Acute Kidney Injury

Question 1

What is the diagnostic criteria for AKI?

Answer 1

A sudden, marked but usually reversible change in kidney function

Based on accumulation of serum creatinine or reduced urine output.

AKI 1: Urine 6 hours
OR
Increase in creatinine by 25umol/L or increase in creatinine by 1.5x

Question 2

What is the most common cause of AKI?

Answer 2

Acute tubular necrosis

Question 3

What is acute tubular necrosis?

Answer 3

Acute necrosis of the renal tubule as the result of an event, usually ischamic (ie prlonged pre renal AKI) or toxic.

Question 4

How much fluid is in the interstitium?

Answer 4

9L

Question 5

How much fluid is IV?

Answer 5

3L (+2 l RED CELLS= 5l TOTAL)

Question 6

Which step of vitamin D activation does the kidney do?

Answer 6

Activation of 25-OH cholecalciferol to 1,25 OH cholecalciferol

Question 7

What are the 3 most easily measured and recognisable indicators of loss of kidney function?

Answer 7

• Change in Na/ H2O balance (variable)
• Accumulation of solutes (creatinine)
• Accumulation of acid

Question 8

What causes pre-renal AKI?

Answer 8

Not enough blood flow to the kidneys–> hypotension/ hypovolemia (any cause of shock) or occlusive vascular ischaemia eg aortic dissection.

Renin-angiotensin-aldosterone system activation.
Urinary concentration capacity is intact.

Question 9

What causes intra- renal AKI (5)?

Answer 9

Direct damage to kidneys:

1. Tubular injury: ischamia/ prolonged hypoperfusion (ATN),
2. Nephrotoxin: aminoglycosides, radiocontrast, IgG from multiple myeloma
3. Interstitial nephritis: drugs (eg omeprazole), infection, sarcoidosis, eosinophilic infiltration
4. Glomeruli: Rapidly progressive GN (eg Goodpasture’s, Wegener’s), thrombosis
5. Vascular disease: vasculitis, occlusion (thrombosis/ embolism)

Question 10

What causes post-renal AKI? In what circumstances does post-renal AKI occur?

Answer 10

Obstruction: prostate, calculi, bladder stones/ injury, ureteric strictures.

Both ureters must be involved (blocked) OR one of the kidneys must have a pre-existing abnormality.

Question 11

What is the triad of drugs which will augment renal impairment (‘triple whammy’), and why?

Answer 11

Ace inhibitor: Angiotensin II usually constricts the efferent arteriole, increasing glomerular filtration pressure

Loop diuretic: decrease plasma volume–> decreased renal plasma flow

NSAID: prostaglandins dilate the afferent arteriole, increasing glomerular blood flow.

Question 12

What causes most community acquired AKI?

Answer 12

Mostly pre-renal causes +/- existing CKD

Question 13

Is oliguria variable in ATN?

Answer 13

YES: can have ATN and still be producing lots of urine- interstitial nephritis caused by aminoglycosides, have decreased renal function even though urine output is maintained.

Question 14

What is the pathophys of ATN?

Answer 14

Initial hypoperfusion–> reperfusion to a vascular network where there has been microvessel thromobisis and occlusion, resulting in further inflammation and injury.

–> Obstructive casts, back leak of tubular fluid.
Most often reversible following regeration of the tubular endothelial cells.

Question 15

How do you assess whether the renal impairment is acute or chronic?

Answer 15

• Compare current investigations with previous ones
• Oliguria suggests acute renal failure
• Pre-existing illness/ RFs: DM, HTN, age, vascular disease
• Small echogenic kidneys on US= chronic
• How well is the patient tolerating their uremia? Acute: feel malaise, fatigue, N+V, itch etch, chronic may not.

Question 16

What are 3 key clinical features of obstruction causing AKI?

Answer 16

1. complete anuria
2. palpable bladder
3. Bilateral hydronephrosis

Question 17

Which haematological malignancy can cause AKI?

Answer 17

Multiple myeloma

• urine Bence-Jones proteins
• plasma electrophoresis looking for M protein

Question 18

Comparing Pre-renal AKI and ATN:
Urine osmolarity
Urine Na
Fraction excretion of Na (%)
Fraction excretion of Urea (%)

Answer 18

Urine osmolarity: AKI normal (500-800 mOsm/kg), ATN LOW (40mmol/DL)

Fraction excretion of Na (%): higher in ATN

Fraction excretion of Urea (%): Higher in ATN

Question 19

What are the principles of treatment of AKI?

Answer 19

Loop diuretics (for volume overload- symptomatic relief only, will not hasten recovery)
Renal replacement therapy (ie dialysis)
Treat the underlying condition if possible

Question 20

How is anuric renal failure defined and what causes it?

Answer 20

Urinary tract obstruction, renal artery obstruction, rapidly progressive glomerulonephritis, bilateral diffuse renal cortical necrosis

Question 21

What is associated with poorer outcomes: fluid overload or fluid depletion?

Answer 21

Fluid overload is associated with poorer outcomes.

Question 22

What are the acute metabolic complications of AKI?

Answer 22

1. Na and H2O overload–> diuretics
2. Hyperkalemia–> restrict intake, IV glucose and insulin, calcium gluconate and dialysis
3. Metabolic acidosis: dialysis or NaCO3 is HCO3 is

Question 23

What are the 2 fuctions of dialysis in AKI?

Answer 23

Fluid balance

Solute removal

Question 24

How do fluids and solutes move in haemodialysis?

Answer 24

Solutes: osmosis
Fluids: ultrafiltration