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MJ- F2 E5- Renal > AKI- MJ > Flashcards

AKI- MJ Flashcards

1
Q

What is the definition of AKI?

A

>50% decrease in GFR over a period of hours to days, with any accompanying accumulation of nitrogenous wastes in the body and inability to maintain fluid and electrolyte balance

(all occuring over less than 3 months)

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2
Q

What is the KDIGO classification of AKI? (3)

A

Increase in creatinine by > 0.3 w/in 48hrs

OR

Increase in creatinine >1.5x baseline, which occured w/in the last 7 days

OR

Urine volume < 0.5mL for 6 hrs

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3
Q

According to KDIGO, what is the creatinine and urine output criteria for stage 1 AKI?

(note: creatinine criteria is more important than urine output)

A

Creatinine criteria: Cr 1.5-1.9x baseline OR Cr increase >0.3

Urine output criteria: <0.5mL x6-12 hrs

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4
Q

According to KDIGO, what is the creatinine and urine output criteria for stage 2 AKI?

(note: creatinine criteria is more important than urine output)

A

Creatinine criteria: Cr 2-2.9x baseline

Urine output criteria: <0.5ml x >12 hours

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5
Q

According to KDIGO, what is the creatinine and urine output criteria for stage 3 AKI?

(note: creatinine criteria is more important than urine output)

A

Creatinine Criteria:

  • Cr >3x baseline OR
  • Cr >4mg/dL OR
  • Initiation of dialysis

Urine output Criteria:

  • <0.3ml x >24hrs OR
  • anuria x >12hrs
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6
Q

What is the main difference between the AKIN (Acute Kidney Injury Network) from the KDIGO classifications for staging of AKI?

A

The main difference is in stage 3 where AKIN also includes the following serum criteria:

Increases in Cr to >3x baseline (or Cr >4mg/dl) w/ an acute increase of at least 0.5mg/dl

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7
Q

What is the RIFLE (Acute Dialysis Quality Initiative) classification for AKI?

(old, not preferred method)

A
  • Risk- Cr 1.5 x normal
  • Injury- Cr 2 x normal
  • Failure- Cr 3 x normal (acute rise > 0.5mg/dl)
  • Loss- Loss of function for > 4 weeks
  • End- ESRD- Complete loss of function > 12 weeks
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8
Q

If a patient is admitted to the ICU due to AKI, what is the mortality rate of this group?

Of those that survive, 30% remain on what?

A
  • In hospital mortality= 40-65%
  • Those who survive, 30% remain on long term dialysis
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9
Q

How much urine produced in 24hrs is considered nonoliguia? Oliguria? Anuria?

How do you monitor urine output in real time?

A

Nonoliguria= >500ml

Oliguria= <500ml

Anuria= <100ml

Monitor using a foley catheter

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10
Q

Is prerenal, intrinsic or postrenal AKI most common?

A

Prerenal (60-70%)

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11
Q

What labs and diagnostic studies should be ordered for evaluation of AKI?

A

•Labs

  • Urine studies (UA, urine Na, urine osmolality)
  • CBC, serum electrolytes

•Diagnostics

  • Ultrasound or possibly CT
  • EKG
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12
Q

What is the first line diagnostic tool for evaluating the kidney?

A

ultrasound

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13
Q

Is the normal range of serum creatinine higher in a male or female?

Greater than 4mg/dl indicates what?

A
  • Higher in males (b/c of muscle mass)
  • Greater than 4mg/dL= serious renal impairment
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14
Q

What is the relationship between creatinine levels and GFR?

(as GFR decreases, what happens to Cr?)

A

Inverse relationship: As GFR decreases, creatinine increases

(If GFR is 1/2 normal, Cr will be 2x normal)

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15
Q

What is the BUN/Creat ratio for prerenal AKI? What is the Fractional excretion NA (FENa)?

A

BUN/Creat ratio= >20:1

FENA= <1%

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16
Q

What is the BUN/Creat ratio for intrarenal AKI? What is the Fractional excretion NA (FENa)?

A

BUN/Creat ratio= <20:1

FENA= >3%

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17
Q

What is the BUN/Creat ratio for postrenal AKI? What is seen on UA?

A

BUN/Creat= <20:1

UA= Hyaline casts

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18
Q

What is seen on UA for intrinsic AKI?

A

Dark Granular casts

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19
Q

What is the most sensitive way to differntiate prerenal vs acute tubular necrosis (intrinsic)?

A

Fractional Excretion of Sodium (FENa)

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20
Q

What is the FENa in prerenal vs intrinsic AKI?

A

prerenal= <1%

intrinsic= >3%

if 1-3%= either or both

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21
Q

T/F: Do low or high fluid statuses cause prerenal AKI?

A

True

Ex of low: anemia, hemorrhage, dehydration

Ex of high: Cardiovascular states (did not focus on this)

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22
Q

Prerenal Azotemia is characterized by what?

