Acute Kidney Injury (AKI)

 

Definition of acute kidney injury

  • Acute kidney injury (AKI): a sudden deterioration in renal function leading to an inability to maintain fluid, electrolyte and acid-base balance
    • AKI has replaced the term acute renal failure (ARF) which nephrologists disliked because it implied complete failure of renal function
  • Oligura: reduced urine output; defined variously as <0.5 ml/kg/hour, <30 ml/hour or <400 ml/day
  • Anuria: complete absence of urine output

 

Staging of acute kidney injury

  • Stage 1: creatinine (Cr) ≥1.5-2 times baseline or urine output (UO) <0.5 ml/kg/hours for >6 consecutive hours
  • Stage 2: Cr ≥2-3 times baseline or UO <0.5 ml/kg/hours for >12 hours
  • Stage 3: Cr ≥3 times baseline or UO <0.3 ml/kg/h for ≥24 hours or anuria for >12 hours
  • Patients should be staged according to their worst criterion

 

Epidemiology of acute kidney injury

  • Common
  • Often accompanies other acute medical or surgical problems due to its wide range of causes

 

Causes of acute kidney injury (AKI)

    • Hypovolaemia
      • Inadequate fluid intake
      • Excess fluid loss
        • Vomiting
        • Diarrhoea
        • Diuresis
        • Early sepsis
        • Haemorrhage
        • Burns
    • Reduced cardiac output
  • Pre-renal: inadequate blood supply to the kidneys
      • Acute coronary syndrome (ACS)
      • Cardiac arrhythmia eg atrial fibrillation (AF)
      • Valvular heart disease
      • Hypertension
      • Cardiomyopathy
      • Cardiac tamponade
      • Late sepsis
    • Renal artery disease
      • Renal artery stenosis
      • Vasculitis
  • Intrinsic renal: direct damage to the kidneys
    • Glomerular
      • Proliferative glomerulonephritis
        • Typically presents as nephritic syndrome characterised by haematuria (with red cells casts on microscopy), mild proteinuria (<3.5 g/day), hypertension, oedema, elevated Cr and oligruia
      • Non-proliferative glomerulonephritis
        • Typically presents as nephritic syndrome characterised by severe proteinuria (>3.5 g/day), hypoalbuminaemia and oedema
    • Tubular
      • Acute tubular necrosis (ATN)
        • Usually occurs secondary to the ischaemia of pre-renal AKI
      • Nephrotoxic drugs
        • Angiotensin converting enzyme inhibitors (ACEIs)
        • Angiotensin receptors blockers (ARBs)
        • Non-steroidal anti-inflammatory drugs (NSAIDs)
        • Aminoglycosides eg gentamicin
        • Radiological contrast
      • Rhabdomyolysis
      • Multiple myeloma
    • Interstitial
      • Acute interstitial nephritis: usually caused by a drug-induced allergic reaction
        • Penicillin
        • NSAIDs
      • Autoimmune disease e.g. systemic lupus erythromatosus (SLE)
      • Infiltrative disease
        • Lymphoma
        • Sarcoidosis
    • Vascular
      • Hypertensive nephropathy
      • Vasculitides
      • Haemolytic uraemic syndrome (HUS)
      • Thrombotic thrombocytopenic purpura (TTP)
      • Disseminated intravascular coagulation (DIC)
  • Post-renal: obstruction to urinary flow
    • Ureters
      • Luminal
        • Ureteric calculi
        • Vesicoureteric reflux
      • Mural
        • Tumour e.g. transitional cell carcinoma
      • Extrinsic
        • Compression from abdominal/pelvic mass
        • Complication of abdominal/pelvic surgery
        • Retroperitoneal fibrosis
    • Bladder
      • Luminal
        • Bladder calculi
      • Mural
        • Tumour e.g. bladder carcinoma
      • Extrinsic
        • Neurogenic bladder
          • Diabetes mellitus
          • Multiple sclerosis
          • Spinal cord compression
          • Cauda equine syndrome
          • Anticholinergic drugs
          • Sympathomimetic drugs
    • Urethra
      • Luminal
        • Blocked urethral catheter
      • Mural
        • Urethral stricture
      • Extrinsic
        • Benign prostatic hypertrophy (BPH)
        • Prostatic carcinoma
        • Pain

 

Risk factors for acute kidney injury (AKI)

  • Age >75 years
  • Chronic kidney disease (CKD)
  • Cardiac failure
  • Peripheral vascular disease (PVD)
  • Hypertension
  • Hepatic disease
  • Diabetes mellitus
  • Nephrotoxic medications

 

History in acute kidney injury

  • Symptoms of dehydration
    • Thirst
    • Light-headedness
    • Dry mouth
    • Dark urine
  • Symptoms of excess fluid loss
    • Vomiting
    • Diarrhoea
    • Diuresis
    • Haemorrhage
    • Burns
  • Symptoms of cardiac failure
    • Fatigue
    • Worsening dyspnoea progressing from an exercise tolerance of dyspnoea on exertion to at rest
    • Orthopnoea
    • PND
    • Cough productive of pink, frothy sputum
    • Ankle swelling
  • Symptoms of sepsis
    • Fever
    • Rigors
    • Symptoms of the focus
  • Symptoms of malignancy
    • Cachexia
    • Anorexia
    • Night sweats
    • Symptoms of the focus
  • Symptoms of ureteric obstruction
    • Severe, colicky loin to groin pain
  • Symptoms of bladder obstruction
    • Complete
      • Painful suprapubic mass
      • Anuria
    • Partial
      • Painful suprapubic mass
      • Urinary frequency
      • Hesitancy
      • Poor stream
      • Terminal dribbling
      • Strangury
  • Drug history
    • Angiotensin converting enzyme inhibitors (ACEIs)
    • Angiotensin receptors blockers (ARBs)
    • Non-steroidal anti-inflammatory drugs (NSAIDs)
    • Aminoglycosides eg gentamicin
    • Anticholinergic drugs
    • Sympathomimetic drugs

