Acute Kidney Injury/AKI (1*)

Question 1

What is it?

What are its risk factors?

How is it classified?

What are the 4 main dangers of it?

Answer 1

➊ Acute and sustained reduction in renal function, resulting in oliguria and a rise in serum urea and creatinine

N.B. The normal Urea:Creatinine ratio is 1:10.

➋ * 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. There’s a false drop in eGFR because of this (eGFR is calculated based on creatinine).

➌ * 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

➍ * Hyperkalaemia
* PH - Metabolic acidosis/alkalosis
* Uraemia - encephalopathy, pericarditis
* Fluid balance - HF, Pulmonary oedema

Question 2

What are the Pre-renal causes (55%)?

What are the Renal causes (35%)?

What are the Post-renal causes (20%)?

Answer 2

➊ Inadequate blood supply to the kidneys - 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

➋ Intrinsic kidney disease, leading to reduced filtration - Can be due to:
* Glomerulonephritis
* Interstitial nephritis
* Acute tubular necrosis

N.B. 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.

➌ Obstruction to urine outflow, leading to back-pressure into kidney and reduced kidney function - Can be due to:
* Luminal - Kidney stones, stricture
* Mural - Malignancy
* Extra-mural - BPH, prostate ca.

Question 3

What are the investigations to do?

Answer 3

• Bloods - FBC, U&E, LFT, Glucose, clotting, Ca, ESR
• Urinalysis - Nitrates, leukocytes, protein, blood
• ECG - hyperkalaemia
• CXR - pulmonary oedema
• US KUB - obstruction, hydronephrosis
• Glomerulonephritis screen

Question 4

How is it managed?

What are the common drugs that need to be stopped during an AKI?

What is the sign to look out for when treating an AKI?

Answer 4

➊ * A-E
* Correct the underlying cause:
‣ Pre-renal - IVF 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

➋* “Stop the DAMN drugs”:*
* Diuretics and Digoxin
* ACEi/ARB
* Metformin and Methotrexate
* NSAIDs

➌ **Polyuria! **- This is a good sign as it shows that the AKI is resolving

Question 5

What are the indications that a patient will need dialysis or haemofiltration?

Answer 5

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)