Acute kidney injury

Question 1

What is an acute kidney injury defined by?

Answer 1

¥ An abrupt (<48hrs) reduction in kidney function defined as
Ð an absolute increase in serum creatinine by >26.4µmol/l
Ð OR increase in creatinine by >50%
Ð OR a reduction in UO

Can only be applied following adequate fluid resuscitation & exclusion of obstruction

Question 2

How is AKI staged?

Answer 2

KDIGO classification (can be classified using Creatinine or urine output):

Stage 1:
Serum Cr - increase in >25nanomol/L OR an increase of X 1.5-1.9 or more reference Cr

Urine output - <0.5ml/kg/hr for >6 consecutive hours

Stage 2:
Serum Cr - increase of 2-2.9 or more X reference Cr

UO: < 0.5ml/kg/hour for >12hrs

Stage 3:
Serum Cr - increase in 3 or more time reference Cr OR increase to 354 nanmol/L or more OR need for RRT

UO: <0.3ml/kg/hr for >24hrs or 12hrs for anuria

Question 3

What are the symptoms of AKI?

Answer 3

Ð	Constitutional symptoms
¥	Anorexia, weight loss, fatigue, lethargy
Ð	Nausea & Vomiting
Ð	Itch (uraemia)
Ð	Fluid overload
¥	Oedema, SOB

Question 4

What are the signs of AKI?

Answer 4

Ð Fluid overload incl HTN, Oedema, Pul oedema, effusions (pleural & pulmonary)
Ð Uraemia incl itch, pericarditis
Oliguria

Question 5

What is a way to classify causes of AKI into 3 main groups?

Answer 5

⇒ Pre- renal (functional)
⇒ Renal (intrinsic structural)
⇒ Post-renal (obstruction)

Question 6

what are 3 different causes for pre-renal AKI?

Answer 6

Reversable volume depletion leading to oliguria and inc. in creatinine

Hypovolaemia
¥ Haemorrhage
¥ Volume depletion (e.g. D&V, burns)

Hypotension
¥ Cardiogenic shock
¥ Distributive shock (e.g. sepsis, anaphylaxis)

Renal Hypoperfusion
¥ NSAIDs / COX-2
¥ ACEi / ARBs
¥ Hepatorenal syndrome

Question 7

What is the management of pre-renal AKI?

Answer 7

¥ Assess for hydration
¥ Clinical observations (BP, HR, UO)
¥ JVP, Capillary Refill Time, Oedema
¥ Pulmonary oedema

¥ Fluid Challenge for hypovolaemia
¥ Crystalloid (0.9% NaCl) or Colloid (Gelofusin)
¥ Do NOT use 5% dextrose
¥ Give bolus of fluid then reassess and repeat as necessary
¥ If >1000mls IN and no improvement, seek help

Question 8

Renal AKI: 4 main causes?

Answer 8

Vascular
Ð Vasculitis ( assoc. with ANCA – e.g. Wegener’s)
Ð renovascular disease

Glomerular
Ð Glomerulonephritis
Ð Anti-GBM disease = goodpastures disease

Interstitial Nephritis
Ð Drugs
Ð Infection (TB)
Ð Systemic (sarcoid)

Acute tubular necrosis
Ð	Ischaemia—prolonged renal hypoperfusion
Ð	Drugs (gentamicin)
Ð	Contrast
Ð	Rhabdomyolysis

Question 9

Which is the most common form of AKI in hospital?

Answer 9

Acute tubular necrosis:
¥ Due to a combination of factors leading to decreased renal perfusion
¥ Common causes include sepsis and severe dehydration
¥ Other important causes include rhabdomyolysis and drug toxicity

Question 10

What are the initial investigations in AKI?

Answer 10

U&Es
Ð Marker of renal function (Na, K, Ur, Cr)
Ð Look at the potassium, is it high?

FBC & Coagulation Screen
Ð Low plts ?HUS ?TTP
Ð Abnormal clotting ?DIC ?Septic
Ð Anaemia ?CKD ?Myeloma

Urinalysis
Ð Haematoproteinuria suggesting active GN

USS
Ð ?Obstruction ?Size (if kidney is small suggests chronic disease)

Immunology
Ð ANA (SLE), ANCA (Vasculitis), GBM (Goodpastures)

Protein electrophoresis & BJP
Ð ?myeloma (everyone over 50yrs)

Question 11

Why is a renal biopsy performed? when would this be indicated urgently? when would this be indicated semi-urgently? What is important to assess before doing this?

Answer 11

Urgent indications
Ð Suspected rapidly progressive GN
Ð Positive Immunology & AKI

Semi-urgent indications
Ð Unexplained AKI to gain a diagnosis
Ð Rule out obstruction, Volume depletion & ATN

Ensure it is safe
Ð Normal clotting, NO warfarin, aspririn etc
Ð Normotensive
Ð No hydronephrosis

Question 12

What is the management of AKI?

Answer 12

Establish good perfusion pressure
Ð Fluid resuscitate
Ð Once fluid resuscitated, if still not achieving an adequate BP inotropes/vasopressors

Treat underlying cause
Ð Antibiotics if sepsis

Stop nephrotoxics

Dialysis if remains anuric & uraemia
Ð Can require urgent dialysis

Question 13

What are the 5 life threatening complications of AKI?

Answer 13

¥	Hyperkalaemia 
¥	Fluid Overload (Pulmonary oedema)
¥	Severe Acidosis (pH < 7.15)
¥	Uraemic pericardial effusion
¥	Severe Uraemia (Ur >40)

Question 14

Post-renal AKI:
causes
treatment

Answer 14

This is AKI due to obstruction of urine flow leading to back pressure (hydronephrosis) and thus loss of concentrating ability

⇒ Causes: stones/strictures/cancers/extrinsic pressure

⇒ Treatment: relieve obstruction (catheter/nephrostomy)
⇒ Refer to urology if ureteric stenting required

Question 15

Hyperkalaemia:
what is the normal range
what is hyperkalaemia

Answer 15

¥ Normal K = 3.5-5.0
¥ Hyperkalaemia = >5.5
¥ Life threatening hyperkalaemia = >6.5

Question 16

What is included in the assessment of hyperkalaemia?

Answer 16

Ð ECG (assoc. with arrythmias)

Ð Muscle weakness (tingling)

Question 17

What ECG changes are seen in hyperkalaemia?

Answer 17

6-7: peaked T waves
7-8: flattened p wave, prolonged PR, depressed ST, peaked T wave
8-9: atrial standstill, long QRS
>9: sine-wave pattern

Question 18

What is the medical treatment of hyperkalaemia?

Answer 18

Cardiac Monitor & IV access

Protect myocardium
Ð 10mls 10% calcium gluconate (2-3mins)

Move K+ back into the cells
Ð Insulin (actrapid 10units) with 50mls 50% dextrose (30 mins)
Ð Salbutamol Nebs (90 mins)

Prevent absorption from GI tract
Ð Calcium resonium (NOT in the acute setting)

Question 19

What are the urgent indications for haemodialysis in AKI?

Answer 19

Hyperkalaemia
Ð	>7
Ð	>6.5 unresponsive to medical therapy
Ð	Severe Acidosis
Ð	pH < 7.15

Fluid overload

Urea >40

pericardial rub/effusion