Acute kidney injury


  • In acute kidney injury (AKI) the ability of the glomeruli to filtrate deteriorates, which leads to a disturbed acid-base and fluid balance as well as to the accumulation of end products of nitrogen metabolism.
  • Within 24 to 48 hours of the onset of the injury the serum creatinine concentration will rise and urine output fall.
  • AKI should be identified before the creatinine concentration is markedly increased and the estimated glomerular filtration rate (eGFR) falls.
  • A typical patient is an elderly individual with pre-existing renal impairment who, for example, contracts acute diarrhoea or receives nephrotoxic drugs (e.g. NSAIDs, ACE inhibitors), i.e. acute-on-chronic kidney disease.
  • Hypovolaemia is the most common cause of oliguria and can be reversed with fluid therapy. The urine output of a seriously ill patient must be monitored.
  • Urinary retention must be identified and treated.
  • The concomitant administration of an ACE inhibitor, diuretic and NSAID [Evidence Level: B] increases the risk of AKI.


  • Pre-renal causes
    • Impaired renal perfusion: hypovolaemia, hypotension, circulatory problems
  • Renal (intrinsic) causes
  • Post-renal causes
  • Risk factors
    • Existing impairment of renal function (eGFR < 60 ml/min, plasma creatinine > 100 µmol/l) (Treatment of chronic renal failure) or other underlying disease, such as diabetes, cardiovascular disease
    • Advanced age
    • Diabetes
    • Vascular diseases
    • Nephrotoxic drugs
    • Surgical procedures in elderly individuals
    • Intravenous contrast media
    • Serious acute illness, such as sepsis, rhabdomyolysis

Clinical picture

  • Oliguria (< 30 ml/hour or < 400 ml/24 hours) or anuria (< 100 ml/24 hours); however, urine output may also be normal
  • Total anuria is usually suggestive of an obstruction to the urine flow resulting in a large, usually palpable bladder.
  • Hypovolaemia is characterised by low blood pressure and cool limbs
  • Hypervolaemia is characterised by oedema, particularly of the lower limbs, increased blood pressure and raised jugular venous pressure.
  • Nausea, loss of appetite
  • Dull pain and percussion tenderness over the kidneys are signs of acute nephritis
  • Deteriorating general health (may be the only sign in an elderly individual)
  • Fever signifying an infection (e.g. sepsis (Septicaemia), pyelonephritis (Urinary tract infections) or epidemic nephropathy (Nephropathia epidemica (NE)))
  • Skin changes (e.g. livedo reticularis in cholesterol embolism (Cholesterol embolization) after a vascular procedure, purpura in vasculitides)


  • Laboratory tests
    • Urinalysis immediately, urinary cell count and bacterial culture
      • A dark colour and a positive urine strip test to Hb are suggestive of rhabdomyolysis – check CK.
      • Proteinuria, haematuria and casts are suggestive of an intrinsic kidney disease.
    • Creatinine and eGFR , plasma electrolytes (sodium, potassium, calcium, phosphate) and, if possible, blood gas analysis
      • Re-check creatinine concentration without delay if it is unexpectedly increased.
      • Hyperkalaemia (Hyperkalaemia) is the most serious complication of AKI.
      • Acidosis worsens hyperkalaemia.
    • CRP, blood count with platelets, glucose
  • ECG (hyperkalaemia?) and chest x-ray (congestion/oedema?)
  • Palpation of the bladder, determination of residual urine (Determining the volume of residual urine by ultrasonography) and digital rectal examination, especially in men.
  • Ultrasonography of the kidneys and urinary tract
    • Hydronephrosis is suggestive of a post-renal obstruction.
    • Oedematous kidneys are suggestive of an acute parenchymal disease.
    • Shrunken kidneys are suggestive of an underlying chronic kidney disease (acute-on-chronic).
  • Kidney biopsy is carried out in specialist care when acute glomerulonephritis is suspected (heavy proteinuria, haematuria, red cell casts).
  • Classification of acute kidney injury: see table T1

Table 1. Classification of AKI (AKIN criteria)
Grade Creatinine Urine output
1 An increase of ≥ 27 µmol/l or 1.5 to 2-fold from baseline Less than 0.5 ml/kg/hour for > 6 hours
2 A 2 to 3-fold increase Less than 0.5 ml/kg/hour for > 12 hours
3 An increase of > 3-fold or > 354 µmol/l or treatment with dialysis Less than 0.3 ml/kg/hour for 24 hours or anuria for 12 hours