 

Examination of the patient with acute kidney injury

  • Signs of hypovolaemia
    • Cold, pale peripheries
    • Prolonged capillary refill times (CRT >2 s)
    • Decreased skin turgor
    • Reduced jugular venous pressure (JVP)
    • Sunken eyes
    • Dry lips, mouth and tongue
    • Tachycardia
    • Postural hypotension
    • Absolute hypotension
    • Dark urine
  • Signs of cardiac failure
    • Respiratory distress
    • Tachypnoea
    • Bibasal crepitations
    • Cardiac wheeze
    • Tachycardia
    • Displaced apex beat
    • Third heart sound
    • RV heave
    • Raised JVP
    • Hepatomegaly
    • Peripheral oedema
  • Signs of sepsis
    • Pyrexia
    • Tachypnoea
    • Tachycardia
    • Altered mental state
    • Hypotension in septic shock
    • Signs of the focus
  • Signs of malignancy
    • Cachectic
    • Signs of the focus
  • Signs of ureteric obstruction
    • Unable to get comfortable
    • Tender loin
  • Signs of bladder obstruction
    • Tender suprapubic mass that is dull to percussion; palpation may generate the urge to urinate
    • Enlarged prostate on digital rectal examination

 

Investigation of acute kidney injury

  • Urea & electrolytes (U&Es)
    • Although there may be prior clinical suspicion, comparison of current Cr to previous values will make the diagnosis, grade the severity and identify any accompanying electrolyte abnormalities
  • Full blood count (FBC)
    • May reveal elevated white cell and neutrophil count suggesting infection
  • Venous blood gas (VBG)
    • May reveal a metabolic acidosis and will provide certain electrolytes faster than laboratory blood tests
  • Urinalysis
    • Proteinuria may be part of nephrotic syndrome and should be quantified with a urinary protein:creatinine ratio (PCR)
    • Haematuria may be part of nephritic syndrome and should prompt a nephritic screen
    • Leucocytes and nitrites suggest infection and should prompt a urine culture
  • Urinary & plasma osmolality and sodium: may help distinguish between pre-renal AKI and ATN
    • Pre-renal AKI: kidney is functioning maximally to retain salt and water; urinary osmolality is high (600-900 mosm/L) and urinary sodium is low (<10 mM)
    • ATN: kidney is functioning inadequately and is unable to retain salt and water; urinary osmolality approaches that of plasma(280 mosm/L) and urinary sodium rises (>30 mM)
  • Bladder scan
    • Will reveal the volume of urine in the bladder and suggests retention if >600 ml
    • If the patient is able to pass urine, perform a post-void bladder scan: if the volume is still significant, this suggests incomplete voiding and partial retention
  • Renal ultrasound scan (USS)
    • May reveal the source of any post-renal obstruction

 

Initial management of acute kidney injury (AKI)

  • Stop/avoid nephrotoxic drugs;
    • If they are absolutely necessary adjust dosages accordingly
  • Fluid resuscitation
  • Monitor fluid balance with input/output chart and daily weights
  • Daily U&Es
  • Urinary osmolality and sodium
  • Urinalysis +/- culture, urinary PCR or nephritic screen
  • Urethral catheterisation to relieve bladder outflow obstruction and/or accurately monitor urine output
    • When considering urethral catheterisation for urine output monitoring, weigh the benefits of accurate urine output monitoring against the risks of introducing infection
  • Renal USS
    • Consider if suspicious of post-renal obstruction, especially if not resolved by urethral catheterisation
  • Treat the cause
  • Treat any complications

 

Further management of acute kidney injury (AKI)

  • Indications for renal replacement therapy (RRT):
    • Urine output <0.3 ml/kg for 24 hours
    • Absolute anuria for >12 hours
    • Multi-organ failure
    • Refractory volume overload
    • Complications of uraemia
      • Uraemic encephalopathy
      • Uraemic pericarditis
    • Severe poisoning or drug overdose
    • Severe hypo/hyperthermia
    • Refractory hyperkalaemia >6.5 mM
    • Serum urea >27 mM
    • Refractory metabolic acidosis pH <7.15
    • Refractory electrolyte abnormalities
      • Hyponatraemia <115 mM
      • Hypernatraemia >165 mM
      • Hypercalcaemia
  • Types of continuous renal replacement therapy (CRRT):
    • Continuous venovenous haemodialysis (CVVHD)
    • Continuous venovenous haemofiltration (CVVHF)
    • Continuous venovenous haemodiafiltration (CVVHDF)

 

Complications of acute kidney injury

  • Hyperkalaemia
  • Hypo/hypernatraemia
  • Hypercalcaemia
  • Metabolic acidosis
  • Pulmonary oedema
  • Hypertension
  • Uraemic encephalopathy
  • Uraemic pericarditis

 

Prognosis of acute kidney injury

  • When mild and treated promptly and aggressively, AKI is usually reversible
  • When severe and/or unrecognised and/or treated inadequately, there is usually at least an element of chronic renal impairment

 

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