Acute Kidney Injury

Question 1

In acute kidney injury, there is a reduction in _____ resulting in ______ developing over days

Answer 1

GFR; azotemia

Question 2

What are common causes of acute kidney injury?

Answer 2

Renal ischemia or toxins

Question 3

How is kidney size affected in AKI?

Answer 3

Kidney size is usually preserved

Question 4

What are some of the diagnostic criteria for AKI?

Answer 4

• An abrupt (within 48 hours) reduction in kidney function defined as
  
  • An absolute increase in serum creatinine level of 0.3 mg/dl or
  • A percentage increase in serum creatinine level of ≥ 50% or
  • A reduction in urine output < 500 mL in 24 hours

Question 5

Define the following:

• Oliguria:
• Azotemia:
• Uremia:

Answer 5

• Oliguria: Urin output < 400-500 ml/day
• Azotemia: Elevation of nitrogen waste products related to insufficient filtering of blood by the kidneys
• Uremia: The illness accompanying kidney failure which results from the toxic effects of abnormally high concentrations of nitrogenous substances in the blood

Question 6

Serum creatinine levels are inversely proportionate to ___

Answer 6

GFR

Question 7

What are the limitations of creatinine compared to inulin?

Answer 7

Unlike inulin, creatinine is also secreted in the nephron and creatinine clearance overestimates GFR

Question 8

What is BUN and when is it used to diagnose renal disease?

Answer 8

Blood Urea Nitrogen - nitrogenous waste product of protein metabolism

Useful in conjunction with creatinine in the differential diagnosis of renal disease - less accurate than creatinine due to variation in protein intake, catabolic rate, and tubular reabsorption

Question 9

How are casts formed and how do they present in acute tubular necrosis?

Answer 9

Casts are caused by the trapping of cellular elements in a matrix of protein secreted by renal tubules

Granular casts - muddy brown urine - are seen in cases of acute tubular necrosis

Question 10

Autoregulation of GFR and RBF is effective between the blood pressures of __ and __

Answer 10

80 and 160

Question 11

What GFR autoregulation mechanisms can compensate for decreased perfusion pressure?

Answer 11

Increased vasodilatory prostaglandins - dilate afferent arterioles

Increased angiotensin II - Constrict efferent arteriole

Question 12

With impaired autoregulation _____ _____ has greater effect on GFR

Answer 12

arterial pressure

Question 13

What are the three categories of AKI?

Answer 13

• Pre-renal: imparied effective renal perfusion
• Renal: intrinsic renal disease
• Post renal: obstruction of urinary flow

Question 14

Pre-renal AKI consists of decreased GFR without _____ or _____ injury to tubules

Answer 14

ischemic or nephrotoxic

Question 15

How does pre-renal AKI lead to oliguria?

Answer 15

Decreased effective renal perfusion → increased Ang II and vasopressin → increased reabsorption of sodium (at proximal tubule) and water → concentrated urine → oliguria

Question 16

Pre-renal AKI is associated with increased reabsorption of urea

Elevation of ____is out of proportion to creatinine?

Answer 16

elevation of BUN is out of proportion to creatinine (>20:1)

Question 17

How does the tubular epithelium appear in pre-renal AKI?

Answer 17

normal

Question 18

What is the most common cause of renal AKI?

Answer 18

Acute tubular necrosis

Question 19

What are some causes of Renal AKI?

Answer 19

• ATN
• Inflammation: glomerulonephritis, tubulointerstitial nephritis, vasculitis
• Embolism, thrombosis, thrombotic miroangiopathy
• Neoplasms: infiltrating tumors

Question 20

What are some morphologic features of acute tubular necrosis (ATN)?

Answer 20

• Tubular dilation
• Attenuation of tubular epithelium
• Loss of epithelial cell brush border
• Granular cast material
• Mitotic figures (regenerative change)

Question 21

How do tubules regenerate after ATN?

Answer 21

Sublethally injured tubular epithelial cells repopulate the tubules by:

De-differentiation → proliferation → migration → re-establishing cell polarity

Question 22

What are some causes of Post-renal AKI?

Answer 22

Bladder outlet obstruction

Ureteral obstruction

Question 23

How many kidneys are affected in Post-Renal AKI?

Answer 23

both

Question 24

What is hydronephrosis (in post renal AKI)?

Answer 24

Distension and dilation of the renal pelvis calyces

Question 25

How can fractional excretion of sodium (FENa) distinguish pre-renal AKI from acute tubular necrosis?

Answer 25

• In the setting of volume depletion urine Na reabsorption should be increased in the proximal tubules → FENa < 1%
• If the proximal tubules are injured (ATN), sodium reabsorption will be impaired → FENa > 2%

Question 26

How do you calculate FENa?

Answer 26

FENa = [(UNa x PCr)/ (PNa x Ucr)] x 100