Acute Kidney Injury Flashcards

1
Q

How is AKI staged?

A

Stage 1-3

  • based on serum creatinine or urine output, whichever is worse
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2
Q

What is the most common cause of AKI? (2)

A
  1. Prerenal azotemia

2. Acute tubular necrosis

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3
Q

What can cause acute tubular necrosis? (cause of AKI)

A
  1. ischemia
  2. Toxins
    • Antibiotics
    • IV iodine contrase dye
    • heme pigments
    • light chains from myosin
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4
Q

What is activated from prerenal azotemia?

A

Prerenal azotemia activates RAAS and ADH

  • RAAS and ADH cause a decrease urine output to restore ECV
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5
Q

What is FeNa in prerenal azotemia?

A

FeNa<1%

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6
Q

What is FeNa in ATN?

A

> 2%, cells are damaged

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7
Q

What parts of the kidney receive the most and least blood?

A
  • Renal Cortex receives the most blood

- Renal medulla is a watershed area susceptible to ischemia

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8
Q

What parts of the kidney have the highest metabolic activity?

A

Proximal tubule and thick ascending limb ( both in medulla susceptible to ischemia)

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9
Q

Why would you see a decreased GFR in acute tubular necrosis?

A
  1. Tubule is obstructed from the formation of casts

2. Urine leaks back because tight junctions are lost

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10
Q

How can you distinguish prerenal azotemia from ATN

A

-Prerenal azotemia has bland urne with hyaline casts

  • ATN has UA with
    1. hyaline casts
    2. renal tubular epithelial cells
    3. transitional epithelial cells
    4. granular casts

PRERENAL AZOTEMIA WILL RESOLVE WITH NORMAL SALINE TX

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11
Q

What drugs can cause interstitial nephritis?

A
  1. NSAIDs
  2. Antibiotics
  3. PPIs
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12
Q

What labs/ diagnostic test should be ordered on all patients with AKI?

A
  1. Urinalysis with microscopy
  2. Urine Albumin/Creatinine ratio or urine protein/creatinine ratios
  3. renal U/S
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13
Q

What 2 renal US signs suggest CKD?

A
  1. cortical thinning

2. Small kidneys

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14
Q

Why would you order FeNa or FeUrea?

A

To differentiate prerenal azotemia from intrinsic renal injury (ATN)

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15
Q

FeNa/ FeUrea is only valid for what type of patients?

A

Oligurua <400-500 ml per day ( more than 100)

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16
Q

Why do urea levels increase in dehydration?

A

In dehydration (prerenal azotemia) ADH is secreted–> ADH binds V2 receptors in basolateral membrane–> increases intracellular cAMP–> leased to insertion AQP and urea on the apical membrane –> increased absorption of urea

BUN/Cr ration is >20:1 in prerenal azotemia

17
Q
  • Renal tubular epithelial cells
  • transitional epithelial cells
  • granular casts
  • waxy casts

is the urinary pattern seen when?

A

Acute tubular necrosis

18
Q

WBC, WBC cast, or urine eosinophils are seen in urine when?

A
  • Acute interstitial nephritis

- Pylonephritis

19
Q

Dysmorphic RBCs and RBC casts are seen in urine when?

A
  • vasculitis

- glomerulonephritis

20
Q

-Proteinuria <3.5 g.day
-hematuria
-dysmorphic RBC
-RBC casts
are seen when?

A

Nephritic syndrome

21
Q

Heavy proteinuria >3.5 g/day

  • lipiduria
  • minimal hematuria

are seen in urine when?

A

Nephrotic syndrome

22
Q

Hyaline casts are seen in urine when?

A

Prerenal azotemia

-nonspecific sign

23
Q

WBCs, RBS, and bacteria would be seen in urine when?

A

UTI

24
Q

What are the indications for dialysis?

A
AEIOU
A: Severe Acidosis
E:Electrolyte disturbance
I: Ingestion
O:volume overload
U:Uremia
25
Q

What is the expected recovery time of AKI?

A

Most recover some degree of renal function within 7-21 days

if they don’t recover in 3 months–> they have CKD