Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

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

(55 cards)

Start Studying
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

HIV, sepsis, legionella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the ischemic causes of ATN?

A
  • Pre-renal
    • Pre-renal AKI that persists can cause ATN
      (an intrinsic AKI)
  • Sepsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

List 3 risk factors for developing AKI

A

Hypvolemia

Older age

Underlying chronic kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

Renal ultrasound

Foley catheter placement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

Study These Flashcards
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

Study These Flashcards
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
What features of a patient’s history and physical exam would be consistent with post-renal AKI?
* **History** * Decreased urinary stream * Nocturia * Frequency * Dribbling * Flank pain * Anuria * **Physical exam** * **​**Distended bladder * Enlarged prostate * Abdominal or pelvic masses
26
Describe the pathophysioogy of hepatorenal syndrome
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
The US Renal Data System suggests that ESRD accounts for nearly \_\_\_\_\_% of all Medicare expenditures.
The US Renal Data System suggests that ESRD accounts for nearly **_7%_** of all Medicare expenditures.
28
What is the effect of Angiotensin II on GFR? Explain
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
If a patient has AKI, are they more likely to have hyperkalemia or hypokalemia?
Hyperkalemia The kidneys are not doing a good job secreting K+
30
Acute tubular necrosis may be ________ or \_\_\_\_\_\_\_\_ in etiology
Acute tubular necrosis may be **_ischemic_** or **_nephrotoxic_** in etiology
31
What causes of intra-tubular obstruction can cause ATN?
* Myeloma * -\> Proteins aggregate and block tubules * Tumor lysis syndrome * -\> Uric acid crystalization * Drugs: Acyclovir, methotrexate
32
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+?
RBCs, RBC casts = Glomeruloneprhitis Urine Na+ \< 20 mEq/L (This implies that the tubules are working to properly reabsorb Na+)
33
What is hepatorenal syndrome?
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
What causes post-renal AKI?
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
Would a patient with post-renal AKI more likely be hyperkalemic or hypokalemic?
Hyperkalemic Impaired K+ excretion (Chronic: Decreased Na+ reabsorption -\> Decreased K+ secretion)
36
What factors are released when glomerular filtration is reduced?
Renin -\> RAAs -\> Angiotensin II Prostaglandins Aldosterone ADH
37
What is the prognosis for a patient with post-renal AKI for \<1 week? What about \>12 weeks?
\< 1 week = likely to have a near complete recovery \> 12 weeks = almost no recovery possible
38
Would a patient with post-renal AKI more likely have metabolic acidosis or alkylosis?
Acidosis Impaired H+ secretion
39
What is the most common cause of intrinsic AKI in hospitalized patients?
Tubular problems (Acute Tubular Necrosis) -\> AKI Usually caused by ischemia, toxins, or pigments
40
What nephrotoxins cause ATN?
* 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
Aldosterone and ADH are secreted in response to \_\_\_\_\_\_\_\_ glomerular filtration. What is the effect?
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
What do you look for in a urine sediment if you suspect intrinsic AKI?
* Renal epithelial cells * Muddy brown casts * =\> Tubular problem (Acute Tubular Necrosis) * RBC casts * =\> Glomerular problem (glomerular nephritis) * WBC casts * =\> Inflammation (Acute Interstitial Nephritis)
43
What is normal for serum creatinine?
**Adult Male:** 0.6 - 1.2 mg/dL **Adult Female:** 0.5 - 1.1 mg/dL
44
What drugs are associated with acute interstitial nephritis (AIN)?
* Penicillins * Rifampin * Cephalosporins * Allopurinol * NSAIDs
45
What are the most common vascular etiologies of AKI?
* Vascular obstruction/occlusion * Thrombosis or embolism of the renal artery or vein * Must be bilateral to cause AKI * Vasculitis
46
In what scenarios would you have a increased FENa in pre-renal AKI?
If the patient is taking duretics (Usually FENa \<1% in pre-renal AKI becuase the tubules are able to appropriately reabsorb Na+)
47
How is AKI diagnosed?
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
Does post-renal AKI cause sodium reabsorption or sodium wasting?
* Acute -\> Na+ reabsorption * Chronic -\> Na+ wasting
49
What is the effect of decreased effective blood volume + ACEI or ARB on GFR?
**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
What are the most common causes of pre-renal AKI?
* **Hypovolemia – most common** * Hypotension * Pharmacologic * Large-vessel compromise
51
s post-renal AKI more common in the inpatient or outpatient setting?
Outpatient
52
If a patient has AKI, are they more likely to have metabolic acidosis or alkylosis?
Acidois (W/ urine that is not acidified/does not contain NH4+, which implies that the kidneys are not properly secreting H+)
53
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
e. All of the above Goal = increase EBV, increase perfusion to the kidney
54
AKI complicates \_\_\_\_% of all hospital admissions and \_\_\_\_\_% of critical care admissions
AKI complicates **_5-7%**_ of all hospital admissions and _**65%_** of critical care admissions
55
Pre-renal AKI is the most common cause of AKI in the _________ setting
Pre-renal AKI is the most common cause of AKI in the **_outpatient_** setting

Renal by Minnie: AH Version (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions