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Renal by Minnie: AH Version > SM 195a - AKI: Pre, Post, and Intrinsic > Flashcards

SM 195a - AKI: Pre, Post, and Intrinsic Flashcards

1
Q

What diagnostic studies could help you diagnose post-renal AKI?

A
  • Post-void residual bladder volume reveals lower tract obstruction
  • Renal ultrasound reveals upper tract obstruction
  • Non-contrast CT
  • BUN/Serum Cr ratio
    • >20:1 implies enhanced urea reabsorption
    • Also elevated in prerenal AKI
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2
Q

How are electrolyte derangements in post-renal AKI resolved?

A

They resolve on their own after post-obstructive duresis

(Diuresis naturally occurs after obstruction is relieved; will stop when the patient achieves electrolyte and volume homeostasis)

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3
Q

What infections are associated with acute interstitial nephritis (AIN)?

A

HIV, sepsis, legionella

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4
Q

The presence of eosinophils, WBCs, and WBC casts in the urine would increase your suspicion for which cause of AKI?

What would you expect from urine Na+?

A

Acute Interstitial Nephritis (AIN)

Urine Na+ >30 mEq/L
(This implies that the tubules are not working to reabsorb Na+)

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5
Q

What laboratory results would be consistent with pre-renal AKI?

  • Urin Na:
  • FENa:
  • BUN/SCr:
  • Sediment:
A
  • Urin Na: < 20 mmol/L
    • ​Implies increased Na+ reabsorption
  • FENa: <1%
  • BUN/SCr: >20
    • ​Implies increased reabsorption of urea
  • Sediment: bland
    • Implies no intrinsic kidney injury

These numbers are consistent with physiological responses to decreased perfusion to the kidney

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6
Q

What are the ischemic causes of ATN?

A
  • Pre-renal
    • Pre-renal AKI that persists can cause ATN
      (an intrinsic AKI)
  • Sepsis
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7
Q

As blood pressure falls, what adaptations occur in the kidney in order to maintain blood flow into the glomerulus?

As mean arterial pressure falls, when does this mechanism begin to fail??

A

Autoregulation

  • Afferent arteriole dilates
    • Due to prostaglandins
  • Efferent arteriole constricts
    • Due to RAAs activation -> ANG II secretion

Autoregulation begins to fail when mean arterial BP falls below 80 mmHg

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8
Q

What are the broad categories of causes of intrinsic AKI?

A
  • Glomerular
    • Acute glomerular nephritis (AGN)
  • Tubular
    • Acute tubular necrosis (ATN)
  • Interstitial
    • Acute interstitial nephritis (AIN)
  • Vascular
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9
Q

What is the effect of decreased effective blood volume + NSAIDS on GFR?

A

Decreased EBV + NSAIDS -> Decreased GFR

NSAIDS inhibit the vasodilatory prostaglandins that normally cause vasodilation of the afferent artriole when EBV drops (autoregulation)

Inability to dilate the efferent arteriole -> decreased GFR

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10
Q

What is the most common cause of AKI in hospitalized patients?

  1. Pre renal
  2. Intrinsic
  3. Post renal
A

b. Intrinsic

Usually tubular etiology (ex: acute tubular necrosis)

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11
Q

What is Acute Interstitial Nephritis (AIN)?

A

Interstitial etiology of intrinsic AKI

Most often associated with drugs/medications, also think of infection, cancer, or autoimmune

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12
Q

What lab results would be consistent with interstitial AKI?

A
  • Blood, WBCs in the urine
  • Eosinophils in the urine
  • WBC casts

Use of nephrotoxic drugs and/or recent infection increase suspicion for acute interstitial nephritis (AIN) as a cause of AKI

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13
Q

All of the following physical or laboratory findings would be suggestive of pre-renal AKI except:

A. Orthostatic hypotension

B. Urine sodium of 75

C. BUN/Cr ratio of 30

D. Urine Osmolality of 500

A

B. Urine sodium of 75

Usually urine Na+ is low (<20) in pre-renal AKI

Most signs of pre-renal AKI are consistent with low EBV

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14
Q

What are the major interstitial causes of intrinsic AKI?

A
  • Acute Interstitial Nephritis
    • Usually drug-induced, abx a common culprit
  • Infiltration
    • Lymphoma, sarcoidosis
  • Some herbs
    • Aristolochic acid
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15
Q

How does obstruction distal to the kidney lead to post-renal AKI?

A
  • Obstruction distal to the kidney
  • -> Increased hydrostatic pressure in the renal pelvis
  • -> Decreased GFR

Can also cause…

  • Derangements in urinary concentrating ability
  • Na+ imbalance
    • Acute -> Na+ reabsorption
    • Chronic -> Na+ wasting
  • Defects in K+ and H+ secretion
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16
Q

List 3 risk factors for developing AKI

A

Hypvolemia

Older age

Underlying chronic kidney disease

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17
Q

AKI due to hypo-perfusion to the kidney is classified as _____________

A

AKI due to hypo-perfusion to the kidney is classified as pre-renal AKI

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18
Q

What is the effect of prostaglandins on GFR?

