Diagnosis of acute kidney injury (AKI)

byAbdelwahab Ward, BS Pharm, PharmD - last updated
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OVERVIEW — Acute kidney injury (AKI) is a term covering a spectrum of injury to the kidneys which can result from a number of causes. It is a clinical syndrome rather than a biochemical diagnosis. The term "acute kidney injury" has replaced the concept of acute renal failure as it more accurately describes that injury to the kidney can occur before function fails. It is characterized by a decline in renal excretory function over hours or days that can result in failure to maintain fluid, electrolyte, and acid-base homeostasis.

CAUSES OF ACUTE KIDNEY INJURY

The causes of acute kidney injury can be divided into (see Table 1):
    • Pre-renal (most common) — due to reduced perfusion of the kidneys and leading to a decreased glomerular filtration rate (GFR). It is usually reversible with appropriate early treatment.
    • Intrinsic renal — a consequence of structural damage to the kidney, for example, tubules, glomeruli, interstitium, and intrarenal blood vessels. It may result from persistent pre-renal or post-renal causes damaging renal cells.
    • Post-renal (least common, accounting for around 10% of acute kidney injury) — due to acute obstruction of the flow of urine resulting in increased intratubular pressure and decreased GFR.
Table (1). Causes of acute kidney injury
Pre-renal Renal Post-renal
Hypovolaemia (e.g. inability to maintain hydration without help from others, haemorrhage, gastrointestinal losses, renal losses, burns) Toxins and drugs (for example antibiotics, contrast, chemotherapy) Obstruction (e.g. renal stones, blocked catheter, enlarged prostate, genitourinary tract tumours/masses, neurogenic bladder)
Reduced cardiac output (e.g. cardiac failure, liver failure, sepsis, drugs) Vascular (e.g. vasculitis, thrombosis, athero/thromboembolism, dissection)
Drugs that reduce blood pressure, circulating volume, or renal blood flow (e.g. ACE inhibitors, ARBs, NSAIDs, loop diuretics) Glomerular (e.g. glomerulonephritis)

Tubular (e.g. acute tubular necrosis, rhabdomyolysis, myeloma)
Interstitial (e.g. interstitial nephritis, lymphoma infiltration)

DIAGNOSIS

SUSPECTING ACUTE KIDNEY INJURY — Suspect acute kidney injury (AKI) in anyone with symptoms and signs such as: nausea and vomiting, or diarrhoea, evidence of dehydration, reduced urine output or changes to urine color with confusion, fatigue, and drowsiness. 

SUSPECTING AKI
Suspect acute kidney injury (AKI) in anyone with an acute illness and any of the following..
  • Age of 65 years or over.
  • A history of acute kidney injury.
  • Chronic kidney disease (estimated glomerular filtration rate [eGFR] less than 60 mL/min).
  • Symptoms or history of urological obstruction or conditions which may lead to obstruction.
  • Chronic conditions such as heart failure and liver disease and diabetes mellitus.
  • Neurological or cognitive impairment or disability (which may limit fluid intake because of reliance on a carer).
  • Sepsis.
  • Nephrotoxic drug use within the last week (especially if hypovolaemic) — for example, nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor antagonists (ARBs), and diuretics. 
  • Exposure to iodinated contrast agents within the past week.
  • Cancer and cancer therapy (risk will depend on the type of cancer, proposed treatment and premorbid risk factors).
  • Immunocompromise (for example HIV infection).
  • Toxins (for example some herbal remedies, poisonous plants and animals).
  • An illness with no clear acute component and any of the following:
      • Chronic kidney disease (especially stage 3B, 4, or 5), or urological disease.
      • New onset or significant worsening of urological symptoms.
      • Symptoms or signs of a multi-system disease affecting the kidneys and other organ systems (for example signs or symptoms of acute kidney injury, plus a purpuric rash in thrombotic thrombocytopenic purpura).
      • Symptoms suggesting the presence of complications of acute kidney injury (hyperkalemia, metabolic acidosis, peripheral and pulmonary edema and uremia).

