0812 - Pathophysiology of AKI - RM

Question 1

What are the RIFLE stages of AKI?

Answer 1

Risk - Creatinine >1.5x baseline or >25% decrease in GFR, OR 2x baseline or 50% decrease in GFR, OR 3x baseline or >75% decrease in GFR, OR 12hrs
Loss - Dialysis dependent >4 weeks
End-Stage - Dialysis dependent >3 months.

Question 2

What is an AKI?

Answer 2

Sudden and acute loss of renal function (RIFLE criteria). Can be pre-renal (affects perfusion), intra-renal, or post-renal (obstruction or backflow of urine). In many cases, there is a cascade of damage, as the inflammatory response exacerbates the injury.

Question 3

What is the physiologic basis of renal autoregulation?

Answer 3

Renal Autoregulation - ability of the kidney to maintain a constant GFR despite changes in MAP. Predominantly comes from constriction or dilation of afferent and efferent arterioles.
Afferent preferentially affected by prostaglandins and NO (both dilate).
Efferent preferentially affected by Angiotensin II (constrict).
Both are constricted by SY tone.

Question 4

What mechanisms can affect autoregulation and result in AKI?

Answer 4

Autoregulation can be affected by:
Autonomic dysfunction (as in diabetes - poor vascular tone)
Medications - NSAIDs block prostaglandins, ACE inhibitors block Angiotensin II.
Vascular disease (e.g. atherosclerosis)
Reduced kidney function to start with.

Question 5

What are the four types of intra-renal kidney injury?

Answer 5

Tubular - Ischaemic or toxic necrosis tubule - most common cause. Cells detatch from basement membrane, clump together and obstructs lumen.
Interstitial - Inflammatory response to drug or antigen, resulting in interstitial immune complexes and consequent kidney injury. Second most common cause.
Glomerular - Glomerulonephritis
Vascular - thrombosis or vasculitis

Question 6

What is the cycle of immune-mediated kidney injury?

Answer 6

Ischaemic damage incites an immune response and inflammation, resulting in oxidative stress and further kidney injury, starting the cycle again.