Acute Kidney Injury AKI

Question 1

What is Acute Kidney Injury (AKI)?

Answer 1

AKI is a rapid deterioration in kidney function, commonly occurring in hospitalised patients.

Question 2

What are the common symptoms of AKI?

Answer 2

AKI is often asymptomatic or presents with non-specific symptoms such as fatigue, nausea, and confusion.

Question 3

What are the primary classifications of AKI aetiology?

Answer 3

AKI aetiology is classified into pre-renal (reduced perfusion), intra-renal (structural/functional nephron changes), and post-renal (obstructive pathology) causes.

Question 4

What are pre-renal causes of AKI?

Answer 4

Pre-renal causes include reduced kidney perfusion due to factors like hypovolaemia, heart failure, renal artery stenosis, NSAIDs, and ACE inhibitors.

Question 5

What are intra-renal causes of AKI?

Answer 5

Intra-renal causes involve structural or functional changes in the nephron, such as acute tubular necrosis, acute interstitial nephritis, glomerular disease, and intra-tubular obstruction.

Question 6

What are post-renal causes of AKI?

Answer 6

Post-renal causes are due to obstructive pathologies like nephrolithiasis, bladder or prostate cancer, urethral stricture, and external compression.

Question 7

What are the risk factors for developing AKI?

Answer 7

Risk factors include chronic kidney disease, heart failure, liver disease, diabetes, previous AKI, oliguria, cognitive impairment, hypovolaemia, nephrotoxic drugs, iodine-based contrast media, urological obstruction, sepsis, and age over 65.

Question 8

What clinical findings might suggest AKI?

Answer 8

Clinical findings can include oliguria or anuria, signs of hypovolaemia (dry mucous membranes, tachycardia, hypotension), signs of volume overload (hypertension, pulmonary or peripheral oedema), signs of uraemia (ecchymosis, asterixis, confusion), and signs of post-renal obstruction (distended bladder).

Question 9

What laboratory investigations are important in AKI?

Answer 9

Important laboratory investigations include urea and electrolytes, full blood count (FBC), liver function tests (LFTs), and venous blood gas (VBG) analysis.

Question 10

What urine studies are useful in AKI assessment?

Answer 10

Useful urine studies include urinalysis, measurement of urine volume, microscopy, osmolarity, and specific gravity.

Question 11

What imaging modalities are used in AKI evaluation?

Answer 11

Imaging modalities include bladder scanning, renal ultrasound, and computed tomography (CT) scans (non-contrast, urogram, or triphasic kidneys).

Question 12

What criteria are used to diagnose AKI?

Answer 12

The KDIGO criteria are used, which include urine output less than 0.5 ml/kg/hr for 6 hours, an increase in creatinine to 1.5 times the baseline over 7 days, or an increase in creatinine by 26.5 µmol/L (0.3 mg/dL) in 48 hours.

Question 13

What general management steps are taken in AKI?

Answer 13

General management includes withdrawing nephrotoxic drugs, adjusting doses of renally cleared medications, fluid resuscitation, catheterisation, and managing sepsis using the sepsis six care bundle.

Question 14

What targeted treatments are available for AKI?

Answer 14

Targeted treatments may involve diuretics for fluid overload, immunosuppression for acute interstitial nephritis or rapidly progressive glomerulonephritis, and urinary catheterisation or stenting for obstruction.

Question 15

When is renal replacement therapy (RRT) indicated in AKI?

Answer 15

RRT is indicated for severe cases of AKI presenting with acidosis, electrolyte abnormalities, toxin accumulation, fluid overload, or uraemia.

Question 16

What are potential complications of AKI?

Answer 16

Complications can include fluid overload, electrolyte derangement, metabolic acidosis, uraemia, progression to chronic kidney disease (CKD), end-stage renal disease (ESRD), and death.

Question 17

How is AKI differentiated from chronic kidney disease (CKD)?

Answer 17

AKI is characterised by a rapid decline in kidney function, whereas CKD involves a gradual loss of function over months to years.

Question 18

What role do NSAIDs play in AKI?

Answer 18

NSAIDs can cause pre-renal AKI by reducing kidney perfusion through inhibition of prostaglandin synthesis, leading to afferent arteriole constriction.

Question 19

How does hypovolaemia contribute to AKI?

Answer 19

Hypovolaemia leads to decreased renal perfusion, resulting in reduced glomerular filtration rate (GFR) and potential pre-renal AKI.

Question 20

What is the significance of oliguria in AKI?

Answer 20

Oliguria, defined as low urine output, is a common clinical finding in AKI and indicates impaired kidney function.

Question 21

How can sepsis lead to AKI?

Answer 21

Sepsis can cause AKI through systemic inflammation, leading to decreased renal perfusion, endothelial injury, and direct tubular damage.

Question 22

What is acute tubular necrosis (ATN)?

Answer 22

ATN is a common cause of intra-renal AKI, involving damage to renal tubular cells due to prolonged ischaemia or nephrotoxic agents.

Question 23

What is the role of diuretics in AKI management?

Answer 23

Diuretics may be used cautiously in AKI to manage fluid overload but are not a primary treatment for the condition.

Question 24

How is post-renal AKI treated?

Answer 24

Post-renal AKI is treated by relieving the obstruction, which may involve catheterisation, stenting, or surgical intervention.

Question 25

What is the prognosis for patients with AKI?

Answer 25

The prognosis depends on the underlying cause, severity, and timely intervention, with some patients recovering fully and others progressing to chronic kidney disease.