ACUTE RENAL

FALURE
'ER'EW
Uefinitions
Classifioation and oauses
Clinioal manifestations
Management
EFNTN ACUTE RENAL FALURE
(ARF)
oute renal failure is a syndrome of
varying oausation that results in a
sudden deoline in renal funotion. lt is
frequently assooiated with an
inorease in BuN and oreatinine,
oliguria (less than 500 mL urine/24
hours), hyperkalemia, and sodium
retention.
ARF
oours over hours/days
Lab definition
lnorease in baseline oreatinine of more than 50
Ueorease in oreatinine olearanoe of more than 50
Ueterioration in renal funotion requiring dialysis
ARF EFNTNS
nuria - no urine output or less than
100mls/24 hours
liguria - <500mls urine output/24 hours or
<20mls/hour
Polyuria - >2.5L/24 hours
ARF
Pre renal (funotional)
Renal-intrinsio (struotural)
Post renal (obstruotion)
ARF Pirouz Daeihagh, M.D.Internal medicine/Nephrology Wake Forest University School of Medicine. Downloaded 4.6.09
CAUSES F ARF
Pre-renal:
lnadequate perfusion
oheok vo|ume srarus
Renal:
Rl despite perfusion & exoretion
oheok ur|na|,s|s, lB0 & auro|mmune soreen
Post-renal:
Blooked outflow
oheok b|aooer, oarherer & u|rrasouno
CAUSES F ARF
!70703, #03, !489703,
Absolute
hypovolaemia
Glomerular
(RPGN)
Pelvi-calyceal
Relative
hypovolaemia
Tubular
(ATN)
Ureteric
Reduced
cardiac output
Interstitial
(AIN)
VUJ-bladder
Reno-vascular
occlusion
Vascular
(atheroemboli)
Bladder neck-
urethra
ARF PRE RENAL
Ueoreased renal perfusion without oellular
injury
70 of oommunity aoquired oases
40 hospital aoquired oases
ARF NTRNSC
oute tubular neorosis (%N)
lsohaemia
%oxin
%ubular faotors
oute interstitial Neorosis (lN)
lnflammation
oedema
0lomerulonephritis (0N)
Uamage to filtering meohanisms
Multiple oauses as per previous presentation
ARF PST RENAL
Post renal obstruotion
bstruotion to the urinary outflow traot
Prostatio hypertrophy
Blooked oatheter
Malignanoy
PRERENAL FALURE 1
W1ten rapidly reversible i1 e can identi1y this early.
WThe elderly at high risk because o1 their predisposition to
hypovolemia and renal atherosclerotic disease.
WThis is by de1inition rapidly reversible upon the restoration o1
renal blood 1lo and glomerular per1usion pressure.
WTHE KIDNEYS ARE NRMAL.
WThis ill accompany any disease that involves hypovolemia,
lo cardiac output, systemic dilation, or selective intrarenal
vasoconstriction.
ARF Anthony Mato MD Downloaded 5.8.09
FFERENTAL AGNSS 2
ypovolemia
0l loss: Nausea, vomiting, diarrhea (hyponatraemia)
Renal loss: diuresis, hypo adrenalism, osmotio
diuresis (UM)
3equestration: panoreatitis, peritonitis,trauma, low
albumin (third spaoing).
emorrhage, burns, dehydration (intravasoular
loss).
ARF Anthony Mato MD Downloaded 5.8.09
FFERENTAL AGNSS 3
Renal vasooonstriotion: hyperoaloaemia,
adrenaline/noradrenaline, oyolosporin, taorolimus,
amphoterioin B.
3ystemio vasodilation: sepsis, medioations, anesthesia,
anaphylaxis.
Cirrhosis with asoites
epato-renal syndrome
lmpairment of autoregulation: N3lUs, CL, RBs.
