Document 6431038

University of Szeged
Faculty of Medicine
Albert SzentSzent-Györgyi
Medical and Pharmaceutical Center
First Department of Internal Medicine
Acute renal
failure
Péter Légrády MD
Acute renal diseases
without renal
failure
or
with renal
failure
glomeruli
and / or
tubuli and
interstitium
nephrosis
and / or
nephritis
Definition
• Quick decline in renal function (hours
hours,, days,
days, weeks)
weeks)
– the previously normal serum creatinine increases
over 180 umol
umol/l
/l or 1.5 folder of previous value
– accumulation of nitrogenous waste products
– electrolyte
l t l t imbalance
i b l
– less urine output ((usually
usually,, but not always)
always)
• oliguria 500 ml/24 hs
• anuria 5050-100 ml/24 hs
Definition
Acute renal failure is a syndrome
defined by a sudden loss of renal
function over several hours to
several days.
Mayo Clin Proc. 2001;76:67-74
1
Basic Facts
Classic laboratory definition
• Renal failure over the course of hours
to days
days..
• The result will be failure to excrete
nitrogenous waste and electrolyte
imbalance..
imbalance
• Hard to define:
define: in 26 studies, no two
used the same definition!!!
• Increase in more than 50
50%
% over
baseline Cr
Cr..
• Decreased
D
d in
i calculated
l l t d Cr
C Clearance
Cl
b
by
more than 50%
50%.
• Any decrease in renal function that
requires dialysis.
dialysis.
What constitutes the syndrome of
ARF?
Etiology of ARF among
outpatients
• Accumulation of nitrogenous waste
products.
• Increased sCr.
sCr.
• Decreased
D
d GFR.
GFR
• Derangement of extracellular fluid
balance.
• Acid
Acid--base disturbance.
• Electrolyte and mineral disorders.
Prerenal (70%)
Intrarenal (11%)
Obstruction(17%)
idiopathic(2%)
AJKD 17:191-198, 1991
2
Etiology of ARF among
inpatients
ATN (45%)
Prerenal (21%)
ARF on CKD (13%)
(
)
Obstruction (10%)
GN/vasc (4%)
AIN (2%)
Atheroemboli (1%)
Natural history of ARF
• 48% ICU p
patient
atientts
ts require dialysis
• 58% inpt mortality among patients who
develop ARF in the ICU
Crit Care Med 24(2);192
24(2);192-198
198, 1996
• 36 % mortality among all inpts with ARF
• 20% of survivors received dialysis
JASN 9(4):692-698, 1998
KI 50:811-818, 1996
Symptoms of acute renal
failure
•
•
•
•
•
•
•
•
•
sudden oliguria,
oliguria, anuria
waist pain
nausea
nausea,, vomitus
peripheral and/or
and/or pulmonary
oedema
hypertension
Kussmaul breathing
convulsions
depression of consciousness
hyperkalemia
The amount of urine
BUT!
• by abdominal ultrasound
(US):
Oliguria: urine output less than 500 ml/24hr.
– kidney size
• < 10 cm and
d parenchyma
h
< 10
mm
Nonoliguria: urine output greater than 500 ml/24hr.
It is chronic
chronic!!
Anuria: urine output less than 50 ml/24hr.
3
Clinical presentation of acute
renal failure
•
•
•
•
•
Acute renal failure
Prerenal
decreased renal perfusion
80% of cases
ARF settled on previous chronic
kidney disease
Renal
intrinsic renal disease
10% of cases
Postrenal
obstruction
10%
The pathophysiology of ARF
•
nephrosis syndrome
ischemic nephropathy
prolonged NSAID therapy
prolonged ACEI therapy
nephrotoxic drugs,
drugs contrast agents added on renal
failure
acute exacerbation of some immunological GN:
–
–
–
–
IgA nephropathy
lupus nephritis
membranoproliferative GN
vasculitis
Factitious ARF
• Interference with laboratory measurement of
Scr (Jaffe Method)
Acute renal failure
Prerenal
Vascular
Intrarenal
Glomerular
Postrenal
Tubular
Factitious
Interstitial
Ischemia
Toxins
– cefoxitin
– ketoacids
• Competitive inhibition of creatinine secretion
in the proximal tubule
– cimetidine
– trimethoprim
• Increased production of creatinine
– fenofibrate
Pigments
JASN 1998;9(4):710-718
4
PrePre
-renal failure
• Often rapidly reversible if we can identify this early.
• The elderly at high risk because of their predisposition to hypovolemia
and renal atherosclerotic disease.