Explain

A

Prostaglandins -> Incresae in GFR

Dilate the afferent arteriole to increase perfusion to the glomerulus

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19
Q

The presence of muddy brown casts in the urine would increase your suspicion for which cause of AKI?

What woudl you expect from urine Na+?

A

Muddy brown casts = Acute Tubular Necrosis (ATN)

Urine Na+ > 30 mEq/L

(This implies that the tubules are not working to reabsorb Na+)

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20
Q

Name 2 diagnostic tests/maneuvers to rule out post-renal problems as the cause of AKI

A

Renal ultrasound

Foley catheter placement

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21
Q

What features of a patient’s history and PE are consistent with pre-renal AKI?

A
  • History - Anything that causes decreased effective blood volume
    • Vomiting, diarrhea
    • Hemorrhage
    • Overdiuresis
    • Burns
    • Fevers
    • Pancreatitis, Heart failure, liver disease
  • Physical exam - Any signs of volume depletion
    • Decrease in SBP ≥20 mm Hg or DBP ≥10 mmHg whn going from sitting to standing
    • Poor skin turgor
    • Dry buccal mucosa
    • Congestive HF
    • Edema
    • Signs of liver disease
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22
Q

What features of a patient’s history and PE are consistent with intrinsic AKI?

A
  • History
    • Recent infection
      • Hemoptysis, sinusitis, pharyngitis, other infection
    • Muscle trauma w/rhabdomyolysis
    • Red urine
    • Use of nephrotoxic medications
    • IV contrast
  • Physical exam
    • Edema
    • Signs of recent infection
      • Rash
    • Muscle tenderness
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23
Q

What is the effect of decreased effective blood volume on GFR?

A

Decreased blood volume -> GFR remains normal

(Up to a point, and then GFR decreases)

  • Vasodilatory prostaglandins -> afferent arteriole dilation
    • Local angiotensin II -> efferent arteriole constriction
24
Q

Describe the proper management of a patient with post-renal AKI

A

Rapid diagnosis and relief of obstruction are necessary to preserve kidney function

  • Relief of obstruction
    • Percutaneous nephrostomy tube placement
    • Bladder catheter placement

Expect post-obstructive diuresis; resolves on its own when the patient returns to electrolyte and volume homeostasis

25
Q

What features of a patient’s history and physical exam would be consistent with post-renal AKI?

A
  • History
    • Decreased urinary stream
    • Nocturia
    • Frequency
    • Dribbling
    • Flank pain
    • Anuria
  • Physical exam
    • ​Distended bladder
    • Enlarged prostate
    • Abdominal or pelvic masses
26
Q

Describe the pathophysioogy of hepatorenal syndrome

A

Healthy kidneys, diseased liver

  • Splanchnic artirial vasodilation
  • -> Compensatory vasconstriction in other systems
  • -> Impaired Na+ and H2O handling
  • -> Ascites, edema
  • -> Further decrease in effective blood volume

PE findings are consistent with prerenal AKI that is unresponsive to volume repletion

27
Q

The US Renal Data System suggests that ESRD accounts for nearly _____% of all Medicare expenditures.

A

The US Renal Data System suggests that ESRD accounts for nearly 7% of all Medicare expenditures.

28
Q

What is the effect of Angiotensin II on GFR?

Explain

A

Angiotensin II -> increased GFR

Causes constriction of the efferent arteriole to increase hydrostatic pressure in the glomerulus

(Note: Decreased volume and solute delivery to the macula densa
-> Renin secretion -> Increased RAAs activity ->
increased Angiotensin II production)

29
Q

If a patient has AKI, are they more likely to have hyperkalemia or hypokalemia?

A

Hyperkalemia

The kidneys are not doing a good job secreting K+

30
Q

Acute tubular necrosis may be ________ or
________ in etiology

A

Acute tubular necrosis may be ischemic or
nephrotoxic in etiology

31
Q

What causes of intra-tubular obstruction can cause ATN?

A
  • Myeloma
    • -> Proteins aggregate and block tubules
  • Tumor lysis syndrome
    • -> Uric acid crystalization
  • Drugs: Acyclovir, methotrexate
32
Q

The presence of RBCs and RBC casts in the urine would increase your suspicion for which cause of AKI?

What would you expect from urine Na+?

A

RBCs, RBC casts = Glomeruloneprhitis

Urine Na+ < 20 mEq/L

(This implies that the tubules are working to properly reabsorb Na+)

33
Q

What is hepatorenal syndrome?

A

Basically, pre-renal AKI caused by liver failure

  • A consequence of renal vasoconstriction in the setting of normal kidneys and andvanced liver disese
  • Pre-renal AKI unresponsive to volume repletion
  • Oliguria, bland urine sediment, UNa <10
34
Q

What causes post-renal AKI?

A

Obstruction anywhere in the urinary tract (distal to the kidney) that causes AKI

  • Ureters
    • Must be bilateral to cause AKI if there are 2 functional kidneys
    • Tumors, calculi, clots, fibrosis, lymphadenopathy
  • Bladder neck
    • Tumors, calculi, clots, prostate enlargement, neurogenic
  • Urethra
    • Strictures, tumors, obstructed catheters
35
Q

Would a patient with post-renal AKI more likely be hyperkalemic or hypokalemic?