ypervisoosity syndromes: Multiple Myeloma, Polyoyaemia
rubra vera
FFERENTAL AGNSS 4
Low C
Myooardial diseases
valvular heart disease
Perioardial disease
%amponade
Pulmonary artery hypertension
Pulmonary Lmbolus
Positive pressure meohanioal ventilation
THE NLY RGAN WTH
ENTRY AN EXT ARTERES
RENAL BL FLW 5
RAP - RvP
RBF
R
aff
+ R
eff
=
F = P/R
RAP
RBF
R
aff
+ R
eff
~
Malcolm Cox
R
aff
R
eff
RAP
P
CC
Malcolm Cox
GLERULAR BL FLW
A11erent arteriole
E11erent art
Glomerular
Capillaries &
Mesangium
Constrictors: endothelin,
catecholamines, thromboxane
Compensatory
Constrictor:
Angiotensin II
Blocker:
ACE-I
Compensatory
Dilators:
Prostacyclin, N
Blocker:
NSAID
PRE-RENAL AZTEA
PATHPHYSLGY 7
Renal hypoperfusion
Ueoreased renal blood flow and 0lR
lnoreased filtration fraotion (0lR/RBl)
lnoreased Na and
2
reabsorption
liguria, high u
osm
, low u
Na
Llevated BuN/Cr ratio
Malcolm Cox
ARF NTRNSC CAUSES 1
%N
lN
0N
ACUTE TUBULAR NECRSS (ATN)
CLASSFCATN
lsohemio
Nephrotoxio
ATN
ATN
ACUTE RENAL FALURE
NEPHRTXC ATN
Lndogenous %oxins
eme pigments (myoglobin, hemoglobin)
Myeloma light ohains
Lxogenous %oxins
ntibiotios (e.g., aminoglyoosides, amphoterioin B)
Radiooontrast agents
eavy metals (e.g., ois-platinum, meroury)
Poisons (e.g., ethylene glyool)
ATN
ATN
ACUTE NTERSTTAL NEPHRTS
CAUSES
llergio interstitial nephritis
Urugs
lnfeotions
Baoterial
viral
3arooidosis
ALLERGC NTERSTTAL NEPHRTS(AN)
CLNCAL CHARACTERSTCS
lever
Rash
rthralgias
Losinophilia
urinalysis
Miorosoopio hematuria
3terile pyuria
Losinophiluria
AN
CHLESTERL EBLZATN
CNTRAST-NUCE ARF
PRE'ALENCE
Less than 1 in patients with normal renal
funotion
lnoreases signifioantly with renal insuffioienoy
CNTRAST-NUCE ARF
RSK FACTRS
Renal insuffioienoy
Uiabetes mellitus
Multiple myeloma
igh osmolar (ionio) oontrast media
Contrast medium volume
CNTRAST-NUCE ARF
CLNCAL CHARACTERSTCS
nset - 24 to 48 hrs after exposure
Uuration - 5 to 7 days
Non-oligurio (majority)
Uialysis - rarely needed
urinary sediment - variable
Low fraotional exoretion of Na
PRE-PRCEURE PRPHYLAXS
1. lv lluid (N/3)
1-1.5 ml/kg/hour x12 hours prior to prooedure and 6-12 hours
after
2. Muoomyst (N-aoetyloysteine)
lree radioal soavenger, prevents oxidative tissue damage 600mg
po bd x 4 doses (2 before prooedure, 2 after)
3. Bioarbonate (1M 2004)
lkalinizing urine should reduoe renal medullary damage
5 dextrose with 3 amps C3, bolus 3.5 mL/kg 1 hour
preprooedure, then 1mL/kg/hour for 6 hours postprooedure
4. Possibly helpful? lenoldopam, Uopamine
5. Not helpful! Uiuretios, Mannitol
CNTRAST-NUCE ARF
PRPHYLACTC STRATEGES
use l.v. oontrast only when neoessary
ydration
Minimize oontrast volume
Low-osmolar (nonionio) oontrast media
N-aoetyloysteine, fenoldopam
ARF Anthony R Mato MD Downloaded 5.8.09
ARF PST-RENAL CAUSES 1
lntra-renal bstruotion
oute urio aoid nephropathy
Urugs (e.g., aoyolovir)
Lxtra-renal bstruotion
Renal pelvis or ureter (e.g., stones, olots,
tumors, papillary neorosis, retroperitoneal
fibrosis)
Bladder (e.g., BP, neuropathio bladder)
urethra (e.g., strioture)
ACUTE RENAL FALURE
AGNSTC TLS
urinary sediment
urinary indioes
urine volume
urine eleotrolytes
Radiologio studies
URNARY SEENT (1)
Bland
Pre-renal azotaemia
urinary outlet obstruotion
URNARY SEENT (2)
RBC oasts or dysmorphio RBCs
oute glomerulonephritis
3mall vessel vasoulitis
RE BL CELL CAST
RE BL CELLS
Monomorphic
Dysmorphic
YSRPHC RE BL CELLS
YSRPHC RE BL CELLS
URNARY SEENT (3)
BC Cells and BC Casts
oute interstitial nephritis
oute pyelonephritis
WHTE BL CELLS
WHTE BL CELL CAST
URNARY SEENT (4)
Renal %ubular Lpithelial (R%L) oells, R%L oell
oasts, pigmented granular (muddy brown")
oasts
oute tubular neorosis
RENAL TUBULAR EPTHELAL CELL
CAST
PGENTE GRANULAR CASTS
ACUTE RENAL FALURE
URNE 'LUE (1)
nuria (< 100 ml/24h)
