Acute Kidney Injury

Question 1

What is acute kidney injury?

Answer 1

• Reduction in glomerular filtration rate resulting in azotemia developing over days
• Commonly due to renal ischemia or toxins
• Usually reversible
• Absence of symptoms of chronic uremia
• Kidney size usually preserved

Question 2

What are the diagnostic criteria for acute kidney injury (AKI)?

Answer 2

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% (1.5-fold from baseline), or
• A reduction in urine output < 500 ml in 24 hours

Question 3

Why do we worry about severe AKI?

Answer 3

there are mild, moderate and severe forms of AKI. the mortality rate jumps in severe AKI especially when the pt requires dialysis.

Question 4

What is oliguria?

Answer 4

urine output < 400-500 ml/day

Question 5

What is azotemia?

Answer 5

elevation of nitrogen waste products related to insufficient filtering of blood by the kidneys

Question 6

What is uremia?

Answer 6

the illness accompanying kidney failure which results from the toxic effects of abnormally high concentrations of nitrogenous substances in the blo`od

Question 7

How are GFR and serum creatinine related?

Answer 7

Serum levels are inversely proportionate to GFR (GFR~100/Cr) and the relationship is not linear

Question 8

What is Blood Urea Nitrogen (BUN)?

Answer 8

Nitrogenous waste product of protein metabolism- Less accurate indicator of GFR than creatinine due to variation in:
– protein intake
– catabolic rate
– tubular reabsorption

Question 9

What are casts?

Answer 9

can be seen in urinalysis caused by trapping of cellular elements in a matrix of protein secreted by renal tubule cells

Question 10

What kind of casts are seen in acute tubular necrosis?

Answer 10

Granular casts (“muddy brown urine”)

Question 11

What is the range of BP in which autoregulation works the best to regulated GFR and RBF?

Answer 11

from 80 to 160 mmHg the kidney can keep blood flow relatively constant.

Question 12

During decreased perfusion pressure, what substances act on the afferent and efferent vessels of the glomerulus?

Answer 12

prostaglandins increase dilation of afferent arteriole and angiotensin II constricts the efferent

Question 13

What are few things that can inhibit vasodilation of afferent arteriole by prostaglandins?

Answer 13

age, NSAIDs and CKD

Question 14

What are few things that can inhibit vasoconstriction by Ang II in the efferent arteriole?

Answer 14

ACEI and ARBs

Question 15

What happens to autoregulation of GFR in normotensive ischemic AKI?

Answer 15

they cannot autoregulate at decreased perfusion pressure therefore the stable range of kidney blood pressure is decreased

Question 16

What are the 3 AKI categories?

Answer 16

Pre-renal:Impaired effective renal perfusion without ischemic injury
Renal:Intrinsic renal disease (glomerular, tubular, interstitial, vascular)
Post-renal:Obstruction of urinary flow

Question 17

What are some common causes of pre-renal AKI?

Answer 17

• Volume depletion
• Heart failure
• Liver failure

Question 18

What are some common causes of renal AKI?

Answer 18

• Acute tubular necrosis
• Interstitial nephritis
• Glomerulopnephritis
• Vascular diseases

Question 19

What are some common causes of post-renal AKI?

Answer 19

• Obstruction:
Prostate
Bladder
Stones
Tumors

Question 20

In pre-renal AKI decreased perfusion causes increase in AngII and vasopressin, what does that do?

Answer 20

increased reabsorption of sodium (at proximal tubule) and water → concentrated urine = oliguria

Question 21

Pre-renal AKI: urea is also retained what does that do to lab values?

Answer 21

elevation of BUN out of proportion to creatinine

Question 22

What do we see on histology with pre-renal AKI?

Answer 22

normal tubular epithelium

Question 23

What is renal AKI?

Answer 23

Acute injury involving the tubules, glomeruli, interstitium, or vasculature causing decreased GFR

Question 24

What is the most common cause of renal AKI?

Answer 24

Acute tubular necrosis or ischemia/toxins

Question 25

How does acute tubular necrosis cause AKI?

Answer 25

necrosis causes debris obstructing tubule and fluid back flow which results in decreased GFR

Question 26

What are the morphologic features of acute tubular necrosis?

Answer 26

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

Question 27

Can tubules be regenerated after acute tubular necrosis?

Answer 27

Yes, Sublethally injured tubular epithelial cells repopulate the tubules (not stem cells)

Question 28

What do we see in the urine with renal AKI?

Answer 28

epithelial/granular casts

Question 29

What is post-renal AKI?

Answer 29

Obstruction of the urinary tract at any level that affects both kidneys

Question 30

What does post-renal AKI result in?

Answer 30

Results in hydronephrosis - distension and dilation of the renal pelvis calyces

Question 31

What is the top cause of acute renal failure?

Answer 31

acute tubular necrosis followed by pre-renal AKI

Question 32

If pt has oliguria how do we determine what kind of AKI there is?

Answer 32

Exclude post-renal AKI with renal imaging and differentiate between pre-renal and ATN by urine sodium excretion

Question 33

What is normal Fractional Excretion of Sodium (FENa)?

Answer 33

Normally ~ 1% (i.e. 99% Na reabsorbed)

Question 34

What is the FENa in pre-renal or volume depletion?

Answer 34

In the setting of volume depletion, urine Na reabsorption should be increased in the proximal tubules = FENa < 1%

Question 35

What is the FENa in ATN?

Answer 35

If the proximal tubules are injured (ATN), sodium reabsorption will be impaired = FENa > 2%

Question 36

What is the equation for:

FENa (%) =

Answer 36

UNa x PCr
———————– X 100
PNa x UCr