A

Hyperkalemic

Impaired K+ excretion

(Chronic: Decreased Na+ reabsorption ->
Decreased K+ secretion)

36
Q

What factors are released when glomerular filtration is reduced?

A

Renin -> RAAs -> Angiotensin II

Prostaglandins

Aldosterone

ADH

37
Q

What is the prognosis for a patient with post-renal AKI for <1 week?

What about >12 weeks?

A

< 1 week = likely to have a near complete recovery

> 12 weeks = almost no recovery possible

38
Q

Would a patient with post-renal AKI more likely have metabolic acidosis or alkylosis?

A

Acidosis

Impaired H+ secretion

39
Q

What is the most common cause of intrinsic AKI in hospitalized patients?

A

Tubular problems (Acute Tubular Necrosis) -> AKI

Usually caused by ischemia, toxins, or pigments

40
Q

What nephrotoxins cause ATN?

A
  • Exogenous
    • Aminoglycosides
    • IV contrast dye
    • Some herbs
  • Endogenous
    • Myoglobinuria
      • Muscle trauma, crush injury, malignant hyperthermia, drug-induced
    • Hemoglobinuria
      • Mechanical destruction of RBCs,
      • Transfustion reaction
      • Heat stroke
      • Burns
      • Venoms
41
Q

Aldosterone and ADH are secreted in response to
________ glomerular filtration.

What is the effect?

A

Aldosterone and ADH are secreted in response to
decreased glomerular filtration.

Aldosterone -> increased Na+ reabsorption

ADH -> increased H2O reabsorption

The result is concentrated urine with low Na+ content

(conservation of sodium and water to increase blood volume)

42
Q

What do you look for in a urine sediment if you suspect intrinsic AKI?

A
  • Renal epithelial cells
  • Muddy brown casts
    • => Tubular problem (Acute Tubular Necrosis)
  • RBC casts
    • => Glomerular problem (glomerular nephritis)
  • WBC casts
    • => Inflammation (Acute Interstitial Nephritis)
43
Q

What is normal for serum creatinine?

A

Adult Male: 0.6 - 1.2 mg/dL

Adult Female: 0.5 - 1.1 mg/dL

44
Q

What drugs are associated with acute interstitial nephritis (AIN)?

A
  • Penicillins
  • Rifampin
  • Cephalosporins
  • Allopurinol
  • NSAIDs
45
Q

What are the most common vascular etiologies of AKI?

A
  • Vascular obstruction/occlusion
    • Thrombosis or embolism of the renal artery or vein
    • Must be bilateral to cause AKI
  • Vasculitis
46
Q

In what scenarios would you have a increased FENa in pre-renal AKI?

A

If the patient is taking duretics

(Usually FENa <1% in pre-renal AKI becuase the tubules are able to appropriately reabsorb Na+)

47
Q

How is AKI diagnosed?

A

ONE of the following

  • Increase in serum creatinine
    • Increase of 0.3 mg/dL above baseline in 48h
    • Increase in serum creatinine of 1.5x baseline in 7 days
  • Decrease in urine output
    • <0.5 mL/kg/hr for 6 hours
48
Q

Does post-renal AKI cause sodium reabsorption or sodium wasting?

A
  • Acute -> Na+ reabsorption
  • Chronic -> Na+ wasting
49
Q

What is the effect of decreased effective blood volume + ACEI or ARB on GFR?

A

Decreased GFR

Angiotensin II normally causes constriction of the efferent arteriole as a part of autoregulation of GFR

ACEI or ARB -> Decreased RAAs -> Decreased Angiotensin II -> efferent arteriole does not constrict

The result is low GFR

50
Q

What are the most common causes of pre-renal AKI?

A
  • Hypovolemia – most common
  • Hypotension
  • Pharmacologic
  • Large-vessel compromise
51
Q

s post-renal AKI more common in the inpatient or outpatient setting?

A

Outpatient

52
Q

If a patient has AKI, are they more likely to have metabolic acidosis or alkylosis?

A

Acidois

(W/ urine that is not acidified/does not contain NH4+, which implies that the kidneys are not properly secreting H+)

53
Q

Which of the following would be appropriate for the management of a patient with pre-renal AKI?

  1. Start iv fluids, eg normal saline
  2. Stop ACE Inhibitor (Lisinopril)
  3. Stop ibuprofen
  4. Check for post-void residual urine; place catheter into the bladder
  5. All of the above
A

e. All of the above

Goal = increase EBV, increase perfusion to the kidney

54
Q

AKI complicates ____% of all hospital admissions and _____% of critical care admissions

A

AKI complicates 5-7%** of all hospital admissions and **65% of critical care admissions

55
Q

Pre-renal AKI is the most common cause of AKI in the _________ setting

A

Pre-renal AKI is the most common cause of AKI in the outpatient setting

Renal by Minnie: AH Version (27 decks)

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