8-19 Acute Renal Failure DSA Flashcards
What are the essentials of Dx for acute kidney injury? (very general)
- Sudden increase in BUN or creatine
- Oliguria can be associated
- Sx and signs depend on cause
What is the RIFLE criteria?
describes 3 progressive levels of acute kidney injury
- risk, injury, failure
Based on serum creatine or decline in urinary output
- 2 outcome measures: loss and ESRD
In other words, takes signs of acute kidney injury, quantifies magnitude of problem
How are risk, injury, and failure defined with the RIFLE criteria?
risk = 1.5x increased serum creatine
injury = 2x increase in serum creatine
failure = 3x increase in serum creatine
- or-
0. 5mL/kg/hr decline in urinary output over 6, 12, or 24 hours, respectively
What is an additional criteria for quantifying damage/outcomes with acute kidney injury?
AKIN criteria, which is close to RIFLE
change in serum creatine > or = 0.3 mg/day
What are the signs and symptoms you should look out for with AKI?
Nonspecific Sx, oft due to uremia
uremia causes:
nausea, vomiting, malaise, altered senses
Also look for HTN and altered fluid homeostasis
You are examining a patient who is complaing of oliguria. If they have AKI, what might you hear when you ausculate their heart? Why?
pericardial friction rub
- uremia can cause pericardial effusions, resulting in cardiac tamponade (yikes!)
Might also hear arrhythmias, d/t hyperkalemia
Continuing with your evaluation of your patient with suspected AKI, what might you hear in their lungs?
rales in presence of hypervolemia
(Hypervolemia causes what kind of AKI? That’s right, post-renal)
Your patient is pretty much a trainwreck with their acute kidney injury (AKI), and you’re suspecting acute kidney failure. What symptoms are associated with acute kidney failure?
Abdominal pain - nonspecific, diffuse
ileus dysfxn
platelet dysfxn
What sort of hematological problems are associated with acute kidney failure?
platelet dysfxn
leads to bleeding and clotting disorders
You want to ask your patient with acute kidney failure some questions regarding their stomach pain, but find their mental status altered. What neurological Sx are present? What do you do now?
asterixis - flapping tremor
confusion
seizures
Patient pretty out of it, better order labs at this point.
Your patient is out of it, but lab work coming in is indicating acute kidney failure. What do you expect to see?
Elevated BUN, serum creatine
Hyperkalemia –> peaked T waves, PR prolonged, widened QRS on EKG
hypocalcemia –> long QT segment on EKG
Anion gap, or normal anion gap metabolic acidosis –> decreased acid clearance
Hyperphosphatemia
Anemia, platelet dysfxn
To sum: increased BUN, serum creatin, K+, PO4. Decreased Ca++, RBCs. Metabolic acidosis, platelets messed up.
What would you expect with prerenal azotemia as far as:
etiology
serum BUN/Cr
Una
FEna (%)
Urine osmolality (mosm/kg)
urinary sediment
etiology - poor renal perfusion
serum BUN/Cr - >20:1
Una - <20
FEna (%) - <1
Urine osmolality (mosm/kg) - >500
urinary sediment - hyaline casts
What would you expect for postrenal azotemia as far as:
etiology
serum BUN/Cr
Una
FEna (%)
Urine osmolality (mosm/kg)
urinary sediment
etiology - obstruction of urinary tracy
serum BUN/Cr - >20:1 (according to Lange)
Una - variable
FEna (%) - variable
Urine osmolality (mosm/kg) - <400
urinary sediment - normal or red cells, white cells or crystals
What would you expect with acute tubular necrosis as far as:
etiology
serum BUN/Cr
Una
FEna (%)
Urine osmolality (mosm/kg)
urinary sediment
etiology - ischemia, nephrotoxins
serum BUN/Cr - <20:1
Una - >20
FEna (%) - >1 (when oliguric)
Urine osmolality (mosm/kg) - 250-300
urinary sediment - granular (muddy brown) casts, renal tubular casts
What would you expect with acute glomerulonephritis as far as:
etiology
serum BUN/Cr
Una
FEna (%)
Urine osmolality (mosm/kg)
urinary sediment
etiology - immune complex mediated, pauci-immune, anti-GBM related
serum BUN/Cr - >20:1
Una - <20
FEna (%) - <1
Urine osmolality (mosm/kg) - variable
urinary sediment - red cells, dysmorphic red cells and red cell casts
What would you expect with acute interstitial nephritis as far as:
etiology
serum BUN/Cr
Una
FEna (%)
Urine osmolality (mosm/kg)
urinary sediment
etiology - allergic rxn, drug rxn, infection, collagen vascular disease
serum BUN/Cr - <20:1
Una - variable
FEna (%) - less or greater than 1
Urine osmolality (mosm/kg) - variable
urinary sediment - white cells, white cell casts, with or without eosinophils
What is prerenal azotemia caused by? How often is it the cause of AKI? Is damage permanent?
Caused by renal hypoperfusion
Cause of 40-80% of acute kidney injury/insult
Damage doesn’t occur if hypoperfusion is fixed quickly
Acute kidney injury with permanent damage happens if ischemia occurs
What happens with renal medullary hypoxia leading to ischemia?
Hypoxia
Increased Na+ to macula densa
Increased renal arteriolar vasoconstriction
Ischemia-induced rearrangement of cytoskeleton in renal tubule cells
Loss of polarity, integrins, adhesion in renal tubular cells
tubule cells slough off
Tubules are filled with crap and obstructed
Tubule damage
acute renal failure
- add complicating factors too: NSAIDs, myoglobin ppt, BJ proteins, hypovolemia, sepsis
What are some things that can cause renal hypoperfusion?
Things that cause volume depletion:
hemorrhage
GI losses
dehydration
excessive diuresis
extravascular space sequestration
pancreatitis
burns
trauma
peritonitis
What medications can affect renal perfusion and GFR?
(RAS blockers)
ACE inhibitors - efferent arteriolar constriction, decreased GFR
NSAIDs - reduce afferent arteriolar vasodilation, really bad with cirrhosis and HF
Epinephrine
norepinephrine
high dose dopamine
anesthetic agents
cyclosporine
Also, renal aa stenosis
Why is FEna helpful in diagnosing acute kidney injury?
Decreased GFR = kidney absorbs more Na+ and water if tubules intact
So, prerenal causes will have low excreted Na+ or low FEna
Oligura + intrinsic kidney dysfxn will excrete more Na+, or high FEna
Accuracy may vary if measured during active half life of diuretics