Acute Kidney Injury Flashcards Preview

Renal Exam > Acute Kidney Injury > Flashcards

Flashcards in Acute Kidney Injury Deck (36):
1

What is acute kidney injury?

• 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

2

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

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

3

Why do we worry about severe AKI?

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

4

What is oliguria?

urine output < 400-500 ml/day

5

What is azotemia?

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

6

What is uremia?

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

7

How are GFR and serum creatinine related?

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

8

What is Blood Urea Nitrogen (BUN)?

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

9

What are casts?

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

10

What kind of casts are seen in acute tubular necrosis?

Granular casts (“muddy brown urine”)

11

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

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

12

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

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

13

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

age, NSAIDs and CKD

14

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

ACEI and ARBs

15

What happens to autoregulation of GFR in normotensive ischemic AKI?

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

16

What are the 3 AKI categories?

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

17

What are some common causes of pre-renal AKI?

•Volume depletion
•Heart failure
•Liver failure

18

What are some common causes of renal AKI?

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

19

What are some common causes of post-renal AKI?

• Obstruction:
Prostate
Bladder
Stones
Tumors

20

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

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

21

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

elevation of BUN out of proportion to creatinine

22

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

normal tubular epithelium

23

What is renal AKI?

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

24

What is the most common cause of renal AKI?

Acute tubular necrosis or ischemia/toxins

25

How does acute tubular necrosis cause AKI?

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

26

What are the morphologic features of acute tubular necrosis?

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

27

Can tubules be regenerated after acute tubular necrosis?

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

28

What do we see in the urine with renal AKI?

epithelial/granular casts

29

What is post-renal AKI?

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

30

What does post-renal AKI result in?

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

31

What is the top cause of acute renal failure?

acute tubular necrosis followed by pre-renal AKI

32

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

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

33

What is normal Fractional Excretion of Sodium (FENa)?

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

34

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

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

35

What is the FENa in ATN?

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

36

What is the equation for:
FENa (%) =

UNa x PCr
----------------------- X 100
PNa x UCr