• This is by definition rapidly reversible upon the restoration of renal
blood flow and glomerular perfusion pressure.
• THE KIDNEYS ARE NORMAL (>10 cm).
• This will accompany any disease that involves hypovolemia, low cardiac
output, systemic dilation, or selective intrarenal vasoconstriction.
- 70%
70% of community acquired cases
cases..
- 40%
40% of hospital acquired cases
cases..
The causes of pre
pre-renal ARF
Reduction in effective extracellular
volume
• hypovolemia
–
–
–
loss of fluid (trauma, surgical, GI,
renal, pulmonary, skin)
bleeding
hypalbuminemia
• heart failure
–
–
–
–
Defect of renal autoregulation
• vasoconstriction of afferent
arterioles
myocardial dysfunction
valvular disease
pericardial tamponade
pulmonary hypertension
–
–
–
–
•
hepatorenal sy
sepsis
hypercalcemia
drugs
g (NSAID,
(
, cyclosporine,
y
p
,
epinephrine, norepinephrine)
vasodilation of effernt arterioles
–
–
ACEI
ARB
• vasodilation
–
–
–
–
sepsis
cirrhosis
anaphylaxis
drug
high htc, se BUN/se creat > 80, concentrated urine (density >1020,
Osm > 500 mOsm, low urine Na (< 20 mmol/l)
Klinikai nephrologia. Ed.: Kakuk György, Medicina, Bp. 2004.
Differential diagnosis
• Hypovolemia
– GI loss: nausea,
ausea, vomiting, diarrhea
– Renal loss: diuresis
diuresis,, hypo adrenalism,
adrenalism,
osmotic diuresis (DM)
– Sequestration: pancreatitis,
peritonitis,trauma,, low albumin.
peritonitis,trauma
– Hemorrhage, burns, dehydration.
Differential diagnosis
• Renal vasoconstriction: hyper Ca, norepi,
norepi, epi,
epi,
cyclosporine, tacrolimus
tacrolimus,, ampho B.
• Systemic vasodilation
vasodilation:: sepsis, medications,
anesthesia, anaphylaxis.
• Cirrhosis
Ci h i with
ith ascites
it
• Hepato
Hepato--renal syndrome
• Impairment of autoregulation
autoregulation:: NSAIDs, ACE,
ARBs.
• Hyperviscosity syndromes: MM, WM,
5
The causes of renal ARF
Differential diagnosis
• Low CO
–
–
–
–
–
–
myocardial diseases
valvular heart disease
pericardial disease
tamponande
pulmonart HTN
pos pressure mechanical ventillation
Arterial and venous occlusions of the
renal vessels
• acute occlusion of renal artery
–
–
–
–
atherosclerosis
aorta aneurysm
invasive vascular procedure
jeopardy of embolism
–
–
–
severe nephrosis sy
severe hypalbuminemia (< 15 g/l)
ARF with kidney tumor
Renoparenchymal diseases
• acute tubular necrosis
–
–
ischemic ATN
toxic ATN (endogenous and exogenous
toxic agents)
•
intrarenal obstruction
•
intrarenal vascular damage
•
•
glomerular diseases
interstitial diseases
• thrombosis of renal vein
–
cristals, debris of cells, casts
–
–
–
–
–
–
–
thrombotic microangiopathy
g p
y
HUS
connected to pregnancy
malignant hypertension
scleroderma
vasculitis
cholesterol embolisation
–
–
–
–
drugs
infections
autoimmune procedures
malignant infiltrative diseases
Klinikai nephrologia. Ed.: Kakuk György, Medicina, Bp. 2004.
Intrinsic renal disease
• Anatomic organization seems to work
best.. ARF does not aequal ATN.
best
ATN.
• 30
30%
% of cases of intrinsic renal failure
y evidence of
f ATN on
will not show any
urin analysis
–
–
–
–
glomerulus
Vessels
Interstitum
tubules
Common causes of acute tubular
necrosis
surgical operations, extended
hypovolemia, sepsis
ischemia
exogenous
aminoglikoside, amphotericine,
vancomycine, contrast agent,
cisplatine, acetaminofene, heavy
metals, organic resolvents
endogenous
myoglobin, hemoglobin, light chain,
urates, calcium, phosphorus,
oxalate,
toxic
6
ATN: Toxic
ATN
• Ischemic Injuries to the renal tubule:
– Takes 1-2 weeks to recover from after perfusion
has been normalized.
normalized.
