Acute Kidney Injury Flashcards

1
Q

What elements are used to calculate the MDRD to estimate GFR?

A
  • serum creatinine
  • age
  • female or not
  • african american or not
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2
Q

What elements are used to calculate the cockroft gault equation to estimate GFR?

A
  • age
  • ideal body weight
  • serum creatinine
  • female or not
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3
Q

Using the microalbumin/creatinine ratio, how do you define normal, microalbuminuria, macroalbuminuria?

A

< 30 mg/g - normal
30-300 mg/g - microalbuminuria
> 300 mg/g - macroalbumuria

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4
Q

Criteria for AKI

A

One of the following

  • increase in serum creatinine of > 1.5 times baseline within prior 7 days
  • increase in serum creatinine of > 0.3 mg/dL within 48 hours
  • Urine volume < 0.5 mL/kg per hour for more than 6 hours
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5
Q

Most common cause of AKI

A

Acute tubular necrosis - 45%

most often caused by hypotension/sepsis, ischemia, surgery/burns, nephrotoxins, rhabdo

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6
Q

What is acute interstitial nephritis (AIN), how is it diagnosed, and how is it treated?

A

fever, rash, elevated serum and urine eosinophils
most common cause is medication, also infection, autoimmune disease, infection
Tx: immediate withdrawal of drug and supportive care are essential
- corticosteroids may be beneficial

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7
Q

Drugs commonly associated with acute interstitial nephritis

A
PPI
allopurinol
cimetidine
NSAIDs
phenytoin
Diuretics - thiazides, furosemide
sulfonamides
cephalosporins, rifampin, cipro, PCN
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8
Q

What is the clinical picture of nephritic syndrome?

A
  • RBCs/RBC casts
  • hypertension
  • mild proteinuria
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9
Q

What is the clinical picture of nephrotic syndrome

A
  • massive proteinuria
  • edema/hypoalbuminemia
  • hyperlipidemia
  • hypercoagulable
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10
Q

When someone has postrenal AKI, what additional evaluation is warranted

A

renal US to look for hydronephrosis

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11
Q

When should renal biopsy be performed in setting of AKI?

A
  • Clinical findings: oliguria, rapidly worsening GFR
  • cause of intrinsic injury unclear
  • pre-renal and post-renal causes have been ruled out
  • need for confirmation before disease specific therapies commence
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12
Q

How do you manage at-risk patient before a dye study?

A
  • stop metformin 48 hours before, esp if GFR < 60
  • isotonic solution IV hydration
  • acetyle cysteine 120 mg BID he day before and the day of exam (inconsistent data)
  • high dose statins may be helpful
  • alkalinize the urine (inconsistent data)
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13
Q

When prescribing metformin, how do you use renal function to guide management?

A
  • do not start if eGFR < 45
  • at eGFR < 45 may continue previous therapy but may consider 50% reduction in dose
  • do not use if GFR < 30
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14
Q

When prescribing nitrofurantoin, how do you use renal function to guide management?

A

Avoid using in GFR < 60 ml/min

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15
Q

What lab findings are used to calculate FENa? How do you interpret FENa?

A
FENa = 100 x (urine Na X Plasma Cr)/(plasma Na x Urine Cr)
prerenal = < 1 %
renal = 1-2%
ATN = > 2-3%
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16
Q

components of FeUrea

How do you interpret it?

A

BUN, serum cr, urine urea, urine creatinine
FeUrea < 35% - prerenal
FeUrea > 50% - ATN

17
Q

How do you calculate mean arterial pressure (MAP)?

A

MAP = (systolic + 2x diastolic)/3

18
Q

Treatment of AKI with volume overload

A

Lasix IV Q6 is initial tx
If inadequate response after 1 hr double the dose
repeat until adequate urine output

19
Q

Treatment of hyperkalemia

A
  • IV calcium gluconate (cario protective/membrane stabilizer)
  • Shift K into cells: insulin (10 units IV and glucose 25 gm), albuterol, sodium bicarb (3 amps in 1 L of 5% dextrose
  • eliminate: Oral or rectal Kayexelate
20
Q

In acidosis, what lab finding would prompt you to initiate sodium bicarb

A

Serum bicab < 15 mEq/L or pH < 7.2

21
Q

What are indications for emergent dialysis in patients with AKI?

A
  • metabolic acidosis: ph < 7.1
  • Uremia: pleuritis, pericarditis, neuropathy, encephalopathy/aMS
  • fluid overload refractory to diuretics
  • Hyperkalemia: K > 6.5 of rapid rise
  • poisoning
22
Q

What level of metabolic acidosis should prompt urgent dialysis in renal failure?

A
  • metabolic acidosis: ph < 7.1
23
Q

What potassium level should prompt urgent dialysis in renal failure?

A
  • Hyperkalemia: K > 6.5 of rapid rise
24
Q

What is Cardiorenal syndrome type I?

A

Acute CHF causes acute AKI

25
Q

What is Cardiorenal syndrome type II?

A

Chronic cardiac dysfunction causes progressive CKD

26
Q

What is Cardiorenal syndrome type III?

A

AKI causes acute cardiac dysfunction

27
Q

What is Cardiorenal syndrome type IV?

A

Primary CKD contributes to cardiac dysfunction - CAD, CHF, or arrhythmia

28
Q

What is Cardiorenal syndrome type V?

A

acute or chronic systemic disorders cause both cardiac and renal dysfunction - sepsis or diabetes

29
Q

What is the mechanism of an ACE inhibitor?

A

blocks conversion of Angiotensin 1 to angiotensin 2

  • Lowers arteriolar resistance
  • increase venous capacity
  • prevents aldosterone secretion from adrenal gland (which ends up preventing sodium retention)
  • prevents vasopressin release from the posterior pituitary ( which ends up preventing H2O retention at distal tubule
  • causes central enhancement of parasympathic activity, breaks sympathetic system activation, reduces plasma NE
30
Q

What change in creatinine is tolerable after administration of ACE-I/ARB?

A

20-30% increase in cr which then stabilizes represents hemodynamic change, not structural change