A

Inadequate blood perfusion to the kidneys

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23
Q

What are the 3 main overarching etiologies of prerenal azotemia?

A
  1. Vascular Depletion
  2. Low Cardiac Output
  3. Change in vascular resistance
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24
Q

Prerenal Azotemia etiologies:

Vascular depletion–> hypovolemia from what?

A
  1. Renal loss
    1. Addisons, DKA, etc
  2. Extrarenal loss
    1. Vomiting, diarrhea, pancreatitis, burns, sweating, etc
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25
Q
A
26
Q

A cause of prerenal azotemia is low cardiac output. What are the 6 possible causes of this and of those, which is the most common?

A
  • CHF (MC)
  • Pulmonary embolism
  • Cardiac Tamponade
  • Positive pressure ventilation
  • Arrhythmia
  • Cardiogenic shock
27
Q

A cause of prerenal azotemia is vascular resistance caused by what 3 things? (in general)

A
  1. Systemically (sepsis, anaphylaxis, anesthesia)
  2. Medications (ACE, NSAIDs, Vasopressors)
  3. Renal artery stenosis (increased resistance and decreased perfusion)
28
Q

What 7 meds can cause vascular resistance resulting in Prerenal Azotemia?

A

1. ACE-inhibitors

2. NSAIDs

  1. Epinephrine
  2. norepinephrine
  3. high dose dopamine
  4. anesthetic agents
  5. cyclosporine
29
Q

What are the 9 signs and symptoms of prerenal azotemia?

A
  • Low urine output
  • Dry mouth
  • Hypotension
  • Tachycardia
  • Thirst
  • Weight loss (weight gain in CHF)
  • Decreased skin turgor
  • Edema (in CHF)
  • Also symptoms related to heart/liver disease/sepsis
30
Q

Do the following diagnostic studies indicate prerenal azotemia, intrinsic renal disease or postrenal azotemia as the cause of AKI?

  • BUN/creatinine ratio: > 20:1
  • Urine sodium: < 20 mEq/dL
  • FENa: < 1%
A

Prerenal azotemia

31
Q

What is the treatment for prerenal azotemia if the cause is a volume depletion?

A

Fluid Resuscitation

32
Q

What is the treatment for prerenal azotemia if the cause is a volume overload? (3 things)

A
  1. Diuresis
  2. Inotropes
  3. Fluid restriction
33
Q

What is the treatment for prerenal azotemia if the cause is a vascular resistance? (2 things)

A
  1. Treat cause
  2. Inotropes
34
Q

What are the 4 causes of intrinsic renal disease (a cause of AKI) and which one is most common?

A
  1. Tubular disease- Acute Tubular Necrosis (MC- 85%)
  2. Glomerular Disease
  3. Vascular Disease (ex: clots in the kidney)
  4. Intersitial disease
35
Q

Intrinsic Renal Disease causing AKI:

What are the 2 most common causes of Acute Tubular Necrosis?

A
  1. Ischemic
  2. Toxin Exposure
36
Q

Ischemic causes of acute tubular necrosis are usually preceded by what?

A

Prerenal azotemia

  • Prolonged low perfusion states (dehydration, sepsis)
  • decreased GFR and parenchymal cellular perfusion
37
Q

AKI: Intrinsic Renal Disease

What are the 5 exogenous nephrotoxins that can cause Acute Tubular Necrosis?

A
  1. Vancomycin
  2. Aminoglycosides
  3. Amphotericin B
  4. Antineoplastics (Cyclosporine)
  5. Contrast Nephropathy
38
Q

AKI: Intrinsic renal disease is characterized by what?

A

Damage or injury within renal parenchyma making it unable to keep its gradients

  • Necrosis
  • Apoptosis
  • Inflammatory response (Nephritic syndromes)
39
Q

AKI: Intrinsic Renal Disease–> Exogenous nephrotoxins causing ATN

The level of nephrotoxicity of Vancomycin increases when combined with which medication?

A

Pipercillin-tazobactam

40
Q

AKI: Intrinsic Renal Disease–> Exogenous nephrotoxins causing ATN

Amphotericin B can cause severe _______ and ______

A

vasoconstricion and tissue damage

41
Q

AKI: Intrinsic Renal Disease–> Exogenous nephrotoxins causing ATN

  • Contrast nephropathy is the ____ leading cause of renal failure in hospitalized patients
  • This is caused by what 2 things?
A
  • Contrast nephropathy is the 2nd leading cause of renal failure in hospitalized patients
  • Caused from renal tubular epithelial cell toxicity and renal medullary ischemia
42
Q

