Acute Kidney Injury Flashcards
What are three characteristics of renal failure (acute and chronic)?
impairment of gfr
elevation of BUN/creatinine
decreased GFR leads to accumulation of substances/drugs normally excreted by the kidney
What is the definition of AKI?
rapid deterioration of renal fxn (hours tod ays but less than 1 month)
greater than .5 mg/dl increase in serum creatinine or increase of 50% over baseline value
sometimes decreased urine output but not always
inability of kidney to regulate electrolytes/water
What is oliguria?
Anuria?
oliguria is decreased urine output below 400 ml/d
anuria is less than 100ml/day (almost none)
T of F:
1) AKI is usually symptomatic, discovered after pain
2) Most cases are irreversible if underlying disease is treated
1) False, most are asymptomatic and discovered in routine labe
2) False, most are reversible if underlying disease is treated
What are the three classifications of AKI?
Prerenal (55%)
Intrinsic Renal (40%)
Postrenal (5%)
What is preprenal ARF?
something before the kidneys is wrong, i.e. insufficient blood flow
What is intrinsic ARF?
something is damaged in the kidney
What is postrenal ARF?
something after the kidney, i.e. problem with bladder or ureter
What is found in the urine sediment of pts with prerenal ARF?
normal or few red blood cels or wbcs
In intrinsic ARF, what does one see in the urine sediment?
rbc casts, granular casts, eosinophils (primarily with allergic interstitial nephritis)
Tell if more characteristic of prerenal or intrinsic ARF:
Uosm: >500
Urine to plasma Osmolality: 20
Urine sediment: hyaline casts
Uosm>500 Prerenal
Intrin - 20 intrinsic
<10 prerenal
Hyaline casts - prerenal
What are things that can cause postrenal ARF?
prostate disease!!!!
cancer
What are symptoms associated with post-renal arf?
voiding complaints
may have distended bladder
u/a unremarkable
dx for ultrasound
What is the typically characteristic of the kidney on ultrasound during post-renal arf?
dilated calyxes
What is the key cause of prerenal arf?
additional causes?
volume depletion (gi, renal)
CHF Shock from fluid losses, sepsis hepatorenal syndrome renal artery stenosis NSAIDS
What do hyaline casts look like on UA (present in prerenal disorders)
they are clear, cylindrical rods
What does a Una less than 25 tell us about the type of ARF?
Una<25 = pre-renal (taking up all the na that it can)
Why is Uosm>500 in prerenal ARF?
all the vasopressin to fix volume depletion
What is hepatorenal syndrome?
Special case of prerenal AKI due to cirrhosis
Decreased BP despite increased ECFV
Kidneys intact and urinalysis normal (except Una)
worsening azotemia and progressive oliguria
Explain the pathway/pathology of HepatoRenal Syndrome (HRS)
portal htn splanchnic vasodilation decreased effective circulatory volume activation of RAAS (leads to two things: Na -> Ascites Renal vasoconstriction -> HRS)
When is the only time you will see renal artery stenosis?
when it is bilateral. when only occurring on one side, the other kidney will compensate
What are two drug types that can lead to ARF in patients with renal artery stenosis?
Why?
ACEi and Angiotensin II blockers
Decreased levels of Angio II or blocking of it impairs renal auto–regulation (constrictino of efferent arterioles in RAS)
What are the two functions of Angiotensin II?
Aldosterone stimulation
Constriction of efferent arterioles
How do NSAIDs affect the kidneys?
they block prostaglandin synthesis, which dilate the afferent arterioles
What pts are at risk for ARF with NSAIDS?
true volume depletion
CHF
cirrhosis
- basically any time you have impaired blood flow due to volume
What are some intrinsic ARF of the glomerulus?
post-strep gn, lupus, rpgn, hepatitis, IgA nephro
What are intrinsic ARF involved with tubules?
ACUTE TUBULAR NECROSIS (due to prolonged HTN, meds)
Acute interstitial nephritis
What are intrinsic ARF causes involving the vasculature?
vasculitis
What can cause acute tubular necrosis?
ischemic injury (i.e. when prerenal continues too long) toxic injury from radiocontrast or meds
Where does most ischemic injury occur?
in the proximal tubules and talh (where the most active transport needing 02 is occurring)
What are clinical clues of ATN?
muddy brown granular casts on UA
urina Na>20 (have aldo but dying tubules cannot absorb)
PRERENAL VS ATN
BUN/Crea >20:1
Prerenal
10-15:1 favors ATN
PRERENAL VS ATN
UA with granular casts
ATN
hyaline casts seen in prerenal
PRERENAL VS ATN
UNa+ <20 meq/L
Prerenal
> 25 meq/L is in ATN because they cannot reabsorb the Na+
PRERENAL VS ATN
Uosm >500 mosm/kg
Prerenal
300-350 in ATN (isoosmotic because we cannot regulate it due to dying tubules
What causes the muddy brown casts in the UA of ATN?
dead cells coming out of body in urine
What causes the elevated BUN/Crea in ATN?
There is obstruction due to dead epithelial cells in the tubule, that dying, release Bun and crea and it goes back into bloodstream
What are drugs that can cause intrarenal AKI?
aminoglycosides, amphotericin B
What can cause acute interstitial nephritis (drugs)?
penicillins, cephalosporins, sulfonamides, NSAIDS
What percentage of people using aminoglycosides will have an increase in creatinine?
10-20% (more in urine)
Where does aminoglycoside accumulate in the kidney?
the proximal tubule cells
How does contrast nephropathy lead to AKI?
direct vasoconstrictive effects on arterioles and tubular toxicity
How can you avoid aKI in pts who need contrast imaging?
avoid volume depletion and nsaids and aCEI
What drugs typically cause acute interstitial nephritis?
antibiotics (penicillins B.lactams) NSAIDS
with mild dehydration, wil you have increased or decreased bp?
increased
in severe dehydration, increased or decreased bp? why?
decreased bp.
aldosterone is triggered, but there isn’t enough h20 to increase bp
