Acute kidney injury

Essentials

  • 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 as early as possible (before the creatinine concentration is markedly increased and the estimated glomerular filtration rate [eGFR] falls).
  • A common finding especially in hospital patients, weakens the prognosis considerably.
  • A typical patient is an older individual with pre-existing renal impairment who also contracts acute injury as a consequence of, for example, acute diarrhoea or the use of nephrotoxic drugs or drugs affecting blood circulation in glomeruli (e.g. NSAIDs, ACE inhibitors), i.e. acute-on-chronic kidney injury.
  • Hypovolaemia is the most common cause of oliguria and can usually be reversed with fluid therapy. Changes in the fluid balance of a seriously ill patient must be monitored carefully.
  • Urinary retention must be identified and treated.
  • The prevention of AKI should be paid special attention in patients with chronic renal failure, diabetes or hypertension and the elderly.
  • The concomitant use of an ACE inhibitor, diuretic and NSAID [Evidence Level: B] increases the risk of AKI – patient education is important.

Aetiology

  • Traditional classification into pre-renal, renal and post-renal factors is related to the investigation of the aetiology (but not severity) of acute injury. Grouping according to the KDIGO (Kidney Disease: Improving Global Outcomes) classification (table T1) is related to the investigation of the severity (but not the aetiological factor) of the injury.
  • Most common causes (pre-renal causes)
    • Impaired renal perfusion: hypovolaemia, hypotension, circulatory problems
      • For example: diarrhoea, sweating, bleeding, surgical procedures, burns, severe congestive heart failure (Acute heart failure and pulmonary oedema)
      • Drugs (ACE inhibitors, angiotensin II receptor blockers, NSAIDs [Evidence Level: B]) and/or difficult infection (e.g. sepsis (Sepsis)) often contributing to making the kidney situation more difficult
      • Prolonged hypoperfusion of the kidneys leads to ischaemic injury (especially in the deeper parts of the kidney → acute tubular necrosis, ATN).
  • Renal (intrinsic) causes (clearly rarer than pre-renal 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, especially diabetes, hypertension, cardiovascular diseases
    • Advanced age
    • Nephrotoxic drugs or drugs affecting the function of glomeruli (NSAIDs, ACE inhibitors, ATR blockers)
    • Surgical procedures in elderly individuals
    • Intravenous iodine contrast media in a risk patient (especially if eGFR < 30 ml/min)
    • Serious acute illness, such as sepsis (Sepsis), rhabdomyolysis (Rhabdomyolysis)

Clinical picture

  • Oliguria (volume of urine < 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. Is the bladder distended?
  • 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)

Diagnosis

  • Laboratory tests
    • Urine examined immediately, urinary cell count and bacterial culture
      • A dark colour and a positive urine strip test to Hb are suggestive of rhabdomyolysis – check CK and/or myoglobin.
      • Proteinuria, haematuria and casts are suggestive of an intrinsic kidney disease.
    • Plasma creatinine and eGFR , plasma electrolytes (sodium, potassium, calcium, phosphate) and, if possible, blood gas analysis
      • Re-check creatinine concentration after 6–12 hours if it is unexpectedly increased.
      • Hyperkalaemia (Hyperkalaemia) is one of the most serious complications 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 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 renal cause (especially glomerulonephritis [heavy proteinuria, haematuria, red cell casts] or interstitial nephritis, vasculitides) is suspected.
  • 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

Treatment

  • It is not possible to cure AKI with medication – treat the factor that caused the injury!
  • Stop potentially nephrotoxic medications, take into account the dose reduction of other medications according to the renal function.
  • Monitoring of urine output: catheter if the patient is unable to pass urine
    • Hourly urine measurements in the beginning
  • Urinary retention, or other obstruction to urine flow, with a palpable bladder
    • A sudden cessation of urine output without hypovolaemia
    • If bladder retention: an indwelling catheter or percutaneous cystostomy
    • If hydronephrosis: consider puncture pyelostomy (consultation with an urologist)
    • The underlying cause should be corrected.
  • Oxygen therapy as required (SpO2 > 94%)
  • Management of dehydration
    • A patient with cool extremities, low systolic blood pressure (e.g. below 90 mmHg), and no audible rales on pulmonary auscultation (dehydrated patient, for example, an elderly patient with diarrhoea)
    • Balanced electrolyte solution (e.g. Ringer 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 symptomatic fluid overload, hypertension and pulmonary oedema (in which case CPAP is indicated) – monitor carefully the response to rehydration!
  • 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 (10–20–40 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 (3–6 times daily) or a continuous infusion (5–20 mg/hour).
    • No evidence is available on the benefit of furosemide, and it does not improve renal cleansing function [Evidence Level: C].
  • In treatment-resistant cases, renal replacement therapies (haemodialysis, ultrafiltration) should be considered in the following situations (= consult a nephrologist):
    • overhydration or fluid overload with pulmonary manifestations and which does not get resolved by conservative means
    • hyperkalaemia (plasma K > 6.5 mmol/l) persists despite drug therapy
    • 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
    • severe symptoms of uraemia (especially if neurological symptoms).
  • 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. Note that the formula for estimated glomerular filtration rate (eGFR) does not work in acute kidney injury; the GFR of an anuric or oliguric patient is < 15 ml/min in reality.

