AKI 2 Flashcards
renal failure
kidney fails to remove end products of metabolism from blood, regulate fluid, electrolyte and pH balance of extracellular fluid
AKI is _____ risk factor for…
independent risk factor for MORBIDITY and MORTALITY of hospitalized patients
diagnostic criteria of AKI
abrupt reduction in kidney function (48hrs) , on e of:
- increase in serum Cr by 0.3 mg/dL+ in 48hrs
- increased serum Cr by 150% + in 48hrs
- Oliguria less than 0.5 mL/kg/hr for more than 6 hrs
when is serum Cr unreliable
- when pt is not in steady state (hasn’t accumulated properly)
- Dialysis patients
pre-renal azotemia def + cause (5)
decrease in renal blood flow - kidney is STILL being perfused, just not filtered
- Heart failure
- blood loss (surgery, trauma, GI)
- shock
- renal artery stenosis
- dehydration (vomiting, diarrhea, sweat)
renal azotemia
disease of renal parenchyma (Kidney is also not being perfused)
tubular necrosis , caused by
1. HoTN (severe decrease in blood flow)
- Nephrotoxins
- glomerulonephritis and acute interstitial nephritis
most cases of intrinsic AKI are due to
acute tubular necrosis
caused by ischemia and nephrotoxins
post renal azotemia
diseases that involve remainder of urinary tract excluding kidney (down stream obstruction)
- kidney stone
- BPH
- neurogenic bladder
- retroperitoneal fibrosis
- tumor (pelvis - cancers)
best way to diagnose AKI
good history and PE
history questions (7)
- hx of renal fxn and labs
- urinary output (amnt, color, incontinence)
- infection
- HoTN, volume loss
- nephrotoxic agents
- recent sx, anesthesia
- evidence of obstruction
PE findings indicative of AKI
- orthostasis (pre-renal, severe intrinsic)
- fluid overload
- weight loss
- palpable, full bladder (post renal)
- rectal exam/prostate (post renal)
- post void straight cath or bladder scan
s/s of aki
specific for kidney
- decreased/absent urine output
- flank pain
- edema
- HoTN
- discolored urine
General S/s of AKI
weakness/easy fatiguability
anorexia, n/v
mental status change
systemic: fever, arthralgia, pulmonary lesions, lived reticularis
symptoms of AKI suggesting vasculitis
fever, arthralgia, pulmonary lesions
this indicates systemic disease
causes of livedo reticularis in AKI
aortic cat or atheromatous or cholesterol emboli
diagnostic eval of of AKI
plasma CR
serum bicarb, K
urine volume (anuria, can be oliguric, non-oliguric)
urine sediments (cells and casts)
pre-renal azotemia casts
moderate hyaline and finely granular casts but cellular casts are infrequent
ATN casts
dirty brown granular casts
renal tubular epithelial cells, free and in casts
urinary indicies use
helpful in distinguishing ATN and pre-renal azotemia
urine sodium, urine CR, urine osmolarity, FE Na)
urinary indices in prerenal azotemia
can’t filter, so decreased volume therefore
Urine Na = LOW (not as much water out)
Urine Cr = HIGH
Urine osmolarity = HIGH (more concentration)
Fe Na = < 1
urinary indices in ATN
not enough blood flow, decreased function (unable to pull the water in so diluted)
Urine Na = HIGH
Urine Cr = LOW
Urine osmolarity = LOW
Fe Na = > 2
when are imaging tests indicated in AKI ?
- obstructive pathology
- determine if renal failure is acute or chronic
ultrasound of Kidney or CT scan of abdomen/pelvis
if CKD: small, shrunken kidney
when is a renal biopsy indicated in AKI?
- vascular pathology suspected
- progressive AKI and no reason why (non responsive to meds)
- oliguria greater than 4 weeks
early renal bx looks for
vasculitis, TTP, glomerulonephritis, HUS
what might suggest duration of disease if previous labs are unavailable?
- recent onset of symptoms
- little to no urine
- progressively increasing Cr
- rate of rise in Cr (ATN = 0.3-0.5/day, rapid)
- small, echogenic kidney on US (chronic dz)
lab abnormalities of AKI
Hyperkalemia (K > 5.5)
BUN > 80
bicarb levels fall (< 15)
emergent action in AKI
deadly complications
arrhythmias (due to hyperK)
fluid overload
acidosis
emergent AKI complications (8)
- cogaulopathy
- confusion, coma
- pericarditis
- severe itching
- infection
- seizures
- drug toxicity
- nausea/vomiting
indications for “urgent” hemodialysis
- metabolic acidosis
- fluid overload (unresponsive to med)
- hyperkalemia
- affects of uremia (pericarditis, confusion, coma, seizures, coagulopathy, n/v, GIB
pre-renal AKI tx
drop in perfusion pressure
fluids (0.9 NS, LR)
pressers (dobutamine)
post renal AKI tx
imagining and restoration of urine flow
foley cath
stent urethra
nephrostomy tube placement
stages of ATN
ignition phase
mantainence phase
recovery phase
pathophysiology of ATN
due to initiation and injury of tubular cells
- loss of barrier, back leak of filtrate
- damage to Na+/K+ ATPase pump
- sloughing of tubular cells = granular casts
- decreased vasodilator production
- increased free radicals
maintenance phase
stabilization of GFR at low level (1-2 weeks)
uremic complications
recovery phase
cells regenerate
abnormal diuresis can occur - salt and water loss
ischemic ATN cause
low perfusion to parenchyma
can be due to progression of prerenal phase
caused by HoTN, hypoxemia, shock, sepsis, dehydration, hypovolemia
effects of major surgical procedures and ischemia ATN
prolonged hypoperfusion worsened by vasodilation anesthetic agents and narcotics
when is ATN most likely to occur?
