AKI

Question 1

Define AKI.

Answer 1

• Rise in serum creatinine of 26+ µmol/L in 48h
• A 50% greater rise in serum creatinine in the preceding 7 days
• Drop in urine output to 0.5 ml/kg/hour for 6 hours in adult or 8h in children + young people

Question 2

List the prerenal causes of AKI.

Answer 2

1. Absolute fluid loss:
   - burns
   - dehydration
   - long-term vomiting
   - diarrhoea
   - haemorrhage
2. Relative fluid loss:
   - congestive heart failure
   - distributive shock
3. Renal artery stenosis/embolus
4. Liver failure

Question 3

Describe the pathology of prerenal AKI.

Answer 3

• kidney hypoperfusion → increased nitrogenous compounds in blood
• decreased blood flow to kidney → reduced GFR, accumulation of waste products in blood = high nitrogen in blood [azotemia]
• reduced GFR → RAAS activation → aldosterone secretion → Na+ and water retention → urea follows Na+ → increased serum urea:creatinine (>20:1)

Question 4

List the renal causes of AKI.

Answer 4

1. Glomerular injury:
   - glomerulonephritis (post-strep glomerulonephritis, Goodpasture’s syndrome, GPA, IgA nephropathy)
2. Tubular injury:
   - acute tubular necrosis
3. Interstitial injury:
   - acute interstitial nephritis
   - bilateral pyelonephritis
4. Glomerular endotheliopathy
   - thrombotic microangiopathy
   - hyaline arteriosclerosis
   - scleroderma

Question 5

How can glomerulonephritis cause AKI?

Answer 5

• inflammation of glomeruli
• deposition of immune complexes of glomerular basement membrane
• activation of complement system
• chemoattraction of macrophages, neutrophils
• mediator release
• inflammation, podocyte damage
• protein + blood cell leakage
• reduces pressure gradient between arterioles + tubules
• reduced GFR + oliguria

Question 6

What is the most common cause of AKI?

Answer 6

Acute tubular necrosis

Question 7

List the postrenal causes of AKI.

Answer 7

1. Compression:
   - ureters (e.g. intra-abdo tumour)
   - urethra (e.g. BPH)
2. Obstruction:
   - ureters
   - urethra
   - kidney stones
3. Congenital abnormalities:
   - vesicoureteral reflux

Question 8

Describe the pathology of postrenal AKI.

Answer 8

• due to obstructed urine outflow distally → increases nitrogenous compounds in blood
• obstruction of urine outflow → reversal of Starling’s forces → pressure backs up into kidneys → reduced pressure gradient between arterioles → reduced GFR

Question 9

What are the potential complications of an AKI?

Answer 9

1. Hyperphosphataemia (late complication)
2. Uraemia (uraemia toxins accumulate with severe and untreated kidney failure, resulting in lethargy + confusion)
3. Hyperkalaemia (results from impaired excretion of K+, cell lysis, or tissue breakdown → affects the heart)
4. CKD
5. ESRD (particularly common in those with underlying kidney disease or comorbidities)

Question 10

How is AKI diagnosed?

Answer 10

1. fractional excretion of sodium >3%

2. Presence of muddy brown casts on urinalysis

Question 11

How is AKI diagnosed?

Answer 11

1. Baseline bloods:
   - U&Es (inc creatinine)
   - VBG (bicarbonate level + assess acidosis)
2. Also request:
   - LFTs
   - CRP
   - FBC (?Leukocytosis; ?Thrombocytopenia)
   - Blood cultures
   - Serum creatinine (if rhabdomyolysis is suspected)
   - ECG
3. Urinalysis:
   - testing for specific gravity, blood, protein, leukocytes and glucose
   - (consider intrinsic/renal AKI if +ve for blood + protein in the absence of an obvious cause → UTI/trauma)
4. Urine electrolytes:
   - fractional excretion of sodium or urea (not really done, but FEUr is more useful fi pt has received diuretics)
   - urine sodium concentration
   - urine osmolality is rarely requested

Question 12

What results would you expect for each of the types of AKI in the following tests:

(a) Serum Ur:Cr
(b) UNa+
(c) FENa+
(d) Uosm

Answer 12

Prerenal:

(a) >20:1
(b) <20 mEq/L
(c) <1%
(d) >500 mOsm/kg

Renal:

(a) <15:1
(b) >40 mEq/L
(c) <2%
(d) >350 mOsm/kg

Postrenal:

(a) <20:1
(b) <20 mEq/L
(c) >1%
(d) >500 mOsm/kg

Question 13

How should AKI be managed?

Answer 13

1. Immediate management is supportive
   - priority us usually to treat hypovolaemia and correct electrolyte imbalances
2. Use simple care bundle STOP AKI:
   (i) Sepsis:
   - perform an urgent septic screen
   - Sepsis 6 within 1 hour if infection suspected
   (ii) Toxins:
   - nephrotoxic drugs (NSAIDs, aminoglycoside abx, iodinated contrast agents)
   - nephrotoxins
   (iii) Optimise volume status + BP:
   - hypovolaemic → immediate IV bolus of crystalloid (balanced crystalloid unless hyperK+ is confirmed)
   - withhold drugs that may exacerbate AKI (ACE-I, ARBs)
   - escalate to critical care for consideration of vasopressors if the patients remains severely hypotensive
   (iv) Prevent harm:
   - identify reversible causes (e.g. relief of urinary tract obstruction)
   - treat life-threatening complications (e.g. hyperkalaemia and acidosis)
   - review and modify doses of all medications

Question 14

When should a patient be referred fro emergency renal replacement therapy?

Answer 14

1. refractory hyperkalaemia (>6.5 mmol/L)
2. refractory metabolic acidosis (pH <7.15)
3. refractory volume overload ± pulmonary overload
4. end-organ complications of uraemia:
   - pericarditis
   - encephalopathy
   - uraemia bleeding
5. Severe AKI poisoning/drug overdose (e.g. ethylene glycol, lithium)

Question 15

How should the complications of AKI be managed?

Answer 15

1. Hyperkalaemia:
   - cardiac protection with IV calcium chloride or calcium gluconate
   - adjunct IV insulin and nebuliser salbutamol
   - calcium polystyrene sulfonate
   - withhold ACE-I, ARB, K+-sparing diuretics
   - RRT
2. Acidosis:
   - IV sodium bicarbonate
   - RRT
3. Pulmonary oedema:
   - sit patient upright
   - give high-flow O2 and IV glyceryl trinitrate
   - seek senior support
   - loop diuretic (one with specialist supervision)
4. Uraemia:
   - dialysis