AKI: Intrinsic Renal Disease–> Exogenous nephrotoxins causing ATN

  • Contrast nephropathy usually occurs within how many hours after exposure?
A

24-48 hours

43
Q

AKI: Intrinsic Renal Disease–> Exogenous nephrotoxins causing ATN

  • What are the 7 predisposing factors of Contrast Nephropathy?
A
  1. Diabetes (10-50%)
  2. Age
  3. Preexisting renal disease
  4. Volume depletion
  5. CHF
  6. Repeated doses of contrast
  7. ACE-I and NSAID use

(“PAD CAR V”)

44
Q

AKI: Intrinsic Renal Disease–> Exogenous nephrotoxins causing ATN

  • How do you prevent Contrast Nephropathy?
A

1. Hydration is key! (better than any other tx)

  1. Acetylcysteinie
  2. Sodium Bicarbonate
45
Q

AKI: Intrinsic Renal Disease

  • What are the 4 endogenous nephrotoxins that can cause Acute Tubular Necrosis?
A
  1. Heme containing products (Hemolytic anemia)
  2. Uric acid (Chemo MCC, Tumor lysis syndrome)
  3. Paraprotiens (Bence Jones proteins in multiple myeloma)
  4. Rhabdomyolysis
46
Q

The following describes which cause of intrinsic renal disease?

  • 10-15% of cases of intrinsic renal failure
  • Characterized by edema and tubular damage from interstitial inflammation (cell mediated immune rxn)
  • Drugs- MC cause
  • Can also be Infectious (CMV, Strep)
A

Interstitial Nephritis

47
Q

What 3 drugs are the most common cause of interstitial nephritis (a cause of Intrinsic Renal Disease)

A
  1. PCN
  2. Sulfa
  3. NSAIDs
48
Q

What are the 5 signs/symptoms of intrinsic renal disease caused by interstitial nephritis?

A

•Fever (>80%)

•Rash (20-50%)

  • Arthralgias
  • Plasma eosinophilia
  • RBC, WBC and white cell casts in UA
49
Q

What is the course of Interstitial Nephritis (a cause of intrinsic renal disease)?

  • Usually self-limiting
  • Recovery _____ to ______
  • Rarely progress to ESRD
A

•Recovery weeks to months

50
Q

What 2 things may be needed in the short term to treat Interstitial Nephritis (a cause of intrinsic renal disease)?

A
  • Dialysis may be needed in the short term
  • Steroids may be given- short term, high dose
51
Q

What is the hallmark of intrinsic renal disease (a cause of AKI)

A

Unable to concentrate urine

(will be on exam)

52
Q

The following are diagnostic findings of which cause of AKI? (prerenal, intrinsic or postrenal)

•Urine:

  • Dark granular casts
  • Urine sodium: > 30 mEq/dL
  • ABG: metabolic acidosis
  • Serum:
  • • FENa: > 2-3%
  • •BUN/creatinine ratio: < 20:1
A

Intrinsic Renal Disease

53
Q

The following are causes of what?(prerenal, intrinsic or postrenal)

•OBSTRUCTION!!!

•Nephrolithiasis

•Bladder stones

•BPH

  • Malignancy
  • Medications that cause urinary retention
  • Poorly emptied neurogenic bladder
A

Postrenal azotemia (cause of AKI)

54
Q
A
55
Q

What are the 8 complications of AKI?

A
  1. Volume regulation
  2. Metabolic Acidosis
  3. Hyperkalemia
  4. Hyperphosphatemia
  5. Excertory failure
  6. Metabolic failure
  7. Hypocalcemia and hypermagnesemia
56
Q

What is the course of AKI? (3 phases, how long does each phase last?)

A
  • Initiation
  • Maintenance phase–> days to weeks
  • Recovery (diuresis) phase–> weeks to months
57
Q

What are the 4 causes of death in a person with AKI? What is the most common cause?

A

•Infections (30-70%)

  • Cardiovascular events (5-30%)
  • GI, pulmonary or neurologic complications (7-30%)
  • Hyperkalemia or dialysis related (1-2%)
58
Q

The following describes which complication of AKI?

  • Na and water retention leads to HTN and edema
  • Hyponatremia
A

Volume regulation

59
Q

The following describes which complication of AKI?

  • Tubules fail to regenerate bicarbonate and secrete H+ ions into urine
  • Retention of phosphate causing a wide anion gap
A

Metabolic Acidosis

60
Q

The following describes which complication of AKI?

•Limited potassium secretion and shift out of cells in exchange for H+ ions which accumulates in renal acidosis

A

Hyperkalemia

61
Q

A complication of AKI is hyperphosphatemia. What is this due to?

A

–Due to filtration failure–> leads to hypocalcemia–> PTH release

62
Q

The following describes which complication of AKI?

  • Erythropoietin production falls–> bone marrow is depressed leading to anemia
  • Malabsorption of dietary calcium
  • Renin is overproduced causing HTN
A

Metabolic Failure

MJ- F2 E5- Renal (13 decks)

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