  • It is not possible to treat AKI with medication.
  • Stop potentially nephrotoxic medications.
  • Monitoring of urine output: catheter if the patient is unable to pass urine
    • Hourly urine measurements
    • In anuria, the catheter should be removed due to the risk of infection.
  • Urinary retention, or other obstruction to urine flow, with a palpable bladder
    • A sudden cessation of urine output without hypovolaemia
    • An indwelling catheter or percutaneous cystostomy
    • The underlying cause should be corrected.
  • Oxygen therapy as required (SpO2 > 94%)
  • Management of dehydration
    • A patient with cool extremities, low systolic blood pressure (below 90 mmHg), and no audible rales on pulmonary auscultation (for example, an elderly patient with diarrhoea)
    • Ringer's acetate solution 1,000 ml as an infusion 15 ml/kg/hour or 1,000–2,000 ml over 2–4 hours. The infusion is continued until the symptoms of hypovolaemia improve and diuresis recommences.
    • The target blood pressure (systolic) is above 100 mmHg. If needed, inotropic drugs (e.g. noradrenaline).
    • Observe the patient for excessive fluid overload and pulmonary oedema (in which case CPAP is indicated).
    • The use of colloids [Evidence Level: B] or albumin [Evidence Level: B] is not recommended.
  • Hyperkalaemia (Hyperkalaemia) and acidosis must be corrected.
    • Mild hyperkalaemia (plasma K < 6.0) with no ECG changes
      • Usually requires no specific treatment. Any medication inducing hyperkalaemia should be stopped.
    • Plasma K ≥ 6.0: see (Hyperkalaemia)
  • Furosemide
    • Can be tried in gradually increasing doses (20–40–80 mg i.v.; large doses administered as an infusion over 15–20 minutes), after it has been verified that the patient is not hypovolaemic.
    • If urine output increases, treatment may continue with repeated doses (4–6 times daily) or a continuous infusion (10–15 mg/hour).
    • No evidence is available on the benefit of furosemide , and it does not improve renal function [Evidence Level: C].
  • Renal replacement therapies (dialysis, continuous filtration) should be considered in the following situations:
    • overhydration
    • hyperkalaemia (plasma K > 6.5 mmol/l)
    • metabolic acidosis (pH < 7.2; HCO3 < 15 mmol/l)
    • persistent oliguria (urine output < 200 ml/12 hours) or a markedly increased urea (> 35 mmol/l) and creatinine (> 500 µmol/l ) concentration.
  • In AKI, the patient’s medication list should always be examined and the possible nephrotoxicity of the drugs in use checked in an appropriate database as needed.

Evidence Summaries

Arrangement of treatment

  • Treatment is usually carried out in specialist care.
  • An elderly patient with gastroenteritis can in most cases be treated in a general ward.

Prophylaxis when using intravenous contrast media

  • Important particularly in high-risk patients (see above)
  • The greatest risk is associated with investigations necessitating intra-arterial administration.
  • Nephrotoxic drugs (metformin, ACE inhibitors, ATR blocers, NSAIDs) and diuretics should be stopped 24 hours before the investigation.
  • It is crucial to ensure the adequate hydration of patients in the high risk groups: an infusion of 0.9% NaCl 1 ml/kg/hour, 6–12 hours before and after the investigation. The fluid regime should be agreed on in good time with the unit carrying out the investigation.
  • In emergency situations (in a hospital), administer 500 ml of 0.9% NaCl as a rapid infusion before the investigation and 1 ml/kg/hour after the investigation for 6–12 hours.
  • Sodium bicarbonate appears to be as effective as 0.9% NaCl.
    • 1.4% sodium bicarbonate is given 3 ml/kg over one hour before the investigation, and after the investigation 1 ml/kg/hour is continued for at least 6 hours.
  • Contrast media used in magnetic resonance imaging are (usually) not nephrotoxic.
  • Plasma creatinine should be checked in high-risk patients 2 days after the procedure.


1. Solomon R, Werner C, Mann D, D'Elia J, Silva P. Effects of saline, mannitol, and furosemide to prevent acute decreases in renal function induced by radiocontrast agents. N Engl J Med 1994 Nov 24;331(21):1416-20.  [PMID:7969280]

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