Acute renal failure

Sudden reduction in renal function resulting in the accumulation of nitrogenous wastes.

Principles of renal failure in surgical patient:

• The kidneys cannot function without adequate perfusion
• Renal perfusion is dependent on adequate blood pressure
• A surgical patient with poor urine output usually requires more fluid
• Absolute anuria is usually due to urinary tract obstruction
• Poor urine output in a surgical patient is not initially treated with diuretics

Aetiology

• Pre-renal (75%) - can lead to ATN in hours. The kidney is structurally and functionally intact, but blood flow and GFR are reduced.
  • Sepsis
  • Hypovolaemia
  • Low cardiac output
• Renal (20%) - involves parenchymal damage
  • Acute tubular necrosis - commonest
  • Renal ischaemia - hypoxia, hypo-perfusion
  • Medications
    • Nsaids, ACE inhibitors
    • Note trimethoprim can cause a 30% rise in creatinine, without necessarily reflecting kidney injury, due to competitive inhibition of creatinine metabolism
  • Iodinated contrast media
    • Can occur within 48 hours of administration
    • Pre-hydration
    • ?NAC
    • Systematic reviews now saying this may not really exist
  • Interstitial nephritis
  • Hepatorenal syndrome
  • Abdominal compartment syndrome
• Post-renal (5%) - obstruction and back-pressure
  • Bilateral ureteric obstruction
  • Bladder outlet obstruction

Pathophysiology:

• GFR can be estimated from serum creatinine, BMI and gender
• Pre-renal injuries:
  • Systemic hypoperfusion leads to increased sympathetic neural tone and release of renin and ADH
  • Leads to arteriolar vasoconstriction primarily in the renal, splanchnic and musculocutaneous circulations to preserve blood flow to the heart and brain
  • Renal vasoconstriction leads to reduced blood flow and GFR
• Acute tubular necrosis
  • Occurs in the setting of prolonged or severe ischaemia
  • Renal tubular cells are more vulnerable than the cortex due to their position deep in the medulla
  • May lead to necrosis, with denuding of the epithelium and occlusion of the tubular lumen by casts and cell debris
• Urine output
  • Normal urine output is 0.5-2mL/kg/hr
  • Oliguria is <0.5mL/kg/hr
  • Anuria is <100mL/day (approx 0.1mL/kg/hr)

Diagnosis and classification:

• Oliguric (<400mL/ day or <17mL/hr)
• Non-oliguric (>2L/day)
• After you have excluded post-renal causes, and undertaken adequate fluid resuscitation, you can diagnose and classify as AKI based on:
  • 'Acute Kidney Injury Network' classification is most useful according to CCrISP - one of:

• Three stages of AKI:

Approach to workup/investigation:

• Sudden onset post-op complete anuria is post-renal UNTIL PROVEN OTHERWISE
  • Catheter kinks
  • Surgical damage to urinary tract
  • Probably needs an USS straight away if nothing obvious found
• Initial investigations:
  • Dipstick/MCS/osmolarity
    • Marked proteinuria or microscopic haematuria with casts suggests a primary renal insult
    • Casts
      • ATN: pigmented coarse granular casts and renal tubular epithelial cells
      • Glomerulonephritis: proteinuria, haematuria, red cell casts
      • Pyelonephritis: White and red cell casts
  • USS
    • As above - mandatory in anuric patient
    • The acutely injured kidney will be echo bright due to oedema, but normal size
    • CKD likely shows a small (<9cm) kidney with echo-bright parenchyma
  • Bloods to consider
    • FBE/UEC/CMP
    • LFT (hepatorenal)
    • CK (rhabdomyolysis - dark brown urine that tests positive for myoglobin)
    • CRP
    • VBG/ABG (for lactate and overall physiology)

• Establish aetiology:
  • Is it pre-renal? And do we need to restore volume?
  • Differentiating prerenal from renal
    • Prerenal will be a/w dehydration - consider whether large losses are occurring elsewhere
    • BUN > 20
    • Brown urine? Myoglobinuria?
    • In ATN, expect low osmolar urine with high sodium and low urea/creatinine, because the concentrating ability is impaired. In pre-renal AKI, the concentrating ability is retained, so you tend to get high osmolarity and high urea/creatinine. See full table below.
  • If prerenal - is it hypovolaemia or heart failure?
    • If hypovolaemic - give fluids
    • If heart failure - give diuretics
• Management:
  • IDC?
  • Avoid nephrotoxics - aminoglycosides, NSAIDs, ACE inhibitors, opioids, beta blockers
  • Alter dose of renally excreted meds
  • Careful fluid balance - restore perfusion as much as possible by first restoring euvolaemia, then an accurate maintenance fluid rate
  • Check electrolytes - essentially check indications for dialysis
  • Check for complications below
  • Maintain sats >94%

Complications

• Hyperkalaemia
  • See separate topic
• Pulmonary oedema
  • Sit patient upright
  • Stop all infusions
  • High flow oxygen
  • Monitor saturations
  • ?IV diamorphone 2.5 mg
  • ?IV GTN infusion if SBP > 100
  • ?IV frusemide
  • ?ICU
• Indications for dialysis:
  • Absolute:
    • Refractory hyperkalaemia (>6mmol/L)
    • Refractory pulmonary oedema and fluid overload
    • Uraemic encephalopathy
  • Relative:
    • Acidosis (pH < 7.2)
    • Uraemia
      • Threshold relates to the rapidity of rise as well as the absolute urea level and presence of symptoms
      • Rise above 35mmol/L unresponsive to other therapies is usually an absolute indication
    • Pericarditis
    • Toxin removal