AKI

Question 1

AKI defined

Answer 1

rapid deterioration in kidney function as manifested by a reduction in GFR.

Potentially reversible. <3 months duration

Can be acute, or acute on chronic

Question 2

Markers of AKI?

Answer 2

Serum creatinine

BUN

• nitrogenous wastes accumulate that would/ could be excreted by the kidneys

Question 3

Azotemia defined

Answer 3

buildup of nitrogenous wastes in blood

Question 4

Uremia defined

Answer 4

constellation of signs and symptoms of multiple-organ dysfunction caused by retention of ‘uremic toxins’ in setting of renal failure

Question 5

AKI and urine output?

Answer 5

oliguric (<400mL/ day)

or

could be

polyuric (>3L/ day)

Question 6

anuric

Answer 6

< 100mL/ day or none

Question 7

What’s the problem with measuring serum creatinine?

Answer 7

Can be a poor reflection of true GFR in many patients.

REM: Muscle is the primary source of creatine. It is then converted to creatinine in the liver.

muscle wasting in px can give false low creatinine levels (also females)

Question 8

What’s the problem with BUN and GFR?

Answer 8

• ANY disease state associated with reduced tubular flow rates wil increase urea reabsorption in kidney.
• Many things influence BUN in absence of changes in GFR.

Question 9

What can increase BUN values?

Answer 9

• reduced tubular flow rates will increase urea reabsorption and increase BUN
• protein loading
• hypercatabolic states (maybe due to infection)
• GI bleed - reabsorbed blood converted to urea
• tetracycline antibiotics (increase urea generation)

Question 10

What can decrease BUN levels?

Answer 10

• Liver cirrhosis; reduced urea generation
• poor protein uptake
• protein malnutrition

Question 11

What’s the story with creatinine and AKI?

Answer 11

an abrupt increase in serum creatinine concentration usually reflects a decline in GFR and the devepement of AKI

Question 12

What’s the most common cause of AKI?

Answer 12

Decreased renal perfusion

Question 13

Common causes of AKI are:

Answer 13

Decreased renal perfusion

nephrotoxic drugs - aminoglycosides and NSAIDs

Radiocontrast material

(CKD is common underlying risk factor)

Question 14

pre-renal AKI defined

Answer 14

a decrease in GFR as a consequence

Reduced renal flow

and/ or reduced renal perfusion pressure

Question 15

Pre-renal causes of AKI

• ‘True volume’ causes

Answer 15

True volume depletion; vomiting, diarrhoea,

overdiuresis,

diabetes insipidus,

renal salt wasting,

severe sweating

Question 16

Pre-renal causes of AKI

• ‘Effective volume’ causes

Answer 16

“Effective” volume depletion

Sepsis, cardiomyopathy, cirrhosis/ hepatic insufficiency, nephrotic syndrome, renal artery stenosis, altered intrarenal haemodynamics

• NSAIDs, ACE inhibitors, ARBs

Afferent - NSAIDS

Efferent - ACEs

NB. venous congestion from hypervolaemia also contributes to reduced renal perfusion!

Question 17

Pre-renal causes of AKI - due to renal artery disease

Answer 17

• renal artery stenosis
• small renal vessal narrowing (hypertensive arterionephrosclerosis)

Question 18

What physiologically occurs with “true” and “effective” pre-renal hypoperfusive states?

Answer 18

Various mechanisms to protect circulatory stability.

• catecholamines from the sympathetic n.s.
• endothelin from the vasculature
• angiotensin II
• ADH from neurohypophysis
• myogenic reflex (renal baroreceptors)

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