AKI Flashcards

(42 cards)

1
Q

define acute kidney injury

A
  • abrupt loss of kidney function resulting in
    • retention of urea and other nitrogenous waste products
    • dysregulation of volume status and electrolytes
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2
Q

GFR

A

estimates how much blood passed through the glomeruli each minute to be filtered

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3
Q

what are the criteria for diagnosis of acute kidney injury

A
  1. serum creatinine levels
  2. decrease in urine output
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4
Q

can you still use serum creatinine to assess kidney function in patient undergoing dialysis

A

no, creatinine is removed by dialysis

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5
Q

Define the RIFLE acronym

A
  • Risk
  • Injury
  • Failure
  • Loss
  • ESRD
  • *first three are levels of severity; last two are outcome measures
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6
Q

what three groups have come up with ways to define AKI

A
  • RIFLE
  • AKIN
  • KDIGO
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7
Q

what is RIFLEs definition of AKI using serum creatinine

A
  • increase in serum creatitine > 50% developing over 7 days
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8
Q

what is AKIN’s definition of AKI using serum creatinine

A
  • increase in serum creatinine of 0.3 mg/dL pr > 50% developing over 48 hours
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9
Q

AKI can be classified into what 3 categories

A
  1. Prerenal: decreased renal perfusion
  2. Intrinsic renal: pathology of vessels, glomeruli, or tubules-interstitium
  3. Postrenal: obstructive
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10
Q

What are some causes of Prerenal AKI

A
  1. True volume depeletion
    • V/D; burns, third spacing from crush injury
  2. Hypotension
    • shock or aggressive tx of HTN
  3. Edematous status
    • heart failure, cirrhosis
  4. Bilateral renal artery stenosis
  5. Drugs affecting GFR
    • NSAIDs
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11
Q

What are some causes of Intrinsic renal AKI

A
  • renal ischemia
    • from all causes of severe prerenal dz
  • sepsis
  • nephrotoxins
    • aminoglycosides, IV contrast, rhabdomyolysis
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12
Q

How does IV contrast affect kidneys

A
  • causes renal tubular epithelial cell toxicity and renal medullary ischemia
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13
Q

risk factors for kidney damage by IV contrast

A
  • pre-existing renal disease
  • volume depletion
  • repeated doses of contrast
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14
Q

prevention of kidney damage by IV contrast

A
  • hydration
  • avoidance of nephrotoxic drugs for at least 48 hours after exposure
    • e.g metformin
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15
Q

define Nonoliguric

A

>400 mL/24 hours

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16
Q

Define Oliguric

A

<400mL/24 hr

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17
Q

define Anuric

18
Q

important labs to get when evaluating AKI

A
  • UA
  • creatinine
    • calculation of GFR
    • calculatoin of fractional excretion of sodium (FENa)
19
Q

first line imaging to get when evaluating AKI? what are you evaluating for

A
  • renal US
  • assess for urinary tract obstruction
20
Q

most dipsticks permit the analysis of the following core urine parameters

A
  • Heme
  • Leukocyte esterase
  • Nitrite
  • Albumin
  • Hydrogen ions (pH)
  • specific gravity
  • Glucose
21
Q

muddy brown casts are pathognomonic for

A

Acute tubular necrosis

22
Q

What are the two most commonly used equations for calculating GFR

A
  • Crockcroft-Gault
  • Modification of Diet in renal disease (MDRD)
23
Q

how is the fractional excretion of sodium (FENa) used

A
  • measures urine sodium
  • in an oliguric patient, the FENa may help to distinguish prerenal AKI from intrinsic renal pathology
24
Q

what is the equation for fractional excretion of sodium (FENa)? What values suggest prerenal and ATN?

A

FENa = (urine Na / Serum Na) / (Urine Cr / Serum Cr) x 100

  • < 1% suggests prerenal etiology
  • >2% suggests intrarenal (ATN)
25
when can you not rely on the fractional excretion of sodium (FENa) equation
* cannot be used in patients on diuretics * can't be used with chronic renal failure * only useful in acute renal failure
26
When is a renal biopsy indicated
* for patients who have no clear explanation for AKI * if the creatinine is markedly elevated or if it significantly worsens over the course of days * biopsy will provide more definitive tissue diagnosis
27
contraindications to getting a renal biopsy
* solitary native kidney * bleeding diathesis * hydronephrosis * pyelonephritis * renal tumor
28
List the life-threatening complications that can come from AKI
* volume imbalance: depletion or overload * metabolic acidosis * hyperkalemia * hypocalcemia * hyperphosphatemia * uremia * \*\*generally require hemodialysis
29
if patient has a h/o consistent with fluid loss (V/D), a physical exam consistent with hypovolemia (hypotension, tachycardia) and/or oliguria, treatment is
* IV fluids * fluid challenge attempts to identify prerenal failure * crystalloid isotonic fluid (0.9 nml saline) is preferred
30
how much fluid is given
* begin with 1-3 liters of fluid with careful and repeated clinical assessment * pts who do not respond to fluids are unlikely to have prerenal disease
31
if patient becomes volume overloaded or develops fluid retention from IV fluid therapy then treatment is
* diuretics (typically furosemide) = temporizing measure * should not be prolonged therapy * dialysis offers most efficient method of volume removal
32
how does AKI lead to metabolic acidosis
* excretion of acid and regeneration of bicarbonate is **impaired with a low GFR** * causes of AKI such as sepsis, trauma, and multi-organ failure produces increased amount of acid
33
how does diarrhea worsens metabolic acidosis
causes net loss of bicarbonate
34
treatment options for metabolic acidosis from AKI
1. dialysis 2. bicarbonate administration * choice depends on presence of volume overload and the underlying cause of acidosis
35
when should a patient with metabolic acidosis from AKI be dialyzed
* patients with severe **oligo-anuric AKI** who are **volume overloaded** and have severe metabolic acidosis ( **pH \<7.1**) * bicarb adminstration results in large sodium load that may cause or increase volume overload
36
when should a patient with metabolic acidosis from AKI be given bicarbonate
* patients with AKI who are **not volume overloaded** and * acidosis is related to **diarrhea** * pH \< 7.1 and awaiting dialysis * AKI due to **rhabdomyolysis** * **goal: serum bicarb 20-22 mEq/L and pH \> 7.2**
37
hyperkalemia can cause
* impaired neuromuscular transmission * cardiac conduction abnormalities (arrhythmias)
38
how does AKI cause hypocalcemia and hyperphosphatemia
* increases in serum phosphorus levels is caused by reduced GFR * phosphorus binds to calcium -\> hypocalcemia * \*\*serum ionized calciu, should be measured
39
what is the tx for patients who are symptomatically hypocalcemic but whose phosphate levels are very high?
* dialysis * if you give IV calcium, it may result in deposition of calciu, phosphate into vasculature and organs * however, give IV calcium while waiting for dialysis if pt has tetany, QT prolongation, Chvostek sign
40
Name signs/symptoms of severe hypocalcemia
* tetany * confussion, sz * Trousseau's sign * Chovstek sign * QT prolongation
41
patients with serum phosphate levels \> 6 mg/dL should be treated with
**dietary phosphate binders** * if serum ionized ca2+ is low =\> **calcium acetate** or calcium carbonate * if serum ionized ca2+ is high =\> **aluminum hydroxide**
42
dialysis should be initiated in patients with severe uremia. what are some signs of severe uremia
* pericarditis * neuropathy * unexplained decline in mental status