Acute Kidney Injury Epidemiology, Pre/Post causes Flashcards
What functions of the kidney go wrong to give rise to AKI?
excretion of nitrogenous waste products
maintenance of fluid balance
maintenance of electrolyte balance
What are some risk factors for AKI?
worse if pre-existing chronic kidney disease (CKD)
worse if elderly
What are the clinical signs indicating AKI?
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
How is oliguria defined?
24 hour urine output is less than 500 mL
How is anuria defined?
24 hour urine output of less than 100 mL
presentation of AKI
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
causes of AKI
prerenal failure
postrenal failure
intrinsic renal failure
systemic manifestations of AKI
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
prerenal injury
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
What are the causes of prerenal injury?
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
laboratory studies to help diagnose prerenal injury
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
How does the kidney respond when when the mean arterial blood pressure falls below 80 mmHg and GFR autoregulation fails?
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
fractional excretion (FE)
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)
What is the equation for the fractional excretion of sodium?
FENa, percent = (UNa/SNa)/(Ucr/SCr) x 100
What do the ranges of FENa suggest?
<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
Aside from indicating pre renal injury, what else does urine sodium indicate?
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
What are the limitations of using FENa in establishing the cause of acute kidney injury?
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
What are the categories of AKI?
prerenal causes
intrinsic renal causes
postrenal causes
management of prerenal injury
rapid diagnosis and reversal of the underlying process
volume expansion (if hypovolemic)
blood pressure support (vasopressors, inotropic agents)
removal of offending medication
postrenal injury
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
causes of postrenal injury
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
What are some of the obstructions that can lead to postrenal injury?
acute or chronic
partial or complete
unilateral or bilateral
may occur at any site in the urinary tract
What are some pertinent positives in patient history when it comes to postrenal injury?
decreased urinary stream
nocturia
frequency
dribbling
flank pain
hematuria
anuria
What are some pertinent positives in physical exam when it comes to postrenal injury?
distended bladder
enlarged prostate
abdominal or pelvic masses
obstructed catheter
What medications can lead to postrenal injury?
opiates for pain, causing urinary retention
diagnostic studies for postrenal injury
post-void residual bladder volume
renal ultrasound
non-contrast CT
BUN/Creatinine ratio (>20/1, enhanced urea reabsorption in a decreased urine flow state)
postrenal injury management
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
