Acute Kidney Injury

Question 1

What is the mortality rate in AKI?

Answer 1

40-60% in critically ill patients

Question 2

What factors affect the outcome of AKI?

Answer 2

Age
DM
Hypertension
Congestive cardiac failure
Pre-existing renal disease
Acute MI
Sepsis

Question 3

List some of the extra-renal effects of AKI

Answer 3

Pulmonary function
CNS function
Cardiac function

Question 4

What are the three main categories of acute kidney injury?

Answer 4

Pre-renal AKI
Intrinsic AKI
Post-renal AKI

Question 5

Describe the pathophysiology of pre-renal AKI

Answer 5

Reduced GFR as a result of haemodynamic disturbances that decrease glomerular perfusion

• absence of cellular injury
• normalisation of renal function with reversal of altered haemodynamic factors

Question 6

List four causes of pre-renal AKI?

Answer 6

Intravascular volume depletion

Decreased effective blood volume

Altered intrarenal haemodynamics

Third space sequestration (intravascular fluid loss to interstitium)

Question 7

What are the causes of third space sequestration?

Answer 7

Bowel obstruction, peritonitis, pancreatitis, ascites

• third space results, hypovolaemia occurs
• raised intra-abdo pressure comprising renal blood flow

Question 8

Why must medication not be used to treat oedema in third space sequestration?

Answer 8

Medication has negative effects

Question 9

How must third space sequestration be treated?

Answer 9

Abdominal decompression (AKI usually recovers after)

• paracentesis if massive ascites
• surgical decompression

Question 10

How should pre-renal AKI be treated?

Answer 10

Treat cause(s)
Treat complications

Question 11

What are the four main pathologies associated with intrinsic AKI?

Answer 11

Acute tubular necrosis

Acute tubulo-intersitial nephritis

Acute glomerulonephritis

Acute vascular syndrome

Question 12

What are the causes of Acute tubular necrosis?

Answer 12

Ischaemic (HTN, hypovolaemia, sepsis) = 50%

Nephrotoxic (radio-contrast, drug-induced, pigment nephropathy) = 35%

Multifactorial

Question 13

Give two examples causing pigment nephropathy?

Answer 13

Intravascular haemolysis

Rhabdomyolsis

Question 14

Profound ischaemic injury may cause what?

Answer 14

Bilateral cortical necrosis

Question 15

Describe the recovery of the kidney after acute ischaemic or toxic injury?

Answer 15

Able to restore its structure and function by de-differentiation and proliferation of remaining viable tubular epithelial cells

Question 16

What is the pathogenesis behind radio-contrast causing AKI?

Answer 16

Hypertonic agent that induces transient vasodilation followed by prolonged vasoconstriction
=> renal ischaemia => reactive oxygen species release
=> direct tubular toxicity

Question 17

What are the causes of tubulo-interstitial nephritis?

Answer 17

Drug-induced (Many ABX, NSAIDs, furosemide)

Infection-related (bacterial, viral, rickettsia disease, TB)

Question 18

What are the features of tubulo-interstitial nephritis?

Answer 18

Arthralgia, Eosinophilia, Eosinophiluria, Biopsy (cell infiltrates)

Question 19

How do you treat tubulo-intersitial nephritis?

Answer 19

Withdrawal offending agent

Steroids => excellent outcome

Question 20

What are the main causes of post-renal AKI?

Answer 20

Intrinsic (stone, papillary necrosis, clot, TCC)

Extrinsic (retroperitoneal fibrosis, AAA, malignancy)

Lower obstruction (urethral stricture, BPH, Prostate Ca,..)

Question 21

Describe the pathophysiology of post-renal AKI

Answer 21

Tubular dysfunction in obstruction

• loss of concentration capacity (polyuria)
• loss of acidification capacity (more alkaline urine)
• causes metabolic acidosis

Question 22

How should post-renal AKI be treated?

Answer 22

Treat the cause

After obstruction relief:

• Monitor post-obstructive diuresis
• Monitor for electrolyte loss with polyuria
• Treat metabolic acidosis

Question 23

List three life-threatening complications of AKI?

Answer 23

Metabolic acidosis

Hyperkalaemia

Acute Pulmonary Oedema

Question 24

What is the clinical effect of metabolic acidosis?

Answer 24

Muscle weakness
Altered mental sate
Kussmaul breathing
Hyperkalaemia
Negative inotropic effect => HTN

Question 25

How should metabolic acidosis be treated?

Answer 25

Treat cause Volume expansion IV sodium bicarbonate (only in severe MA) Dialysis

Question 26

What are the risks of treating acidosis with sodium bicarbonate?

Answer 26

``` Hypokalaemia (by shifting K+ into cell) Symptomatic hypocalcaemia (by decreasing Ca2+) ```

Question 27

What is the pathophysiology with hyperkalaemia ?

Answer 27

Acidosis causes H+ to move into cell => K+ moves out of cell

Question 28

What are the clinical effects of hyperkalaemia?

Answer 28

Muscle weakness Constipation Cardiac arrhythmias

Question 29

What ECG changes can occur with hyperkalaemia?

Answer 29

``` P wave loss AV block Broad QRS Tented T waves Bradycardia Ventricular tachycardia Asystole ```

Question 30

How should hyperkalaemia be treated?

Answer 30

``` Treat cause IV fluid Cardiac protection (Calcium gluconate 10% 10mL 10mins) IV insulin dextrose Correct acidosis IV salbutamol (Beta-agonist) - shifts K+ into cell Cation exchange resin Dialysis ```