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Acute Kidney Injury (AKI)

An Acute Kidney Injury (AKI) is an acute and sustained reduction in renal function, resulting in oliguria and a rise in serum urea and creatinine.


Risk factors:

  • CKD

  • HF

  • Diabetes

  • Elderly

  • Nephrotoxicity

  • Contrast administration


N.B. Trimethoprim can cause an isolated rise in creatinine. It competitively inhibits creatinine secretion from the renal tubules, and causing a false drop in eGFR because of this (eGFR is calculated based on creatinine).


Classification

  • Stage 1 - Creatinine rise of 1.5x or urine output < 0.5 ml/kg/hour for 6 hrs

  • Stage 2 - Creatinine rise of 2x or urine output < 0.5 ml/kg/hour for 12 hrs

  • Stage 3 - Creatinine rise of 3x/>354μmol/L or urine output < 0.3 ml/kg/hour for 24 hrs


Causes

  • Pre-renal (55%) - Due to inadequate blood supply to the kidneys. This can be due to:

    • Hypovolaemia - Dehydration, Haemorrhage, Burns

    • Reduced CO - Cardiogenic shock, MI

    • Renal vasoconstriction - Renal artery stenosis, NSAIDs, ACEi/ARB

    • Systemic vasodilation - Sepsis, Drugs

  • Renal (35%) - Due to Intrinsic kidney disease, leading to reduced filtration This can be due to:

    • Glomerulonephritis

    • Interstitial nephritis

    • Acute tubular necrosis

      • Rhabdomyolysis leads to the release of myoglobin, CK, and potassium into the blood. Myoglobin is nephrotoxic, and the accummulation of it in the glomerulus leads to acute tubular necrosis. Myoblobinuria also gives a false +ve result for blood on urine dip.

  • Post-renal (20%) - Obstruction to urine outflow, leading to back-pressure into kidney and reduced kidney function. This can be due to:

    • Luminal - Kidney stones, stricture

    • Mural - Malignancy

    • Extra-mural - BPH, prostate ca.


Investigations

  • Bloods - FBC, U&E, LFT, Glucose, clotting, Ca, ESR

  • Urinalysis - Nitrates, leukocytes, blood, protein

  • ECG - hyperkalaemia

  • CXR - pulmonary oedema

  • US KUB - obstruction, hydronephrosis

  • Glomerulonephritis screen


Management

  • A-E approach

  • Correct the underlying cause:

    • Pre-renal - IV Fluids if hypovolaemic, Abx if septic, Stop nephrotoxic drugs (e.g. NSAIDS, ACEi/ARB)

    • Renal - Nephrology review to identify the less common causes

    • Post-renal - Catheterisation and urology review


The common drugs to stop during an AKI can be remembered by the acronym, "Stop the DAMN drugs":

  • Diuretics and Digoxin

  • ACEi/ARB

  • Metformin and Methotrexate

  • NSAIDs


When treating an AKI, look out for Polyuria! as it's a good sign and indicates that the AKI is resolving.


Indications for Acute Dialysis or Haemofiltration - AEIOU:

  • Acidosis (severe metabolic acidosis with pH of < 7.20)

  • Electrolyte imbalance (resistant hyperkalaemia)

  • Intoxication (drug overdose, poisoning)

  • Oedema (refractory pulmonary oedema)

  • Uraemia (encephalopathy or pericarditis)



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