– In the extreme form this can lead to bilateral renal
cortical necrosis
• Three phases:
phases:
– Initiation phase
– Tubuloglomerular feedback
feedback:: afferent arteriole
constriction triggered by an increase in the salt
delivery sensed by the macula densa
densa..
– Recovery phase:
phase: tubular epithelial cell repair and
regeneration.. This may be associated with a marked
regeneration
diuretic phase.
phase.
Differentiation of prepre-renal kidney
failure and acute tubular necrosis
prepre
-renal
ATN
urine osmol.
> 500 mOsm
< 350 mOsm
urine Na
< 20 mmol/l
> 40 mmol/l
FENa
<1%
>2%
sediment
negative
casts, epithel
cells
urine creat/se.
creat.
> 20:1
10
10--15:1
rate of sese-creat.
< 40 umol/day
> 40 umol/day
• Exogenous
–
–
–
–
–
–
–
Radiocontrast
CSP
TAC
Amino glycosides
Chemotherapy
Ethylene glycol
Tylenol
• Endogenous
–
–
–
–
–
Myoglobin
Hemoglobin
Uric acid
Oxylate
Light chains
Acute interstitial nephritis:
nephritis:
allergic
Allergic reaction in the tubules. IT IS
PARAMOUNT TO IDENTIFY THE
OFFENDING AGENT AND REMOVE
IT. There may be some role for
steroids in the case of AIN.
7
Acute interstitial nephritis
Drugs
• Antibiotics
–
penicillines, cephalosporines,
sulfonamides, rifampicine,
nitrofurantoine, quinolones,
macrolides, tetracycline,
vancomycine, acyclovire
•
Analgetics/NSAIDs
•
Others
–
–
5-ASA, p
paracetamol, aspirin,
p
amidazophene, ibuprofene, stb.,
thiazids, triamterem, furosemide,
chlorthalidon, cimetidine, ranitidine,
famotidine, omeprazole, allopurinol,
propylthiouracil, phenytoine,
carbamazepine, diazepam,
azathioprine, cyclosporine,
interferon, streptokinase, warfarin,
contrast agent, captoprile, „crack”,
„mega”--Vitamin C
„mega”
Infections
• Bacteria
–
Streptococcus, diphtheria,
Leptospira, Legionella, Pneumococcus,
malta fever, typhus, Yersinia
Acute nephritis syndrome
• oliguria
• azotemia
= ARF
•
Viruses
•
Fungi
• hypertension,
hypertension headache
•
Others
• red
red-brown, cola
cola-like colored urine
–
hantavirus, CMV, EBV, adenovirus,
polyoma, HIV, HAV, morbilli, german
measles, influenza, Coxsackie
–
candidiasis, histoplasmosis
–
mycoplasma, toxoplasma, malaria,
schistosomiasis, leishmaniasis
- may be with fever, rash, joint pain, eosinophiles; or only with renal failure,
- pyuria, granular casts, RBCs, eosinophiles in urine in 75 % (except NSAID)
- < 1.5 g protein
Diseases causing acute
nephritis syndrome
• post
post-streptococcal GN: acute diffuse
proliferative GN
• IgA nephropathy
• membranoproliferative GN
• SLE: focal or diffuse proliferative GN
• oedema - periorbital, mainly in the morning
(macroscopic hematuria)
• active urine sediment:
dysmorphic RBCs , RBC casts, WBCs, WBC
and granular casts, amorphic granules
quick (days, weeks) developing symptoms
Rapidly progressive GN
RPGN (Rapidly Progressive
Glomerulonephritis)) is a
Glomerulonephritis
syndrome defined by the rapid
loss of renal function over days
to weeks due to acute
glomerulonephritis..
glomerulonephritis
• RPGN
8
Rapidly progressive GN
• insidious beginning
Rapidly progressive GN
•
• quick and progressive GFR decline
•
• oliguria
•
• hematuria / proteinuria
• kidney size larger, structure slackened,
(abdominal US)
• nephritis sy., rarely nephrosis sy.