surgery
shock (esp. sepsis)
contrast
which patients are susceptible to ATN
underlying CKD
elderly
people on medications (ACE, ARB, diuretics, metformin)
dehydration
how to prevent ATN
correct underlying electrolyte abnormalities
hydration
avoid nephrotoxic drugs
antibiotics that likely cause ATN (class and drug names)
aminoglycosides
Gentamycin
Tobramycin
Amacaine/Neomycin
aminoglycosides and ATN
older patients and those with renal disease are concerns
occurs 5-10 days after exposure (mild and non oliguric)
treatment of ATN caused by aminoglycosides
stop medications
hydrate gently
monitor renal function
NSAIDs/COX-2 and ATN
inhibit prostaglandin synthesis by endothelial cells
not an issue in people with normal function, but some patients depend on constant prostaglandin induced vasodilation of renal arterioles
patients depending on prostaglandin for normal kidney function
HTN Stage III CKD Chronic arteriosclerotic dz volume depletion nephrotic syndrome ESLD severe hypercalcemia
treatment of ATN due to NSAIDs/COX-2
improve in 3-7 days following drug d/c
acute interstitial nephritis
allergy to NSAIDS (ibuprofen, naproxen, fenoprofen)
reaction occurs in the kidney
causes renal insufficiency and nephrotic range proteinuria
other drugs causing ATN
amphotericin B (Antifungal)
vancomycin
acyclovir
cephalosporins
ACE inhibitors/ARBs
Foscarnet
Antivirals
synthetic cannabinoids
contrast dye and ATN
occurs w/in 24-96 hrs of administration
renal function returns in 7-10 days
no effective treatment
risk factors for contrast induced ATN
CKD (stage 3+) DM >65 y/o Volume depletion large volumes/repeated doses
prevention of contrast induced ATN
lower doses
IV hydration before and after
avoid nephrotoxic agents 224-48hrs before and after
mucomyst/m-acetylcystine
exogenous nephrotoxins
cyclosporin immunosuppressant (dose dependent, biopsy needed)
antineoplastics, cisplatin
organic solvents
heavy metals (mercury, cadmium, arsenic)
endogenous nephrotoxins
myoglobin
hemoblogbin
myoglobin and nephrotoxin
from rhabdo
released into blood causing damage to renal tubules
complain of muscular pain (show signs of muscle injury)
myoglobin urine
dark brown without RBCs
serum CPK and myoglobin elevated
dark brown and false positive for RBCs (not on dipstick)
clinical situations where Rhbadomyolysis is seen
statins
elderly people/drugs = fall can’t get up
extreme exercise
crush injuries
clinically relevant CK levels
20k-50k or more
side effects of muscle cell lysis
ATN
hyperkalemia, hyperphostphatemia, hyperuricemia
treatment of ATN due to rhabdo
hydration at high rate
may do alkaline IV
must monitor urine output
alkaline IV in rhabdo
sodium bicarb in D5
forces metabolic alkalosis that protects kidney and body from hyperkalemia and prevents AKI
hemoglobin
causes direct injury
due to massive intravascular hemolysis
treament: reversal of cause and hydration
causes of massive hemolysis
wrong match blood transfusions
hemolytic anemia
uric acid as a nephrotoxin
occurs in rapid cell turnover and lysis (neoplastic diseases)
esp. in chemo
precipitation of uric acid crystals in tubules (+ hyper K and PO4)
prevention of uric acid ATN
UOP of 3l/day
prophylactic allopurinol
multiple myeloma and ATN
nephrotoxicity due to excretion of light chain Igs into urine
light chains are not found on UA so must diagnose with serum electrophoresis
hydration and MM treatment
treatment goals of ATN
avoid volume overload and hyper kalmia (volume restriction and loop diuretics)
nutritional support (catholic state, keep weight up)
indications for hemodialysis in AKI
- life threating electrolyte issue (hyperK)
- volume overload
- worsening acidosis
- avoidance of uremic complications (BUN > 80)
treatment of ATN
correct anemia if symptomatic (don’t want to fluid overload)
appropriately dose drugs
be sure to monitor for infection (decrease number of lines)