RESPONDING TO AKI WARNING STAGE TEST RESULTS — Respond to AKI warning stage test results within an appropriate timescale using clinical judgment, bearing in mind that certain clinical features will prompt an earlier review, for example, poor urine output, evidence of hyperkalaemia, previous AKI, known CKD stage 4 or 5 or renal transplant, frailty, chronic disease such as diabetes or heart failure, suspected intrinsic kidney disease or urinary tract obstruction. As a guide (see Table 2)...
    • If AKI warning stage 1 (current creatinine 1.5 or more times the baseline level or creatinine rise more than 0.3 mg/dL (26.5 micromol/L) or greater within 48 hours) and there is a low pre-test probability of AKI (stable clinical context), consider clinical review within 72 hours of the result and high pre-test probability of AKI (in the context of acute illness), consider clinical review within 24 hours of the result.
    • If AKI warning stage 2 (current creatinine 2 or more times the baseline level) and there is low pre-test probability of AKI (stable clinical context), consider clinical review within 24 hours of the result and high pre-test probability of AKI (in the context of acute illness), consider clinical review within 6 hours of the result.
    • If AKI warning stage 3 (current creatinine three or more times the baseline level, or creatinine 1.5 times baseline and more than 4 mg/dL or 354 micromol/L) and there is a low pre-test probability of AKI (stable clinical context), consider clinical review within 6 hours of the result and high pre-test probability of AKI (in the context of acute illness), consider immediate admission.
Table (2). Stages of Acute Kidney Injury
Stage Change in serum creatinine level Urine output Other
1 Increase ≥ 0.3 mg per dL (26.52 μmol per L) or ≥ 1.5- to twofold from baseline < 0.5 mL per kg per hour for more than six hours —
2 Increase > two- to threefold from baseline < 0.5 mL per kg per hour for more than 12 hours —
3 Increase > threefold from baseline or ≥ 4.0 mg per dL (353.60 μmol per L) with an acute rise of at least 0.5 mg per dL (44.20 μmol per L) < 0.3 mL per kg per hour for 24 hours or anuria for 12 hours Renal replacement therapy required

CONFIRMING AKI

In people with suspected acute kidney injury (AKI) who do not require urgent admission to hospital, measure serum creatinine (or refer to a current result if this has already been done) and, taking into account the clinical context, compare with baseline. To obtain a baseline value for the initial detection of acute kidney injury. Use the lowest creatinine value within 7 days of the current value, or (if this is not available). Look at older results and use the lowest or mean creatinine value from between 7 days and 1 year before the current value. If no baseline creatinine value is available, it may be appropriate to repeat the creatinine measurement after 48–72 hours. Use clinical judgement and monitor the person closely and do not let waiting for a second creatinine result delay treatment or referral if acute kidney injury is possible, particularly if the person is unwell or the serum creatinine level is high. Take into consideration if the patient has:
    • Chronic kidney disease — an increase in creatinine may be because this has progressed.
    • Recently been treated with trimethoprim — this can cause a false positive result as trimethoprim may increase serum creatinine, but not affect glomerular filtration rate.
    • Recently completed a pregnancy — this can cause a false positive result due to an apparent rise in creatinine compared with naturally reduced creatinine values in pregnancy.
diagnosis criteria
Detect AKI by using any of the following criteria...
  • A rise in serum creatinine of  0.3 mg/dL (26 micromol/L) or greater within 48 hours. Be aware that in the absence of a baseline creatinine value, a high serum creatinine level may indicate AKI, even if the rise in creatinine over 48 hours is less than 0.3 mg/dL (particularly if the patient has been unwell for a few days).
  • A 50% or greater rise in serum creatinine (more than 1.5 times baseline) known or presumed to have occurred within the past 7 days.
  • A fall in urine output to less than 0.5 mL/kg/hour for more than 6 hours (if it is possible to measure this, for example, if the person has a catheter).
  • If there is doubt whether a patient with chronic kidney disease has worsening of their condition or has acute-on-chronic kidney disease, consider it to be acute and manage accordingly.

REFERENCES

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