Evidence Summaries

Arrangement of treatment

  • Treatment is usually carried out in specialist care (especially severe AKI), but hydration may be started in primary 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 patients with high risk of AKI (see above) – consider if the use of contrast medium is necessary
  • The greatest risk is associated with investigations necessitating intra-arterial administration and large amounts of iodine contrast medium.
  • Nephrotoxic drugs or drugs affecting the function of glomeruli (ACE inhibitors, ATR blockers, NSAIDs), metformin and diuretics should be stopped for the duration of the investigation, for 2–3 days.
  • It is crucial to ensure the adequate hydration of patients in the at-risk group: balanced electrolyte solution (e.g. Ringer solution) or 0.9% NaCl 1 ml/kg/hour, 3–4 hours before and 4–6 hours 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 500–1,000 ml of balanced electrolyte solution (or 0.9% NaCl) as a rapid infusion before the investigation and 1 ml/kg/hour after the investigation for 4–6 hours.
  • Contrast agents used in magnetic resonance imaging (gadolinium) are only rarely nephrotoxic. Consult a nephrologist if eGFR is < 15 ml/min.
  • Plasma creatinine should be checked in at-risk patients 1 and 2 days after the procedure.

Follow-up

  • The majority of patients who become ill with mild AKI especially recover from it fully.
  • The patients who have previously become ill with AKI have, however, later an increased risk of getting a new injury and/or of developing chronic renal insufficiency.
    • The risk of cardiovascular diseases is also increased.
  • Follow-up according to the level of renal function either at a primary care centre (mild–moderate insufficiency) or in specialist care (moderate–severe).

References

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2. Pickkers P, Ostermann M, Joannidis M et al. The intensive care medicine agenda on acute kidney injury. Intensive Care Med 2017;43(9):1198–1209.  [PMID:28138736]
3. Hodgson LE, Sarnowski A, Roderick PJ et al. Systematic review of prognostic prediction models for acute kidney injury (AKI) in general hospital populations. BMJ Open 2017;7(9):e016591.  [PMID:28963291]
4. Poston JT, Koyner JL. Sepsis associated acute kidney injury. BMJ 2019;364:k4891.  [PMID:30626586]
5. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International, March 2012, Vol 2, Supplement 1 https://kdigo.org/guidelines/acute-kidney-injury/.
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8. Hiremath S, Kayibanda JF, Chow BJW et al. Drug discontinuation before contrast procedures and the effect on acute kidney injury and other clinical outcomes: a systematic review protocol. Syst Rev 2018;7(1):34.  [PMID:29467030]
9. van der Molen AJ, Reimer P, Dekkers IA et al. Post-contrast acute kidney injury – Part 1: Definition, clinical features, incidence, role of contrast medium and risk factors: Recommendations for updated ESUR Contrast Medium Safety Committee guidelines. Eur Radiol 2018;28(7):2845–2855.  [PMID:29426991]
10. van der Molen AJ, Reimer P, Dekkers IA et al. Post-contrast acute kidney injury. Part 2: risk stratification, role of hydration and other prophylactic measures, patients taking metformin and chronic dialysis patients: Recommendations for updated ESUR Contrast Medium Safety Committee guidelines. Eur Radiol 2018;28(7):2856–2869.  [PMID:29417249]
11. Hounkpatin HO, Fraser SDS, Glidewell L et al. Predicting Risk of Recurrent Acute Kidney Injury: A Systematic Review. Nephron 2019;142(2):83–90.  [PMID:30897569]
12. Fortrie G, de Geus HRH, Betjes MGH. The aftermath of acute kidney injury: a narrative review of long-term mortality and renal function. Crit Care 2019;23(1):24.  [PMID:30678696]
13. Wald R, Kitchlu A, Harel Z et al. Care of the Acute Kidney Injury Survivor. Nephron 2017;137(4):306–309.  [PMID:29132132]

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