Acute Kidney Injury (AKI)

Question 1

How common is it?

Answer 1

15% of adults admitted to hospital in developed countries develop AKI.

Question 2

What causes it?

Answer 2

• AKI is a rapid deterioration of renal function, resulting in an inability to maintain fluid, electrolyte and acid-base balance.

Pre-renal - (40-70%) - due to renal hypoperfusion. Eg. hypotension (any cause, including hypovolaemia, sepsis), renal artery stenosis +/- ACE-i.

Intrinsic - (10-50%) may require renal biopsy for diagnosis.

Post-renal - (10-25%) caused by urinary tract obstruction.

• Luminal - stones, clots, sloughed papillae.
• Mural - malignancy (eg. ureteric, bladder, prostate), BPH, strictures.
• Extrinsic compression - malignancy (esp pelvic), retroperitoneal fibrosis.

Question 3

Name some types of intrinsic AKI?

Answer 3

Tubular - acute tubular necrosis (ATN) is commonest renal cause of AKI, often as a result of pre-renal damage or nephrotoxins such as drugs, radiological contrast and myoglobulinuria in rhabdomyolysis.

Glomerular - autoimmune such as SLE, HSP, drugs, infections, primary glomerulonephritides.

Interstitial - drugs, infiltration with e.g. lymphoma, infection, tumour lysis syndrome following chemo.

Vascular - vasculitis, malignant high BO, thrombus or cholesterol emboli from angiography, HUS/TTP, large vessel occlusion eg. Dissection or thrombosis.

Question 4

Who does it affect?

Answer 4

• Old people
• People with co-morbidities like heart disease, liver disease or diabetes.
• People with bad infections
• Children and young people can also get AKI

Question 5

What risk factors are there?

Answer 5

• Age > 75
• CKD
• Cardiac Failure
• Chronic liver disease
• Diabetes
• Drugs (esp newly started)
• Sepsis
• Poor fluid intake/increased losses
• History of urinary symptoms

Question 6

How does it present?

Answer 6

• Rise in creatinine > 26 micromol/L in 48 hrs
• Rise in creatinine > 1.5x baseline
• Urine output 6 consecutive hours.

Question 7

How would you investigate the patient?

Answer 7

• Assess volume status - look for reduced urine volume, non-visible JVP, poor tissue turgor, raised BP, raised JVP, lung creps, peripheral oedema and gallop rhythm on cardiac auscultation.

Question 8

What treatment/s would you consider? What risks and benefits of treatment are there?

Answer 8

• Aim for euvolaemia - Avoid K+ containing fluids unless hypokalaemic.
• Stop nephrotoxic drugs - eg NSAIDS, ACE-i, gentamicin, amphotericin. Stop metformin if creatinine is >150mmol/L. Check and adjust doses of renally excreted drugs.
• Treat underlying cause
• Manage complications - hyperkalaemia, pulmonary oedema, uraemia (maybe dialysis), acidaemia (maybe dialysis, oral sodium bicarbonate.