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Renal > AKI. Large Group 3 -Barnes > Flashcards

AKI. Large Group 3 -Barnes Flashcards

1
Q

What does an elevated BUN: Cr ratio indicate?

A

low perfusion to the kidney==> reabsorb more Urea nitrogen

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2
Q

What will the urine sediment for pre renal azotemia show?

A

nothing!

he showed us a slide with a fiber. pre renal azotemia will not have casts

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3
Q

is there damage to the kidney in pre renal azotemia?

A

NO!

it is reversible without kidney damage

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4
Q

What is renal auto regulation?

A

the ability of the kidney to regulate its own blood flow

through tubulo-glomerular feedback

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5
Q

What causes Pre-renal azotemia?

A

prolonged decreased effective circulating volume–> persistent aggrevation of compensatory mechanism–> overwhelm compensation

maximal water resorption, highly concentrated urine, low urine Na. BUN and PCr maintained

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6
Q

What is the equation for fractional excretion of sodium?

A

%FENa=(Una x Pcr)/(Pna x Ucr) x 100

=CNa/CCr x100

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7
Q

What does a FENa of less than 1% indicate? >2%?

A

pre-renal azotemia (kidneys will hold on to the Na+ b/c dec ECV)

> 2% –> ATN (or not a pre-renal cause)

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8
Q

What is FENa?

How can FENa be affected by diuretics?

What can be tested in pts on diuretics?

A

FENa is the % of filtered Na+ in the final urine.

FENa can be >1% in pts on diuretics that are volume depleted (not necessarily because they have pre-renal)

FEUrea <35%=pre-renal

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9
Q

What is oliguria?

A

<400-500mL urine/24 hours

low urine output

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10
Q

What is anuria?

A

no urine output

<100 mL/24 hours

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11
Q

What can lead to Pre-Renal Azotemia? (4)

A

decrease in ECV

  • volume depletion
  • acute decompensated heart failure
  • hepatic failure
  • sepsis
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12
Q

How does decompensated heart failure lead to pre-renal azotemia?

A
  • cardiorenal syndrome
  • poor renal perfusion secondary to poor forward flow and decreased ECV
  • increased intra-abdominal pressure (ascites and visceral edema)
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13
Q

How does cirrhosis lead to pre-renal azotemia?

A

dilation in the splanchnic vessels due to portal hypertension –> decrease in ECV ==> decreased perfusion of the kidney

also get a increase in RAAS, SNS and ADH –> renal vasoconstriction, salt and water retention ==> ascites –> hepatorenal syndrome (HRS)

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14
Q

What can cause Allergic Interstitial Nephritis?

A

-Methicillin original association
(Other PCN’s as well (naficillin, cephalosporins))

  • PPI’s (very common in recent years)
  • NSAID’s (nephrotic syndrome)
  • Sulfa drugs
  • Allopurinol (CKD, rash, liver dysfunction)
  • Infection much less common cause now
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15
Q

What are the most common symptoms of AIN (allergic interstitial nephritis)?

A 
Fever
Rash
Sterile Pyuria (no bacteria causing WBCs in the urine)
Eosinophilia
Hematuria
Renal Dysfunction
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16
Q

What do you order to confirm AIN? Is this the first step of diagnosis/treatment of suspected AIN?

A

biopsy –> see inflammatory cells lining the kidney interstitial

NOT THE FIRST STEP! if withdraw medications and then pt shows clinical improvement, there is no need for a biopsy.

if no clinical improvement with stopping meds and there is a contraindication for a renal biopsy, consider steroids.

17
Q

What is the treatment for AIN?

A

Remove offending agent

Usually resolves in 2 weeks (up to 6)

10-20% of patients may have permanent renal dysfunction

Steroids may hasten recovery of renal failure if no improvement after 1 week

  • 1mg/kg/day tapered over 30 days
  • Not helpful in NSAID-induced AIN*
18
Q

Why are ACE inhibitors and NSAIDS bad for pts in pre-renal azotemia?

A

ACE inhibitors==> block Ag II –> block efferent constriction –> lose compensation

NSAIDS =block prostaglandin induced vasodilation –> worsen the azotemia

19
Q

What do positive leukocyte esterase and nitrites in the urine indicate?

A

UTI

20
Q

How does the tubular cell structure change in the 3 phases of acute AKI? Which stage shows the largest decrease in GFR?

A

initiation leads to epithelial injury with loss of brush borders and disruption of the cell polarity and cytoskeleton (can fully recover if injury is alleviated at this stage)
**largest drop in GFR

extension phase: cell death, desquamation and inflammation. (tx: inhibition of apoptosis and inflammation)

maintenance: balance between tubule cell death and restoration (dedifferentiation and proliferation)

21
Q

What do muddy brown granular casts in urine indicate?

A

ATN

22
Q

What types of things can lead to ATN?

A
  • contrast induced nephropathy
  • direct damage (from gentamicin)
  • poor renal perfusion
  • cholesterol emboli
  • urinary obstruction
23
Q

How can contrast agents damage the kidneys?

A
  • vasoconstriction
  • oxidative stress
  • direct tubular injury
24
Q

What imagine should be ordered in suspected AKI? What are you looking for?

A

Renal US

hydronephrosis from a urinary obstruction

25
Q

What are the signs/symptoms of urinary obstruction?

A

polyuria

urinary frequency

increased BUN: creatinine >20:1

post-void fullness

nocturia

Dribbling

incontinence

26
Q

What are the acute indications for hemodialysis (HD)?

A

AEIOU

Acidosis 
Electrolyte abnormality (hyperK+)
Intoxicants (volume overload) 
Overload (volume overload)
Uremia
27
Q 
The optimal therapy for ATN is:
A. Furosemide
B. Renal Dose Dopamine 
C. Fenoldepam 
D. ANP 
E. Supportive Therapy
A

E. Supportive Therapy

Volume expansion with isotonic crystalloid, Avoid hypotension, Prevent Sepsis, Discontinue Nephrotoxins

28
Q

How long does it take to recover from ATN?

What should you monitor in the recovery period of ATN?

A

2-8 weeks

**post-ATN Diuresis

persistant tubular dysfunction after Cr drops and UOP increases

AVP resistance –> seen by hypernatremia (unable to concentrate urine)

electrolyte wasting (from the large loss of water)

29
Q

What does an AKI increase the risk of elderly patients developing?

A

ESRD (even in pts that recover from AKI)

30
Q

What is elevated Creatinine linked to in AKI?

A

death

by the time Creatinine is elevated, the kidney damage has already been done (not ideal biomarker because it does not indicate when damage is taking place)

31
Q

What is a better biomarker for AKI than creatinine?

A

urine NGAL (occurs during the tubular damage stage)

32
Q

How will the BUN/Cr ratio differ between Pre-renal azotemia and ATN?

A

BUN/Cr

Pre-renal >20:1

ATN 10-15:1

33
Q

How will the urine sediment differ between Pre-renal azotemia and ATN?

A

urine sediment

pre-renal normal

ATN: granular casts

34
Q

How will the UNa differ between Pre-renal azotemia and ATN?

A

UNa

Pre renal: 40

35
Q

How will the FENa differ between Pre-renal azotemia and ATN?

A

FE Na

Pre-renal: 2%

36
Q

How will the FEUrea differ between Pre-renal azotemia and ATN?

A

FE Urea

Pre-renal: 50%

Renal (9 decks)

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