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98 Cards in this Set

  • Front
  • Back
Acute Renal Failure is...
abrupt decline in renal fxn resulting in an inability to excrete metabolic wastes and maintain proper F&E balance
2 declines that constitute ARF
1)NORMAL renal fxn @ baseline w/ a 50% incr in SCr over 1d
2)SCr is over 2mg/dl @ baseline w/ a greater than 1mg/dl incr
For CrCL use what equation in ARF?
Chiou, not CG (only works in stable renal fxn)
Hospitalized pts that develop ARF have...
sig incr mortality
Why might SCr not be a good measure of acute changes in renal fxn (2)
1)accumulation of metabolic wastes may be out of proportion to the change in SCr
2)SCr may not decline/recover at the same rate as renal fxn
Community ARF
a)incidence
b)common causes (3)
c)surivial
a)less than 1%

b1)volume depletion
b2)prostate obstruction
b3)meds

c)70-95%
Hospital ARF
a)incidence
b)common causes (3)
c)surivial
a)2-5%

b1)volume depletion
b2)hypotension
b3)meds

c)30-50%
ICU ARF
a)incidence
b)common causes (3)
c)surivial
a)6-23%

b1)sepsis
b2)multi-organ failure
b3)meds

c)10-30%
Nonoliguric?
normal urine production (over 400mL/day)
Oliguric?
decr urine production (less than 400mL/d)
Anuric
no urine production (less than 50mL/day)
"Prerenal"

"Postrenal"

"Intrinsic"
a)decr renal perfusion (prerenal azotemia)

b)obstruction of urine flow

c)structural kidney damage
Urinalysis
a)what is it
b)what does it include (5)
a)chemical/microscopic analysis of urine
b1)pH
b2)specific gravity
b3)protein/glucose
b4)ketones
b5)WBC/RBC
Urine Sodium (Una)
a)measures...
b)values (2)
a)urine []ing ability of kidney

b1)5-10 when volume depleted so incr [] of urine
b2)over 30 when kidney can NOT concentrate urine
Urine Osmolality (Uosm)
a)measures... (2)
b)values (2)
a)urine []ing ability of kidney; # of osmotically active particles in urine

b1)normal is 50-1200 (depending on hydration status of pt)
b2)highly []ed urine is over 500
Fractional Excretion of Na (FEna)
a)measures...
b)why gotten? (2)
c)values (3)
a)urine []ing ability
b1)does NOT require 24h collection
b2)reflects acute changes

c)normal is 1%
c)less than 1% when volume depleted (b/c kidney will [] urine by retaining Na)
c)over 1% = kidney can NOT [] urine due to damage/diuretics
FEna equation
(Una x SCr) / (Ucr x Sna)
BUN:SCr ratio
a)normal value
b)values
a)10:1

b1)volume depletion = 20:1 or more = ability to [] urine
b2)10:1 can mean inability to [] urine
Volume depletion =
WILL = CONCENTRATED URINE
PreRenal ARF CAUSES (3)
1)hypovolemia (decr circulating blood volume = decr kidney perfusion; v/d, dehydration, hemmorhage)

2)hypotension (decr effective blood volume; sepsis, CHF)

3)Meds (vasospasm of kidney vessels = decr kidney perfusion; ACEI, NSAIDs)
Clinical Findings of Prerenal ARF (7)
1)hypovolemia (v/d, diuretics, hemorrhage)
2)hypotension (CHF, sepsis)
3)tachycardia
4)orthostatic hypotension (positive tilt test)
5)dry mucous membranes
6)poor skin tugor (tenting)
7)wt loss
"Positive Tilt Test"?
decr BP and incr pulse when going from lying down to upright
Renal assessment in Prerenal ARF (6)
1)oliguria
2)incr BUN:SCr
3)incr Uosm
4)decr Una
5)FEna less than 1%
6)UA normal
Tx of Prerenal ARF (4)
1)hypovolemia
a)FLUID REPLACEMENT
b)stop v/d, diuretics, bleeding

2)hypotension (treat CHF, sepsis)
What is done in body to incr BP/ maintain kidney perfusion (2)
1)RAAS activation
2)incr Na/water reabsorption
Determine IV fluid to use (2)
1)If serum Na is greater than normal pt is: hypernatremic hypovolemia
a)means they have a greater water deficit than salt deficit so use 0.45% NaCl

