1/25 Acute Kidney Injury - Halevy Flashcards
AKI, acute kidney injury
formerly known as
ARF: acute renal failure
criteria
RIFLE and AKIN criteria
- increases in serum creatinine
- decreases in urine output
physio review graphic
GFR ~ clearance = UV/P
REMEMBER:
- on NORMAL end of spectrum, small changes in creatinine indicate big changes in kidney fx
- once damage has occurred (RENAL IMPAIRMENT, END STAGE RENAL DISEASE), converse is true: big changes in creatinine might not indicate much change in kidney fx at all
- look at right graph and understand it
renal physio review
nephron
glomerulus
GFR
nephron = glomerulus + assoc tubule
- 400k-800k nephrons/kidney → 1-2M nephrons total
- glomerulus: filters plasma of blood flowing through glom cap
GFR = cumulative filtration of all glomeruli in both kidneys = 100-120 ml/min
acute kidney injury flowchart
acute kidney injury
- prerenal (60-70)
- intrinsic (25-40)
- tubular cell injury (80-90)
- ischemia and infl (sepsis, surgery, hypoperfusion)
- toxins
- direct: aminoglycosides, cisplatin
- vasoconstriction: NSAIDs, cyclosporine, radiocontrast
- acute interstitial nephritis (5-10)
- acute glomerulonephritis (<5)
- tubular cell injury (80-90)
- postrenal (5-10)
prerenal vs renal vs postrenal
prerenal: pump problems or depleted intravascular volume
postrenal: outflow issue
postrenal acute renal failure
why?
tumors, stones, enlarged prostate (BPH)
prerenal acute renal failure
- low ECV
- salt/water depletion
- hemorrhage
- heart/liver failure (“ineffective renal perfusion”)
- sepsis
- drugs (IV contrast, indinavir)
- stenosis/thrombosis/embolization
fractional excretion of Na
what kind of ARF?
formula
implication
fraction of filtered Na excreted in urine (not reabs)
helps identify prerenal
FeNa = [U/P] of Na / [U/P] creatinine
if FeNa < 1 → prerenal cause of ARF
if FeNa > 1 → ATN, diuretics
kidney and nephron anatomy
great pic
pick out:
- affa, effa
- JGA
- glomerulus
GFR
vascular regulators/controllers
- tone of affa and effa
- vasodilators and vasoconstrictors acting in affa and effa
- autoregulation
vasodil/vasoconst
renin-angiotensin system
when triggered? 4x
whats the effect?
JGA releases renin in resp to…
- drop in affa pressure
- fall in tubular flow rate
- drop in Na or Cl concentration at macula densa
- stim of beta1 receptors in renin-producing granular cells
renin → AI → AII → predominantly efferent arteriolar constriction (bc more receptors for AII in effa)
JGA/macula densa/effa/affa graphic
vasodil/vasoconst
prostaglandins
vasodil/vasoconst PGs x2 apiece
when are prostaglandins critical? → what can mess it up?
vasodilatory PG:
- PGE2
- PGI2
vasoconstrictors (AII, endothelin, norepi) stimulate production of PGE2 and PGI2 → attenuate/WEAKEN vasoconstrictor effect
- **in conds where vasoconst levels increase (vol depletion, CHF, ascites, nephrotic syndrome), GFR becomes critically dependent on PGE2/PGI2
- i.e. use of NSAIDs in these conds can cause ARF!!!
vasoconstrictor PG:
- PGE2alpha
- TXA2
autoregulation of GFR
1. myogenic reflex
- rise in bp in lumen of arterioles → wall stretch
- causes reflex constriction of smooth muscle cells → reducing blood flow and pressure
- intact endothelium necessary
2. tubuloglomerular feedback
- incr glomerular cap bp
- incr GFR, incr tubular fluid flow rate, incr [Cl] in tubular lumen at macula densa
- signals JGA to release adenosine → constriction of affa → reduction in GFR toward normal
intrarenal acute renal failure
3 parts potentially involved
- tubulointerstitial
- hold in good things (proteins), expel waste (urea), maintain balance
- glomerulus
- vascular
acute tubular necrosis
phases: initiation, extension, maintenance, recovery
causes:
- post-ischemic
- drugs (aminoglycosides, amphotericin, etc)
- infection (staph sepsis)
- toxin (rhabdomyolysis, tumor lysis, hemolysis)
AKI drugs
AKI u/a results
heme positive urine, no RBCs
hematuria
RBC casts
WBC casts
muddy brown casts
proteinuria
