AKI. Large Group 3 -Barnes Flashcards
(36 cards)
What does an elevated BUN: Cr ratio indicate?
low perfusion to the kidney==> reabsorb more Urea nitrogen
What will the urine sediment for pre renal azotemia show?
nothing!
he showed us a slide with a fiber. pre renal azotemia will not have casts
is there damage to the kidney in pre renal azotemia?
NO!
it is reversible without kidney damage
What is renal auto regulation?
the ability of the kidney to regulate its own blood flow
through tubulo-glomerular feedback
What causes Pre-renal azotemia?
prolonged decreased effective circulating volume–> persistent aggrevation of compensatory mechanism–> overwhelm compensation
maximal water resorption, highly concentrated urine, low urine Na. BUN and PCr maintained
What is the equation for fractional excretion of sodium?
%FENa=(Una x Pcr)/(Pna x Ucr) x 100
=CNa/CCr x100
What does a FENa of less than 1% indicate? >2%?
pre-renal azotemia (kidneys will hold on to the Na+ b/c dec ECV)
> 2% –> ATN (or not a pre-renal cause)
What is FENa?
How can FENa be affected by diuretics?
What can be tested in pts on diuretics?
FENa is the % of filtered Na+ in the final urine.
FENa can be >1% in pts on diuretics that are volume depleted (not necessarily because they have pre-renal)
FEUrea <35%=pre-renal
What is oliguria?
<400-500mL urine/24 hours
low urine output
What is anuria?
no urine output
<100 mL/24 hours
What can lead to Pre-Renal Azotemia? (4)
decrease in ECV
- volume depletion
- acute decompensated heart failure
- hepatic failure
- sepsis
How does decompensated heart failure lead to pre-renal azotemia?
- cardiorenal syndrome
- poor renal perfusion secondary to poor forward flow and decreased ECV
- increased intra-abdominal pressure (ascites and visceral edema)
How does cirrhosis lead to pre-renal azotemia?
dilation in the splanchnic vessels due to portal hypertension –> decrease in ECV ==> decreased perfusion of the kidney
also get a increase in RAAS, SNS and ADH –> renal vasoconstriction, salt and water retention ==> ascites –> hepatorenal syndrome (HRS)
What can cause Allergic Interstitial Nephritis?
-Methicillin original association
(Other PCN’s as well (naficillin, cephalosporins))
- PPI’s (very common in recent years)
- NSAID’s (nephrotic syndrome)
- Sulfa drugs
- Allopurinol (CKD, rash, liver dysfunction)
- Infection much less common cause now
What are the most common symptoms of AIN (allergic interstitial nephritis)?
Fever Rash Sterile Pyuria (no bacteria causing WBCs in the urine) Eosinophilia Hematuria Renal Dysfunction
What do you order to confirm AIN? Is this the first step of diagnosis/treatment of suspected AIN?
biopsy –> see inflammatory cells lining the kidney interstitial
NOT THE FIRST STEP! if withdraw medications and then pt shows clinical improvement, there is no need for a biopsy.
if no clinical improvement with stopping meds and there is a contraindication for a renal biopsy, consider steroids.
What is the treatment for AIN?
Remove offending agent
Usually resolves in 2 weeks (up to 6)
10-20% of patients may have permanent renal dysfunction
Steroids may hasten recovery of renal failure if no improvement after 1 week
- 1mg/kg/day tapered over 30 days
- Not helpful in NSAID-induced AIN*
Why are ACE inhibitors and NSAIDS bad for pts in pre-renal azotemia?
ACE inhibitors==> block Ag II –> block efferent constriction –> lose compensation
NSAIDS =block prostaglandin induced vasodilation –> worsen the azotemia
What do positive leukocyte esterase and nitrites in the urine indicate?
UTI
How does the tubular cell structure change in the 3 phases of acute AKI? Which stage shows the largest decrease in GFR?
initiation leads to epithelial injury with loss of brush borders and disruption of the cell polarity and cytoskeleton (can fully recover if injury is alleviated at this stage)
**largest drop in GFR
extension phase: cell death, desquamation and inflammation. (tx: inhibition of apoptosis and inflammation)
maintenance: balance between tubule cell death and restoration (dedifferentiation and proliferation)
What do muddy brown granular casts in urine indicate?
ATN
What types of things can lead to ATN?
- contrast induced nephropathy
- direct damage (from gentamicin)
- poor renal perfusion
- cholesterol emboli
- urinary obstruction
How can contrast agents damage the kidneys?
- vasoconstriction
- oxidative stress
- direct tubular injury
What imagine should be ordered in suspected AKI? What are you looking for?
Renal US
hydronephrosis from a urinary obstruction