2)If serum Na is less than normal then pt is hyponatremic hypovolemia
b)means greater salt deficit than water deficit so use 0.9% NaCl
Calculating how much to use for
a)0.45% NaCl
b)0.9% NaCl
a)formula given on exam (so don't worry)

b)formula's given just remember to convert to L of NS to infuse (154mEq/L)*****
Other Fluid replacement steps after calculating need (6)
1)Serum Na correction should never be more than 0.5mEq/L/hr*******
2)How much will we change the serum Na--(Na-140)=mEq/L to correct
3)(mEq/L to correct) x ((L/hr)/(0.5mEq)) = minimum hours to infuse volume
4)IV bolus rate (fluids gotten in first 24h) should replace half of deficit in first 24hrs (unless this requires replacement faster than 0.5mEq/L/hr)
6)Continuous IV infusion rate (rate after 1st 24h); infuse @ rate of 1mL/kg/hr
When to incr/decr rate of IV bolus of fluids

When to incr/decr rate of continuous IV infusion rate
1)incr if acute onset of hypovolemia
2)decr if prolonged onset of hypovolemia


1)incr if symptomatic, nonolguric, can tolerate
2)decr if oliguric/anuric, heart disease, unable to tolerate fluid load
S/sx of volume overload that tell you to DECREASE IV FLUIDS (4)
1)edema
2)pulmonary edema (rales)
3)incr BP
4)wt gain
S/sx of volume depletion that tells you to INCREASE IV FLUIDS (6)
1)wt loss
2)decr BP
3)tenting (poor skin tugor)
4)dry mucous membranes
5)positive tilt tachycardia
6)BUN:SCr is increased
PostRenal ARF CAUSES (3)
1)ureter obstruction (in both kidneys or 1kidney if pt only has 1)
2)bladder obstruction
3)urethra obstruction
PostRenal ARF
a)clinical findings (4)
b)renal assessment (2)
a1)decr urine stream/output
a2)distended bladder
a3)enlarged prostate
a4)pelvic/abdominal mass

b1)oliguria
b2)UA normal
Treatment of PostRenal ARF
a)Ureter obst (2)
b)Bladder obst (2)
c)Urethra obst (2)
a1)crystal/calculi: analgesics and IV fluids to incr urine flow
a2)clot/tumor: surgery

b1)prostatic hypertrophy/tumor: surgery
b2)Neurogenic bladder: alpha-antagonist, I/O catheterization

c1)catheter
c2)surgery
Intrinsic ARF BROAD CAUSES (4)
1)damage to renal vasculature/vessels
2)damage to glomerulus (glomeruluonephritis)
3)damage to interstitium (intersitial nephritis)
4)acute tubular necrosis (ATN--damage to tubules)
Damage to renal vasculature/vessels (INTRINSIC ARF)
a)causes
b)manifestations (2)
c)tx
a)vasculitis

b)systemic vasculitits
b)UA normal

c)tx underlying cause
Glomerulonephritis (INTRINSIC ARF)
a)causes (2)
b)manifestations (5)
c)tx (2)
a1)lupus
a2)post infectious (immune mediated damage to glomerulus) glomerulonephritis

b1)s/sx of lupus
b2)h/o of recent infexn
b3)UA shows heavy protein (>3g/day), "foaming" urine (severe proteinuria)
b4)RBCs, RBC casts
b5)"cola-colored" urine (hematuria)

c1)tx underlying cause
c2)immunosuppressants
Interstitial nephritis (INTRINSIC ARF)
a)cause
b)manifestations (4)
c)tx (2)
a)allergic rxn to meds (MOSTLY ABX)

b1)rash
b2)h/o of abx use
b3)loss of urine []ing ability (Fena over 1%, incr Una, decr Uosm)
b4)WBCs and eosinophils in UA

c1)dc offending med
c2)consider corticosteroids
ATN (INTRINSIC ARF)
a)what is ATN? (3)
b)cause (3)
a1)predominant cause of ARF in hospitalized pts
a2)tubule cells die and slough off into tubule lumen
a3)this forms casts that obstruct the tubule and prevent glomerular filtration

b1)tubules are highly susceptible to injury b/c of high metabolic activity
b2)ischemia (hypovolemia, hypotension, vasoconstrictors)
b3)toxins (nephrotoxic meds)
ATN (INTRINSIC ARF)
a)clinical findings (3)
b)renal assessment (3)
a1)s/sx of hypovolemia/hypotension (h/o PreRenal)
a2)h/o of vasoconstricting meds
a3)h/o of nephrotoxin meds

b1)loss of urine []ing ability (FEna over 1%, incr Una, decr Uosm)
b2)DIRTY BROWN CASTS IN UA****
b3)oliguria
ATN (INTRINSIC ARF)
a)tx (3)
b)maintaining fluid status (3)
c)goal
a1)treat underlying cause
a2)avoid nephrotoxic meds
a3)provide hemodynamic support

