically ill patients with acute kidney injury". The New England Journal of Medicine 359 (1): 7–20. July 2008. doi:10.1056/NEJMoa0802639. PMC 2574780. PMID 18492867. Accessed from http://www.ncbi.nlm.nih.gov/pubmed/18492867.

6 Mayo Clinic. Acute kidney failure. Accessed from http://www.mayoclinic.org/diseases-conditions/kidney-failure/basics/treatment/con-20024029.

7 Mehta RL, Cerda J, Burdmann EA, Tonelli M et al. International Society of Nephrology's 0by25 initiative for acute kidney injury (zero preventable deaths by 2025): a human rights case for nephrology. Lancet Commissions, 385(9987):2616-2743. June 27, 2015. Accessed from http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(15)60126-X/abstract.

8 Chawla LS, Kimmel PL. Acute Kidney Injury and Chronic Kidney Disease: An Integrated Clinical Syndrome. Kidney Int., 82(5):516-524; doi:10.1038/ki.2012.208; published online June 6, 2012.

9 Li PKT, Burdmann EA, Mehta RL. Acute kidney injury: Global health alert. J Nephropathol, 2(2):90-97. April 2013. 10.12860/JNP.2013.15. Accessed from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3891141/.

Please note: this brief summary of AKI is intended to be a primer. For more complete and detailed information, see references above and the following:

KDIGO Clinical Practice Guidelines for Acute Kidney Injury, 2012 (PDF, 1.7MB).

National Institute for Health and Care Excellent (NICE) Clinical Guideline: Acute Kidney Injury, 2013.

Essentials of Chronic Kidney Disease. Nova Science Publishers Inc ISBN-978-1-63482-542-9, 2015.

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