• crescents > 70 %
Rapidly progressive GN –
treatment
Rapidly progressive GN
I. Anti
Anti--GBM antibodies (linear IF)
Goodpasture--sy.,
• Goodpasture
• anti
anti--GBM sy.,
• without pulmonological symptoms, only kidney affected
II. Immunocomplex GN (granular IF)
• primary GN: IgA GN, membranoproliferative GN
• postinfectious: sepsis, abscess, endocarditis, HBV,
post--streptococcal GN
post
• autoimmune: SLE
III. ANCA associated GN (no IF = „pauci” immune)
• Wegener granulomatosis
• microscopic polyarteritis
• Churg
Churg--Strauss sy
• RPGN with ANCA
• „idiopathic” crescent GN
Clinical features:
– cold or viral prodrome
Symptoms: weakness, nausea, vomitus, waist pain, hemophtysis, oliguria,
rised BP
Dg.:
– urine:
• hematuria (dysmorphic RBCs)
• 100 % casts (granular, RBC)
• 100 % proteinuria
– kidney function:
• creatinine
creatinine--clearance: < 20 ml/min approx. 30 %
– normal kidney size
– anemia: normocyter, normochrom
– serologycal disparities
– histology: renal biopsy
• quick diagnosis
• steroid
• cytotoxic agents
•
•
•
•
•
– cyclophosphamide,
cyclophosphamide chlorambucil,
chlorambucil azathioprine
micophenolate mofetil
plasmapheresis
extracorporal immunoabsorption
dialysis (depending on kidney function)
transplantation
9
Rapidly progressive GN –
steroid therapy
• Intravenous pulse therapy followed with
oral supporting therapy:
– methylprednisolone 1 g/day for 33-5 days,
and after
– orally 1 mg/kg/day decreasing step by step
to 4
4--8 mg/day for 12
12--24 months
• Continuous oral therapy:
– methylprednisolone 1-1.5 mg/kg for 4
4--6
weeks, decreasing step by step to
supporting dose
Rapidly progressive GN –
plasmapheresis
• change of 4 litre plasma
• 7-10 times
• with fresh frosened plasma
Rapidly progressive GN –
cytostatic therapy
• cyclophosphamide
– oral 150
150--200 mg/day
– i. v. 10 mg/kg monthly
• chlorambucil
– oral 5 mg/day
• azathioprine
– oral 100
100--150 mg/day
• dose reduction:
– no. of WBCs < 4.000
– no. of platelets < 100.000
Acute urate nephropathy
(AUAN)
- blood uric acid level suddenly increased
- insufficient proximal tubular reabsorption
- uric acid crystals precipitating in tubules → damage of tubular epithel
cells
- bigger crystal precipitates → renal colic, obstruction of ureters
Klinikai nephrologia. Szerk.: Kakuk György, Medicina, Bp. 2004. 417417-420.
10
Acute urate nephropathy
(AUAN)
Clinical features:
• oligo
oligo--anuric ARF
• urate crystals in urine sediment
(BUT! not with obstructed ureters)
• no specific symptoms
• waist p
pain, renal colic
• labs: uric acid ↑ (even > 900
+
µmol/l),
P ↑, K ↑, Ca ↓,
yes
tumorlysis syndrome
after therapy
no
spontaneous
tumorlysis syndrome
Treatment of acute urate
nephropathy
Prevention
With ARF
• high dose (600
(600--900 mg) allopurinol
started 2 days before chemotherapy or
irradiation
• rasburicase (urate
(urate--oxidase)
• normalise metabolic parameters
• urine > 2500 ml/day
• (parenteral) fluid intake (start it before
2 days and stop it after 22-3 days of
therapy)
• diuretics (furosemide, mannitol)
• alkalify urine (NaHCO3)
pH: 7.0 – 7.5
– ph < 7.0 uric acid precip.
– ph > 7.5 xantine percip.
• allopurinol in reduced dose
• forced diuresis (high dose furosemide and
mannitol)
• hemodialysis (if P ↑ -> daily)
daily)
• NaHCO3 is not adviced in oliguria and it
could be dangerous in hyperphosphatemia
(Ca--P deposits)
(Ca
• rasburicase (urate
(urate--oxidase)
Klinikai nephrologia. Ed.: Kakuk György, Medicina, Bp. 2004. 417417-420.
PostPost
-renal causes
If we can identify this early, this can
be readily reversible. This accounts
for fewer than 5% of cases of ARF.