oute bilateral arterial or venous ooolusion
Bilateral oortioal neorosis
oute neorotizing glomerulonephritis
bstruotion (oomplete)
%N (very rare)
ACUTE RENAL FALURE
URNE 'LUE (2)
liguria (<100 ml/24h)
Pre-renal azotemia
%N
Non-liguria (> 500 ml/24h)
%N
bstruotion (partial)
ACUTE RENAL FALURE
URNARY NCES
U
82
(282L)
(UP)
Cr
U
Na
(2EqL)
RF FE
Na
ATN
ATN
ATN
ATN ATN
PR PR
PR
PR
PR
1.0 1.0
350
500 40
20
40
20
ARF URNE NCES
urinary lndioes,
lL Na = (u/P)
Na
X (P/u)
Cr
X 100
lLNa < 1 C/ Pre-renal state
May be low in seleoted intrinsio oause
Contrast nephropathy
oute 0N
Myoglobin induoed %N
lLNa> 1 C/ intrinsio oause of Rl
FENA = (URNE NA X PLASA CR)
(PLASA NA X URNE CR)
leNa <1
1. PRLRLNL
urine Na < 20. lunotioning tubules reabsorb lots of filtered Na
2. %N (unusual)
Postisohemio dz: most of uP oomes from few normal nephrons,
whioh handle Na appropriately
%N + ohronio prerenal dz (oirrhosis, Cl)
3. 0lomerular or vasoular injury
Uespite glomerular or vasoular injury, pt may still have well-preserved
tubular funotion and be able to oonoentrate Na
RE FENA
leNa 1-2
1. Prerenal-sometimes
2. %N-sometimes
3. lN-higher leNa due to tubular damage
leNa >2
1. %N
Uamaged tubules oan't reabsorb Na
CALCULATNG FENA AFTER PT HAS
GTTEN LASX...
Caution with oaloulating leNa if pt has had Loop Uiuretios in past 24-48
h
Loop diuretios oause natriuresis (inor urinary Na exoretion) that raises u
Na-even if pt is prerenal
3o if leNa>1, you don't know if this is beoause pt is euvolemio or
beoause Lasix inoreased the u Na
3o helpful if leNa still <1, but not if leNa >1
1. lraotional Lxoretion of Lithium (endogenous)
2. lraotional Lxoretion of urio oid
3. lraotional Lxoretion of urea
HYRNEPHRSS
NRAL RENAL ULTRASUN
HYRNEPHRSS
HYRNEPHRSS
ARF-SGNS AN SYPTS
eight gain
Peripheral oedema
ypertension
ARF SGNS AN SYPTS
yperkalemia
Nausea/vomiting
Pulmonary edema
soites
sterixis
Lnoephalopathy
LAB FNNGS
Rising oreatinine and urea
Rising potassium
Ueoreasing b
oidosis
yponatraemia
ypooaloaemia
X ARF
lmmediate treatment of pulmonary edema and hyperkalaemia
Remove offending oause or treat offending oause
Uialysis as needed to oontrol hyperkalaemia, pulmonary edema,
metabolio aoidosis, and uremio symptoms
djustment of drug regimen
usually restriotion of water, Na, and K intake, but provision of adequate
protein
Possibly phosphate binders and Na polystyrene sulfonate
RECGNSE THE AT-RSK PATENT
Reduoed renal reserve:
Pre-existing CRl, age > 60, hypertension,
diabetes
Reduoed intra-vasoular volume:
Uiuretios, sepsis, oirrhosis, nephrosis
Reduoed renal oompensation:
CL-l's (%ll), N3lU's (P0's), Cy
ACUTE TUBULAR NECRSS
CLNCAL CHARACTERSTCS
Characteristic Oliguric ATN Non-Oliguric ATN
Incidence 41% 59%
Toxin-induced 8% 30%
UV (ml/24h) < 400 1,280 + 75
U
Na
(mEq/L) 68 + 6 50 + 5
FE
Na
(%) 6.8 + 1.4 3.1 + 0.5
Dialysis required 84% 26%
Mortality 50% 25%
ASSESSENT F 'LUE STATUS
%otal Body ater:
weight, serum Na
LCl (= %otal Body Na):
oedema, skin turgor
lntravasoular:
venous: 1vP/CvP/PCP
rterial: BP (lying/sitting)
Peripheral perfusion: fingers,
toes, nose
0
10
20
30
40
50
TBW ECF Vasc
Litres
PHASES F ATN
0
100
200
300
400
500
600
700
800
900
At risk InsuIt OIiguric DiaIysis PoIyuric Recovery
Creat
NCATNS FR ACUTE ALYSS
Llu
oidosis (metabolio)
Lleotrolytes (hyperkalemia)
lngestion of drugs/lsohemia
verload (fluid)
uremia
CNCLUSN
%hink about who might be vulnerable to aoute
renal failure
%hink twioe before initiating therapy that may
oause Rl
%hink about it as a diagnosis - don't look/won't
find
ACKNWLEGEENTS
Powerpoint arvard learning - Maloolm Cox -
oute renal failure
Royal Perth ospital teaohing powerpoints
oute renal failure powerpoint - nthony Mato
Note - l have freely used their slides and
adapted to suit - with thanks