Prerenal Flashcards

1
Q

What does pre-renal azotemia indicate?

A

Renal pathology due to reduced renal blood flow

This occurs over the sub-acute to chronic time frame.

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2
Q

How does the kidney respond to perceived low blood volume in pre-renal azotemia?

A

By increasing retention of fluid through reabsorption of urea and sodium

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3
Q

What is the typical BUN/Cr ratio in pre-renal azotemia?

A

BUN/Cr >20

Indicates high blood urea nitrogen levels.

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4
Q

What is the typical fractional excretion of sodium (FENa) in pre-renal azotemia?

A

FENa <1%

Indicates low sodium levels in urine.

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5
Q

What is the time frame for acute decreased perfusion leading to acute tubular necrosis?

A

Seconds to minutes

This differs from the sub-acute to chronic time frame of pre-renal azotemia.

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6
Q

What conditions can cause acute tubular necrosis due to acute decreased perfusion?

A

Blood loss, acute heart failure exacerbation, or arrhythmia (Example: VFib for 30 seconds before resuscitation.)

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7
Q

What is the expected renal outcome if a patient loses significant blood during surgery and then develops oliguria and decline in renal function two days later?

A

Acute tubular necrosis

Despite decreased renal perfusion, the timing indicates acute tubular necrosis, not pre-renal azotemia.

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8
Q

Why is the proximal convoluted tubule (PCT) particularly susceptible to anoxic/hypoxic injury?

A

Due to the concentration of ATPase transporters

This makes it vulnerable to acute drops in blood flow.

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9
Q

True or False: Pre-renal azotemia is caused by acute drops in renal perfusion lasting seconds to minutes.

A

False

Acute drops in perfusion lead to acute tubular necrosis, not pre-renal azotemia.

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10
Q

What is the cause of oliguria in a post-op patient who was started on ketorolac?

A

Hypoperfusion

This scenario illustrates how NSAIDs can lead to post-operative oliguria due to pre-renal causes.

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11
Q

Name 4 common causes of pre-renal azotemia relevant for the USMLE.

A
  • NSAID use
  • Diuretic use
  • Chronic left heart failure
  • Dehydration from days of vomiting/diarrhea

These are key conditions to consider when evaluating pre-renal azotemia.

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12
Q

What medications are commonly associated with causing pre-renal oliguria in patients?

A

NSAIDs and diuretics

Examples include naproxen and ibuprofen.

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13
Q

What is the effect of NSAIDs on sodium excretion in pre-renal azotemia?

A

Decreased renal excretion of sodium

This occurs due to increased reabsorption of sodium in the proximal convoluted tubule (PCT).

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14
Q

Fill in the blank: In cases of pre-renal azotemia, the fractional excretion of sodium (FENa) is typically _______.

A

<1%

This indicates that the kidneys are conserving sodium due to low perfusion.

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15
Q

Vignette of patient who is on an NSAID + now has peripheral edema + they ask why there’s edema

A

“Decreased renal excretion of sodium.” This is because the PCT reabsorption of sodium in pre-renal (FENa <1%).

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16
Q

What is the recommended action when a patient on an NSAID develops edema?

A

Discontinuation of ibuprofen

This is a common approach to manage NSAID-related edema.

17
Q

What is the typical clinical presentation of a patient experiencing pre-renal azotemia due to dehydration?

A

Oliguria and increased creatinine

This presentation is often seen in patients who have days of vomiting or experiencing diarrhea.

18
Q

Hepatorenal syndrome is

A

A severe form of Prerenal AKI caused by Splanchnic vasodilation causing renal hypoperfusion

19
Q

Hepatorenal syndrome presents with

A

Bland urinalysis (no blood or protein) makes intrinsic AKI unlikely
No obstruction (postrenal) on imaging
Very low urinary sodium
Lack of response volume expansion (albumin)