AKI Flashcards

1
Q

The kidney’s inability to excrete nitrogenous waste, maintain fluid balance, AND maintain electrolyte balance over a period of hours to days is the definition for which condition?

A

acute kidney injury

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2
Q

In global south nations, what is the primary cause of AKI?

A

hypovolemic shock from diarrhea

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3
Q

In global north countries, what is a primary cause of AKI?

A

bypass cardiac surgery

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4
Q

If you have CKD, what is your risk of developing AKI in a hospital?

A

2 to 40x higher

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5
Q

Per KDIGO, what changes in serum creatinine define AKI?

A

o Increase in serum creatinine by ≥0.3 mg/dL within 48 hours; or
o Increase in serum creatinine by ≥1.5 times baseline, which is known or presumed to have occurred within the prior seven days;

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6
Q

per KDIGO, what urine volume changes define AKI?

A

urine volume < 0. 5 mL/kg/h (oliguria) for 6 hours

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7
Q

Define oliguria

A

Oliguria is defined as 24 hour urine output <500 ml.

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8
Q

Define anuria

A

Anuria is defined as 24 hour urine output of <50 ml.

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9
Q

What term is interchangeable with AKI?

A

acute renal failure (ARF)

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10
Q

• Extracellular volume expansion manifesting as hypertension, congestive heart failure, pulmonary or peripheral edema
• Hyperkalemia
• Metabolic acidosis
• Hyperphosphatemia
• Anemia due to a decrease in the production of erythropoietin
• Uremia (a toxic metabolic state due to a variety of accumulated toxins)
These are all systemic manifestations of what syndrome?

A

acute kidney injury

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11
Q

How is pre renal AKI defined?

A

a reduction in the glomerular filtration rate (GFR) as a result of decreased renal perfusion that is reversed with restoration of perfusion and not associated with structural damage of the kidney.

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12
Q

What parameter defines pre renal AKI?

A

effective arterial pressure, as interpreted by the arterial baroreceptors

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13
Q

Name 4 possible causes of pre renal AKI

A
  • Decreased CO: CHF, MI
  • Hypovolemia: Dehydration, GI losses, Blood loss
  • Peripheral vasodilation: Sepsis, Shock
  • Selective renal ischemia: Renal autoregulation disruption (ACE inhibitors, AII receptor antagonists (ARBs), NSAIDs), Renal vascular occlusion
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14
Q

CHF and MI’s could cause pre renal AKI through what mechanism?

A

decreased CO

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15
Q

Dehydration, GI losses and blood loss would cause pre renal AKI through what mechanism?

A

hypovolemia

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16
Q

Sepsis and shock would cause pre renal AKI through what mechanism?

A

peripheral vasodilation

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17
Q

Renal autoregulation disruption (ACE inhibitors, AII receptor antagonists (ARBs), NSAIDs) and renal vascular occlusion would cause pre renal AKI through what mechanism?

A

selective renal ischemia

18
Q

In general, what FeNa suggests prerenal disease?

A

< 1 % but NOT diagnostic

19
Q

How do you calculate FeNA?

A

(UNa X SCr)/ (SNa X UCr) x 100

20
Q

What is the numerator for the FeNa calculation?

A

UNa X SCr

21
Q

What is an appropriate response by the kidney to decreased renal perfusion?

A

reabsorption of almost all Na (i.e. very low FeNa)

22
Q

What FeNa result would suggest that acute tubular necrosis should be considered?

A

1 -2%

>2% is usually ATN

23
Q

What are the 4 limitations for using FeNa in establishing the cause of AKI?

A
  • The FENa criterion of < 1% to diagnose prerenal disease applies only to patients with a marked reduction in GFR.
  • Single measurements of serum creatinine may not provide an accurate estimate of the GFR.
  • There are a number of causes of AKI other than prerenal disease in which the FENa can be <1%.
  • The FENa may be > 1% when prerenal disease occurs in patients with CKD or any cause of sodium wasting, such as diuretic therapy while the diuretic is still acting.
24
Q

How do you manage pre renal AKI?

A

rapid diagnosis, reversal of underlying process (i.e. volume resuscitation or BP support)

25
Q

How is post renal AKI defined?

A

obstruction anywhere in the urinary tract causing renal failure

26
Q

How does obstruction cause AKI?

A

Severe or complete obstruction causes a marked increase in hydrostatic pressure in the renal pelvis causing a marked decrease in glomerular filtration rate. Obstruction may also cause tubular derangements in urinary concentrating ability, sodium reabsorption causing sodium wasting, defects in potassium secretion and impaired hydrogen secretion.

27
Q
These are all causes of what condition? 
	Ureteral obstruction
(bilateral to cause AKI)
•	Nephrolithiasis
•	Blood clots
•	Papillary necrosis
•	Retroperitoneal fibrosis
•	External compression, i.e., malignancy
•	Unintentional ligation intraoperatively
	Bladder obstruction
•	Prostatic hypertrophy
•	Prostate or other malignancy
•	Neurogenic bladder
	Urethral obstruction
A

postrenal AKI

28
Q

What lab study should be ordered to confirm post renal AKI?

A

BUN/Cr ratio

29
Q

What are two procedures that can be done to confirm and treat post renal AKI?

A

renal US and foley catheterization

30
Q

Following relief of obstruction, what is the next step in a post renal AKI?

A

post obstructive diuresis - resolved when electrolyte hemostasis and euvolemia reached

31
Q
These are all causes of what type of AKI? 
o	Vascular
o	Glomerular 
o	Interstitial
o	Tubular
	ATN
A

intrinsic

32
Q

Proteinuria and hematuria in a UA in the setting of possible AKI should indicated what process?

A

intrinsic AKI

33
Q

What lab studies should be ordered in evaluating a possible intrinsic AKI?

A

UA
urine sediment
Renal US

34
Q

What is indicated by urine eosinophils?

A

allergy

35
Q

What should be closely monitored when managing an AKI?

A

• Review electrolytes (Na, K, HCO3, calcium, phosphorous, magnesium), BUN, creatinine, urine output closely.

36
Q

When should kidney replacement therapy (i.e. dialysis) be considered in the management of AKI?

A

If these problems persist despite aggressive conservative therapy or in the presence of uremia (pericardial rub, mental status changes, bleeding) or volume overload compromising pulmonary status, consider kidney replacement therapy, dialysis.

37
Q

When managing an AKI in the setting of acidosis, what is the therapy?

A

bicarbonate

38
Q

When managing an AKI in the setting of a hyperkalemia, what is the therapy?

A
	Modify diet
	Insulin and glucose
	IV calcium
	Bicarbonate (if acidotic)
	Kayexalate (sodium/potassium exchange resin in gut)
	Loop diuretic
	Beta-agonists
	Dialysis

** just for exposure right now**

39
Q

What is kayexalate? when is it given?

A

sodium potassium exchange resin in the gut, used in hyperkalemic aKI

40
Q

When managing AKI in the setting of hyperphosphatemia, what is the therapy?

A

 Modify diet
 Calcium containing binders
 Non-calcium containing binders: sevelamer, lanthanum, aluminum hydroxide

41
Q

When managing AKI in the setting of drug intoxication, what is the therapy?

A

 Gastric lavage, depending on time of ingestion and ingested drug
 Hemodialysis (if indicated)