FRCA Notes

Acute Kidney Injury

There are multiple relevant curriculum items, perhaps the most relevant of which is 'demonstrates knowledge of the pathophysiology of acute renal failure'.

Resources

  • AKI occurs in 7-10% of all inpatients
  • In patients undergoing non-cardiac surgery with normal pre-operative renal function the incidence is approximately 7.5%
  • Higher rates are seen in patients undergoing cardiac surgery (10-36%) and cardiopulmonary bypass (50%)
  • Other at-risk patients include those undergoing aortic aneurysm repair, either open repair or EVAR

  • In critical care, it has a much higher incidence of up to 50%
    • Of these 5% will require RRT
    • Its presence is associated with an increased mortality, as high as 50%

KDIGO Criteria

  • The KDIGO Criteria are a combination of the RIFLE and AKIN criteria
Category Creatinine Urine output
Stage 1 ↑ by 1.5 - 1.9x
or
↑ ≥26.4μmol/L in 24hrs		 <0.5ml/kg/hr for 6-12 hours
Stage 2 ↑ by 2.0 - 2.9x <0.5ml/kg/hr for 12 hours
Stage 3 ↑ by 3x
or
>354μmol/L
or
Receiving RRT		 <0.5ml/kg/hr for 24hrs
or
<0.3ml/kg/hr for 12hrs
or
Anuria for 12hrs

Other Criteria

  • The RIFLE (Risk, Injury, Failure, Loss, End-stage) criteria are based on rising creatinine and/or falling urine output
  • As one progresses down the RIFLE criteria one can expect an increased length of stay, lower chance of renal recovery and higher mortality
  • The AKIN criteria are similar, with no difference in predictive acuity between AKIN and RIFLE criteria

Pre-renal

  • Pre-renal AKI is due to some state of renal hypoperfusion
  • Renal hypoperfusion leads to compensatory mechanisms being activated:
    • Activation of the sympathetic nervous system and RAAS
    • Aldosterone and vasopressin (ADH) secretion
    • Increased reabsorption of sodium, urea and water in order to maintain GFR
  • Restoration of normal renal perfusion via these mechanisms (or resuscitation) should result in a prompt recovery of renal function
  • However, if renal hypoperfusion is persistent then the compensatory mechanisms fail and GFR declines
  • Pre-renal AKI is also a potent risk factor for the development of intrinsic AKI
Aetiology of pre-renal AKI Examples
Hypovolaemia
(absolute fluid loss)		 Haemorrhage
Vomiting
Diarrhoea
Burns
Redistribution
(relative intravascular loss)		 Sepsis
Pancreatitis
Hypoalbuminaemia
Burns
↓ cardiac output E.g. heart failure
Renal vasoconstriction Hepatorenal syndrome
Prostaglandin inhibition
Hypercalcaemia
Malignant hyperpyrexia

Intrinsic renal

  • Parenchymal failure of the kidneys occurs due to intrinsic damage to some part of the glomerulus or nephron
  • It can be subdivided into:
    1. Acute tubular necrosis (commonest)
    2. Acute interstitial nephritis
    3. Glomerulonephritis
Acute tubular necrosis Acute interstital nephritis Glomerulonephritis
Drugs (antibiotics, heavy metals, ionic contrast media) Drugs (NSAIDs, antibiotics) Post-streptococcal
Hyperuricaemia/TLS SLE SLE
Haemolysis (haem molecules) Lymphoma HSP
Rhabdomyolysis (myoglobin) Goodpasture's dx, Burger's dx (IgA nephropathy)
Myeloma (light chains) DIC
MAHA

Post-renal

  • Occurs due to obstruction of urine outflow, which again can be subdivided into different anatomical locations
Upper tract obstruction VUJ obstruction Bladder outlet obstruction
Calculus Calculus Calculus
Trauma inc. surgical Trauma inc. surgical Trauma inc. surgical
Retroperitoneal neoplasm Pelvic neoplasm Bladder neoplasm
Retroperitoneal abscess Pyelonephritis Cystitis
Retroperitoneal fibrosis Prostatism
Pregnancy/labour
Drugs inc. opioids, anticholinergics
Prolapse


Perioperative management of the patient with AKI, and to reduce risk of AKI

  • The majority of peri-operative AKI is multifactorial, with significant overlap between pre- and intrinsic-renal AKI due to prolonged haemodynamic disturbance
  • The pathogenesis of tubular injury after major surgery is due to the interactions between:
    • Pre-existing risk factors and disposition
    • Peri-operative haemodynamic disturbances
    • Nephrotoxic insults
    • Renal venous congestion (BJA, 2022)
    • The inflammatory response, which plays a central role by causing direct injury and inducing microcirculatory dysfunction which contributes to local tissue ischaemia