b1)restrict Na (less than 2g/d)
b2)restrict water (less than 1L/d)
b3)avoid excessive fluid hydration

c)INCR URINE PRODUCTION TO GREATER THAN 1mL/kg/hr
Purpose of Incr Urine Production? (5)
1)convert oliguric to non-oliguric renal failure
2)no evidence that this improves outcomes
3)but may be good at maintaining fluid balance (preventing pulmonary/peripheral edema)
4)forcing elimination of nephrotoxins
5)stabilizing hemodynamics
Incr Urine Production
a)drugs used (3)
b)mechanism
c)adv of them
a)HIGH DOSE: lasix, torsemide, bumetanide
b)incr GFR and cause vasodilation
c)safe, cheap
Equivalent IV dosing of the 3 loops
Furosemide (80mg po) 40mg IV = 20mg torsemide = 1mg bumetanide

Torsemide Twenty
Furosemide Forty
Dosing of furosemide (3)
1)initiated @ 80mg IV q8h
2)or continuous infusion of 10mg/hr
3)TITRATE URINE OUTPUT UP TO GOAL OF 1mL/kg/hr******
Monitoring parameters of loops (5)
1)fluid status (diuresis goal is 1kg/day)
2)BP
3)HR
4)Na, K, Mg, Ca
5)renal fxn
ADR's of loops (4)
1)tinnitus
2)vertigo
3)fullness in ear
4)rates of 4mg/min associated w/ ototoxicity
Diuretic resistance
a)mechanismS (4)
b)methods to overcome (4)
a1)inadequate diuretic dose
a2)excessive Na intake
a3)reduced renal blood flow/perfusion
a4)meds, hypotension, hypovolemia

b1)combine loop and thiazide (metolazone)
b2)continuous IV infusion of IV loop (furosemide 1mg/kg/hr)
b3)Na restriction (less than 1g/day)
b4)renal dose dopamine
ARF Tx Goals of the following COMPLICATIONS:
a)develop chronic renal failure (4)
b)fluid overload (3)
a1)treat reverse underlying cause
a2)maintain hydration
a3)monitor/adjust meds
a4)avoid nephrotoxin meds

b1)restrict Na/water
b2)incr urine production when oliguric
b3)minimize excess exogenous fluids (TPN, IV meds)
ARF Tx Goals of the following COMPLICATIONS:
a)Arrhythmia (due to electrolyte abnormality)
b)Acidosis/Alkalosis (due to electrolyte abnormality)
c)HTN
d)Sepsis
a)manage K
b)manage H
c)manage BP
d)prevent/early recognition/aggressive tx
ARF Tx Goals of the following COMPLICATIONS:
a)GI bleeds
b)altered mentation
c)malnutrition (2)
a)maintain BP
b)manage electrolytes/toxins/meds

c1)enteral/parenteral supplements to meet catabolic state
c2)consider nutrients lost w/ dialysate
Complications of ARF (9)
1)chronic renal failure
2)fluid overload
3)arrhythmia/acidosis/alkalosis due to electrolyte abnormality
4)toxin accumulation
5)HTN
6)sepsis
7)GI bleeding
8)altered mentation
9)malnutrition
Indications for ACUTE Dialysis in ARF (5)
AEIOU

a)Acidosis (resistant to tx)
b)Electrolytes abnormal (incr in K, resistant to tx)
c)Intoxications (ethylene glycol, lithium)
d)Overload (volume overload resistant to tx)
e)Uremia (symptomatic)
Monitor/adjust drug dosing (3)
1)adjust current meds according to renal fxn
2)inability to efficiently estimate CrCL in ARF requires PK monitoring
3)avoid nephrotoxins, but when have to be used take measures to prevent renal damage
Mechanisms of Drug Induced Renal Failure (4)
1)hemodynamic
2)acute tubular necrosis (ATN)
3)allergic interstitial nephritis
4)rhabdomylosis
Drugs that induce hemodynamic renal failure (3)
1)NSAIDs
2)ACEI/ARB
3)contrast media
Regulation of Glomerular Filtration by PG and angiotensin2 (3)
a)PG at the afferent arteriole causes vasodilation (incr renal perfusion)
b)AG2 acts to constrict the afferent arteriole BUT is heavily outweighed by PG effect (so dc this effect)
c)AG2 @ the efferent artierole causes vasoconstriction
NSAIDs effect on kidney (2)
1)vasoconstrict afferent arteriole (decr perfusion)
2)in normal people there will be autoregulation to maintain GFR
COX2 effect on kidney?
1)they may also precipitate renal failure b/c COX2 is in the kidney as well
NSAIDs and people w/ ___ and ___ causes problems...(2)
1)volume depletion (dehydration)
2)effective volume depletion (CHF, cirrhosis)

