Acute Kidney Injury Epidemiology, Pre/Post causes Flashcards

1
Q

What functions of the kidney go wrong to give rise to AKI?

A

excretion of nitrogenous waste products

maintenance of fluid balance

maintenance of electrolyte balance

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2
Q

What are some risk factors for AKI?

A

worse if pre-existing chronic kidney disease (CKD)

worse if elderly

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3
Q

What are the clinical signs indicating AKI?

A

rise in serum creatinine of 0.5 if the baseline is less than 2.5 mg/dL

or of more than 20% if the baseline is greater than 2.5 mg/dL

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4
Q

How is oliguria defined?

A

24 hour urine output is less than 500 mL

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5
Q

How is anuria defined?

A

24 hour urine output of less than 100 mL

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6
Q

presentation of AKI

A

most patients are asymptomatic

malaise, hematuria, flank pain, shortness of breath, edema, hypertension, confusion, lethargy can occur

oliguria or anuria

hyperkalemia (> 5.0 mEq/L)

metabolic acidosis

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7
Q

causes of AKI

A

prerenal failure

postrenal failure

intrinsic renal failure

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8
Q

systemic manifestations of AKI

A

ECF 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

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9
Q

prerenal injury

A

occurs when there is inadequate renal perfusion - either from true volume depletion or ineffective circulating arterial blood volume

the result is a reduction in glomerular filtration rate in the setting of intact renal tubular function

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10
Q

What are the causes of prerenal injury?

A

decreased cardiac output - CHF, MI

hypovolemia - dehydration, GI losses, blood loss

peripheral vasodilation - sepsis, shock

selective renal ischemia - renal autoregulation disruption, renal vascular occlusion

pharmacologic - NSAIDs, ACE inhibitors

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11
Q

laboratory studies to help diagnose prerenal injury

A

urinalysis

urin sodium <20mMol/L (or fractional excretion of sodium - FENa < 1%)

BUN/creatinine ratio (tends to be > 20:1 in prerenal states)

urine sediment is bland, absence of cellular elements of casts

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12
Q

How does the kidney respond when when the mean arterial blood pressure falls below 80 mmHg and GFR autoregulation fails?

A

angiotensin II causes greater constriction of the efferent than the afferent arteriole to preserve ultrafiltration pressure

prostaglandins preferentially vasodilate the afferent arteriole to counteract vasoconstrictor effects of norepinephrine and angiotensin II

aldosterone release is increased, leading to increased distal nephron sodium reabsorption

antidiuretic hormone (ADH) is increased, which decreases free water clearance

result: concentrated urine with low urine sodium and increased blood volume

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13
Q

fractional excretion (FE)

A

clearance principle used to measure fractional excretopm pf sp;ites

clearance (UV/P) of solute divided by clearance of creatining (as a surrogate for GFR)

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14
Q

What is the equation for the fractional excretion of sodium?

A

FENa, percent = (UNa/SNa)/(Ucr/SCr) x 100

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15
Q

What do the ranges of FENa suggest?

A

<1% suggests prerenal injury

1-2% is seen with either prerenal or ATN (acute tubular necrosis)

>2% indicates ATN

<1% is not diagnostic

reabsorption of almost all of the filtered Na represents an appropriate response to decreased renal perfusion

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16
Q

Aside from indicating pre renal injury, what else does urine sodium indicate?

A

reflective of the rate of water reabsorption

a low urine sodium (< 10 mEq/L) is helpful, but a higher sodium level does not exclude pre renal injury

17
Q

What are the limitations of using FENa in establishing the cause of acute kidney injury?

A

the FENa criterion of < 1% to diagnose prerenal disease applies only to patients with a marked reduction in GFR

single measurements of serum creatining may not provide an accurate estimate of GFR

there are a number of causes of AKI other than prerenal disease in which the FENa can be < 1%

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

18
Q

What are the categories of AKI?

A

prerenal causes

intrinsic renal causes

postrenal causes

19
Q

management of prerenal injury

A

rapid diagnosis and reversal of the underlying process

volume expansion (if hypovolemic)

blood pressure support (vasopressors, inotropic agents)

removal of offending medication

20
Q

postrenal injury

A

obstruction anywhere in the urinary tract, causing renal failure

severe or complete obstruction causes a marked increase in hydrostatic pressure in the renal pelvis

leads to a marked decrease in GFR

obstruction may also cause tubular derangements in urinary concentrating ability and sodium reabsorption

causes sodium wasting, defects in potassium secretion, and impaired hydrogen secretion

21
Q

causes of postrenal injury

A

ureteral obstruction (bilateral) - nephrolitiasis, blood clots, papillary necrosis, retroperioneal fibrosis, external compression, unintentional intraoperative ligation

bladder obstruction - prostatic hypertrophy, prostate or other malignancy, neurogenic bladder

urethral obstruction - urethral stricture, obstructed urinary catheter

22
Q

What are some of the obstructions that can lead to postrenal injury?

A

acute or chronic

partial or complete

unilateral or bilateral

may occur at any site in the urinary tract

23
Q

What are some pertinent positives in patient history when it comes to postrenal injury?

A

decreased urinary stream

nocturia

frequency

dribbling

flank pain

hematuria

anuria

24
Q

What are some pertinent positives in physical exam when it comes to postrenal injury?

A

distended bladder

enlarged prostate

abdominal or pelvic masses

obstructed catheter

25
Q

What medications can lead to postrenal injury?

A

opiates for pain, causing urinary retention

26
Q

diagnostic studies for postrenal injury

A

post-void residual bladder volume

renal ultrasound

non-contrast CT

BUN/Creatinine ratio (>20/1, enhanced urea reabsorption in a decreased urine flow state)

27
Q

postrenal injury management

A

goal is to preserve renal function, rapid diagnosis, and relief of obstruction

postobstructive diuresis due to volume expansion and osmotic diuresis from solute retention - resolves once electrolyte homeostasis and euvolemia is achieved

this is done through bladder catheter placement, percutaneous nephrostomy tube placement, or alleviation of blockage of urinary flow