  • Perioperative tubular injury can increase pre-glomerular resistance, causing renal hypoperfusion independent of systemic haemodynamics
  • This limits the reversibility of AKI by optimising systemic circulation and global renal oxygen delivery

Assessment

  • Identify those at risk of AKI (see risk factors below)
  • Establish the aetiology of the patient's AKI if pre-existing
  • Recent U&E including trend
  • Urine output, weight, fluid balance
  • Existing management to date e.g. need for RRT, fluid resuscitation
  • Optimisation where possible e.g. further fluid resuscitation, RRT timing, Renal team input
  • Plan suitable post-operative location if more intensive monitoring is required e.g. HDU

Risk factors for perioperative AKI

Patient factors Pharmacological factors Surgical factors
Male gender NSAIDs Emergency surgery
↑ Age ACE-I/ARA Cardiac surgery
Existing CKD Antibiotics inc. aminoglycosides, glycopeptides Liver surgery
Cardiovascular disease inc. HTN Hydroxyethyl starch colloids Intra-peritoneal surgery
Chronic liver disease Radiological contrast media Prolonged duration of surgery
Diabetes mellitus esp. if poor control Calcineurin inhibitors Major haemorrhage/blood transfusion
Sepsis Platinum-based chemotherapy Hypovolaemia/hypotension
Limited cardiopulmonary reserve


  • A targeted approach to peri-operative haemodynamic management improves patient and renal outcomes after surgery

Monitoring

  • AAGBI as standard
  • Consider arterial line for those in whom closer haemodynamic monitoring is require with respect to AKI
  • Monitor urine output; intra-operative oliguria is associated with (but doesn't necessarily predict) post-operative AKI (BJA, 2021)

Fluid therapy

  • Patients with high risk of AKI or undergoing high-risk surgery should undergo goal-directed perioperative fluid management strategies
  • This may include:
    • Cardiac output monitoring
    • Organ perfusion monitoring e.g. arterial lactate
    • Strict fluid balance monitoring
    • Cautious fluid therapy

  • Fluid overload is associated with worsening AKI and worsening morbidity/mortality
  • The timing of fluid administration may be of importance too, with earlier resuscitation reducing renal inflammation and improving microvascular perfusion
  • Balanced crystalloids > 0.9% NaCl > HES

Blood pressure management

  • Maintenance of adequate MAP is important in preserving renal function, by:
    • Maintaining trans-glomerular pressure gradient for ultrafiltration
    • Preserving renal perfusion pressure
  • Peri-operative hypotension is associated with post-operative AKI
    • Both the degree and duration of hypotension is associated with AKI
    • There is little evidence of absolute MAP values below which AKI will occur
    • Intra-operative hypotension with a MAP <55mmHg was significantly associated with persistent AKI in one study (BJA, 2022)

  • Hypotension associated with systemic vasodilation should be treated with vasopressors, rather than fluids
    • The latter may prolong renal hypotension and cause fluid overload
    • The positive effect vasopressors provide by ↑ renal perfusion pressure outweighs the negative effect caused by ↑ renal vascular resistance
    • However, excessive use of vasopressors without a degree (≥10ml/kg) of fluid resuscitation may also increase risk of post-operative AKI (BJA, 2022)
  • The use of dopamine has not been shown to prevent onset, or halt progression, of AKI in clinical settings
  • Conversely, levosimendan in cardiac surgery is associated with reduced mortality and need for RRT

  • MAP management requires consideration of the normal MAP for the individual
    • Chronically hypertensive or elderly patients may require a higher MAP
    • MAP of 75mmHg has been shown to increase renal oxygen delivery and GFR following cardiac surgery

Drugs

  • Although diuretics may improved urine output, they do not reduce the onset of AKI or alter GFR
    • Excessive use risks hypovolaemia and additional renal injury
    • Diuretics should be used to control fluid balance only
    • Equally, there is insufficient evidence to support the use of recombinant BNP (nesiritide) or theophylline in prevention or treatment of AKI
  • Other drugs which are associated with a degree of reno-protection include (BJA, 2021):
    • Atrial natriuretic peptides
    • Alpha-2-adrenoreceptor agonists e.g. clonidine, dexmedetomidine (poor quality evidence)
    • Calcium channel blockers (poor quality evidence)

  • Caution using drugs with active metabolites relying on renal excretion e.g.:
    • Rocuronium
    • Morphine

  • Consider avoiding drugs associated with worsening renal injury
    • NSAIDs
    • Aminoglycoside antibiotics

  • Ongoing suitable MAP target
  • Monitor urine output
  • Fluid balance monitoring
  • Check U&Es
  • Multi-modal anti-emetic and analgesic approach to encourage early return to oral intake
  • If nephrotoxic drugs are to be used/continued:
    • Ensure a limited course is prescribed e.g. 3 days' NSAIDs then stop
    • Ensure appropriate monitoring e.g. gentamicin levels prior to further dosing