1)PG synthesis is incr to preserve renal blood flow and the GFR
2)these pts are dependent on PGs to maintain renal perfusion
Risk factors for NSAID-induced renal failure (7)
1)renal insufficiency
2)CHF
3)cirrhosis
4)hypovolemia
5)elderly
6)dehydration
7)concomitant ARB/ACEI use
ACEI/ARB and people w/ ___ and ___ causes problems...(3)
1)volume depletion (dehydration)
2)effective volume depletion (CHF, cirrhosis)

1)angiotensin2 increases the intraglomerular pressure in order to maintain/incr GFR
2)these pts are dependent on AG2 to maintain renal perfusion
3)pts w/ bilateral renal artery stenosis are dependent on AG2 to maintain renal perfusion
Risk Factors for ACEI/ARB induced renal failure (7)
1)CHF
2)cirrhosis
3)hypovolemia
4)elderlly
5)dehydration
6)renal insufficiency
7)concomitant NSAID/COX2 use
Mechanism of Radiocontrast media induced renal failure (2)
1)osmotic diuresis (causing volume depletion and hypotension)
2)direct tubular toxin
Risk factors for Radiographic Contrast Media induced renal failure (3)
1)renal insufficiency
2)volume depletion or effective volume depletion
3)large doses of RCM
Manifestations of RCM induced renal failure (3)
1)initial diuresis
2)then a PreRenal state (volume depletion and hypotension)
3)then onto ATN (loss of urine []ing ability) (FEna over 1%, incr Una, decr Uosm)
Prevention of RCM induced renal failure (3)
1)ID high-risk pts
2)saline prehydration (500mL IV over 30min before; 500mL IV over 30min after)
3)Acetylcysteine (600mg po q12h for 4 doses, 2 doses prior/2 doses after RCM)
RCM induced renal failure treatment(2) and prognosis (2)
1)maintain F&E
2)tx as PreRenal or ATN

1)transient/txable PreRenal ARF up to..
2)irreversible renal failure requiring dialysis
Brief ATN description (2)
1)tubule cells die and slough off into tubule lumen
2)forms casts that obstruct the tubule and prevent glomerular filtration
Drugs that induce ATN (3)
1)aminoglycosides
2)amphotericin B
3)cisplatin and carboplatin
Aminoglycosides and ATN
a)drugs (2)
b)prevalence
c)mechanism (3)
a)gentamicin and tobramycin
b)10-20% of pts

c1)AGs filtered/taken up by and stored in the proximal tubular cells
c2)accumulation of AGs induces renal injury
c3)onset of ATN will be 5days after start of therapy (but can cause renal failure several days after stopping therapy)
Aminoglycoside/ATN risk factors (6)
1)high doses/long duration
2)high troughs (over 2)
3)renal insufficiency
4)elderly
5)hypotension/volume depletion
6)decr K/Mg
AG induced ATN manifestations (5)
1)decr K/Mg
2)nonoliguria
3)proteinuria
4)incr SCr
5)ATN (loss of urine []ing ability/dirty brown casts in urine)
Prevention of AG induced ATN (3)
1)fluids
2)PK monitoring
3)extended interval dosing (24hr vs. normal q8h dosing)
Tx of AG induced ATN (3 and one w/ 3)
1)F&E management
2)use alternative abx if possible

3)tx as ATN
a)restrict Na (less than 2g/d)
b)restrict water (less than 1L/d)
c)avoid excess fluid hydration
AG induced ATN prognosis (3)
1)return to baseline renal fxn within 21d after dc of AG
2)will take longer if pt is hypovolemic/hypotensive
3)irreversible renal damage may occur w/ prolonged courses
Amphotericin B desc (5)
1)IV antifungal
2)many ADRs (amphoterrible)
COMMON:
a)infusion-related rxns
b)electrolyte disorders
c)ARF in 80%
Amphotericin B mechanism of nephrotoxicity (6)
1)renal vasoconstriction
2)bind tubular cells
3)incr cell permeability
4)histologic damage
5)ischemia
6)tubule cell death
Amphotericin B risk factors (3)
1)high dose
2)volume depletion
3)renal insufficiency
Amphotericin B induced ATN manifestations (2)
1)decr K/Mg
2)ATN (loss of urine []ing ability--FEna less than 1%, incr Una, decr Uosm & dirty brown casts in urine & oliguria)
Prevention of Amphotericin B induced ATN (3)
1)fluids (500mL IV over 30min before & 500mL IV over 30min after)
2)BUT DO NOT THIS 1) FOR A PT W/ ATN
3)ALSO NOT GOOD FOR PTS UNABLE TO TOLERATE THE NA LOAD
Tx of Amphotericin B induced ATN (3 and one w/ 3)
1)F&E management
2)change antifungal if possible

3)tx as ATN
a)restrict Na (less than 2g/d)
b)restrict water (less than 1L/d)
c)avoid excess fluid hydration
Amphotericin B alternatives (3) and prognosis (2)
1)lipid based AmB products (but these are freakin expensive)
2)these have decr ADRs, decr ARFs
3)only use in pts that fail AmB

1)gradual return to baseline
2)may be irreversible
Incidence of ARF w/ the -platins (3)
1)cisplatin 25-40%
2)less w/ carboplatin
3)rare w/ oxaliplatin
Mechanism of nephrotoxicity/ATN by platins (2)
1)direct tubular damage (impaired enzymes/energy)
2)onset at 10days, but may be cumulative w/ subsequent cycles
Cisplatin induced ATN risk factors (4)
1)radiation/nephrotoxins
2)renal insufficiency
3)elderly
4)hypotension/volume depletion
Cisplatin induced ATN manifestations (3)
1)SEVERE decr Mg (may be irreversible)
2)decr K/Ca
3)ATN (loss of urine []ing ability--FEna over 1%, incr Una, decr Uosm & dirty brown casts in urine & oliguria)
Cisplatin induced ATN
a)prevention (3)
b)tx (3 and one w/ 3)
a)hydration
b)force diuresis
c)but w/ 1&2 monitor chemotherapy efficacy w/ amifostine

b)F&E management
b)alternative chemo if possible
c)tx ATN
a)restrict Na (less than 2g)
b)restrict water (less than 1L)
c)avoid excessive fluid hydration
Cisplatin induced ATN prognosis (2)
1)mild and reversible w/ initial course
2)more severe and less reversible w/ subsequent
Allergic Interstitial Nephritis
a)happens w/... (3)
b)onset
a1)B-lactams (penicillin, cephalosporins
a2)quinolones
a3)sulfonamides
b)7-10d after exposure
Allergic Interstitial Nephritis mechanism (4)
1)drug-host protein antigen enters renal tubule
2)initiates inflammatory rxn and eosinophils in interstitium
3)enlarges kidney
4)tubule damage occurs
Allergic Interstitial Nephritis risk factors (2)
1)idiopathic allergic rxn
2)consider/monitor pts w/ other drug allergies
Allergic Interstitial Nephritis
a)manifestations (4)
b)tx (2)
c)prognosis (2)
a1)fever
a2)rash
a3)loss of urine []ing ability (FEna over 1%, incr Una, decr Uosm)
a4)WBCs and eosinophils on UA

b1)stop offending agent
b2)prednisone 1mg/kg for 7d then taper

c1)most recover to normal renal fxn (when med dc'd)
c2)though permanent damage may occur
Rhabdomyolysis mechanism (4)
1)muscle necrosis
2)release of muscle breakdown products
3)leads to renal damage
4)severity ranges from asymptomatic to life threatening
Rhabdomyolysis
a)drugs causing it (2)
b)drug combo's that incr risk of rhabdo (3)
a1)COCAINE (life-threatening cases are mostly w/ this)
a2)statins

1)gemfibrozil w/ statin
2)niacin w/ statin
3)CYP3A4 inhibitors w/ statin (macrolide, antifungals)
Mechanism of nephrotoxicity w/ rhabdo (3)
1)breakdown of muscle cells releases CPK, lactate deH, myoglobin
2)myoglobin is eliminated by kidneys and forms casts in tubule cells
3)causes obstruction of GFR (CAUSING ATN)
Manifestations of rhabdo (7)
1)myalgias
2)fatigue
3)incr CPK
4)incr LDH
5)incr lactic acidosis
6)incr K
7)myoglobin on UA
Tx of rhabdo incuded nephrotoxicity (3) AND prognosis(2)
1)aggressive fluids (to protect kidney from myoglobins)
2)use vigorous diuresis
3)alkalinization of urine (w/ NaHCO3 in IV)

1)prompt tx may reverse renal damage
2)poor prognosis if untreated