Differential diagnosis
• BPH (No
(No11)
• Prostatitis
• Prostate
/
Cervical
cancer
p
fibrosis
f
• Retroperitoneal
/ disorders
• Extraluminal malignancy
• Neurogenic bladder /
anticholinergic drug use
use::
functional obstruction
• Bilateral renal calculi
• Myeloma light chains
• Papillary necrosis
• Urethritis with spasm
• Inadvertent
surgical
ligature
• Intraluminal Thrombosis
• Intraluminal (collecting
system) crystal disease
• Uric acid
• Calcium oxylate
• Acyclovir
• Sulfonamide
• MTX
11
Acute obstruction of urinary
tract
Intrinsic causes
–
–
–
–
–
–
papillanecrosis
blood clot
stones
tumors (carcinomas
carcinomas))
stricture (trauma)
infections (schistosomiasis)
schistosomiasis)
•
Extrinsic causes
–
–
–
–
–
pregnancy
gynecological tumors
prolapse of the uterus
ovariall cysts
prostatic hyperplasia
hyperplasia,, prostatic
hypertrophy
– M. Crohn
– aorta aneurysm
– surgical causes (ligature
ligature))
Acute renal failure
ailure:: Diagnostic
work
ork-up
• Chem
•
• Urine electrolytes •
•
• Urinalysis with
Microscopic
Mi
i
analysis
*
• Renal ultrasound
BUN/Cr ratio > 1515-20
Na and CO2 may be high
FeNa
FeNa*
* = Cr S x NaU x
100
CrU x Na S
< 1 prerenal,
prerenal, >1 renal
• Urinary Na < 20
• Urine Osms > 500
Klinikai nephrologia. Ed.: Kakuk György, Medicina, Bp. 2004.
Other useful tests
•
•
•
•
24 hour urine for protein and creatinine
urine eosinophils., UPEP
cholesterol,, albumin,, glucose
g
ANA panel, CC-ANCA , SPEP, HIV,
Hepatitis B/C, ASO
• Renal biopsy
• Post
Post--void residual or catheterization
• PSA
Renal failure indices
• Fractional excretion of Na
Na:: this will relate the
clearance of Na to that of Cr.
Cr.
• In the case of prerenal disease Na is actively
reabsorbed to restore intravascular volume.
volume.
• This is not the case in renal injury
j y ((absorptive
p
mechanisms
h i
are broken).
b k ). In
broken)
I either
ith case Cr
C is
i NOT
reabsorbed.. So we have the makings of a
reabsorbed
comparative ratio.
ratio. The cut off is 1%.
U Na / P Na
__________ x 100% = .14% (Prerenal
(Prerenal))
U Cr / P Cr
12
Additional labs
Kidney and the potassium
• Peak Cr:
Cr:
– In prerenal disease : may fluctuate with hemodynamics
hemodynamics..
Rise will be rapid
rapid.. This is true for contrast (5 days to
peak and 7 to normal)
– Atheroembolization (later peak and return to baseline),
peak and return to baseline).
baseline)).
and ischemia ((later p
– Rise will be delayed in toxin exposure.
exposure.
• Rhabdo
Rhabdo:: elevated K, Phos
Phos,, hypocalcemia with elevations in CK
and UA
UA..
• TLS
TLS:: elevated UA, K, Phos
Phos,, low Ca, elevated Cr and elevated
LDH (intracellular enzyme)
enzyme)..
• Elevated anion gap + elevated osm gap
gap:: suggests ethylene
glycol / methanol exposure.
exposure.
• Anemia may suggest hemolysis,
hemolysis, MM, or TTP
TTP..
• Eosinophillia may suggest AIN, atheroembolic disease.
disease.
• Kidney handles it in a
unique way.
way.
• It virtually reabsorbs
100%
100
% of the K in the
proximal tubule (70
70%
%)
and the loop of henle
(30
30%
%).
• We reabsorb almost
all of the K before we
reach
the
distal
segments..
segments
Differential diagnosis
Differential diagnosis
• Increased intake : rare except in iatrogenesis
• Cellular release
–
–
–
–
–
–
–
TLS, Rhabdomyolysis, exercise, trauma
Metabolic acidosis
Insulin deficiency
Hyperkalemic periodic paralysis
Digoxin toxicity, beta blockers
Adrenal insufficiency
Succinylcholine
• Impaired excretion
– Renal failure
– Primary hypoaldosteronism
– Secondary hypoakdosteronism
• ACE,
ACE NSAIDs
NSAIDs, Heparin
Heparin, Type 4 RTA
– Aldo resistance
• K sparing diuretics, bactrim, pentamidine, sickle cell
disease, multiple myeloma.
– Gordon’s syndrome (enhanced Cl reabsorption, less
K secretion, HTN)
– Ureter Diversion to Jejunum.
13
Symptoms / Signs of
hyperkalemia
• Flaccid paralysis
• Arrhythmia
– Peaked T waves
– PR / QRS
prolongation
– AV conduction delay
– Loss of P waves
– Sine wave
– V fib
Treatment
• Prevention is the key.
key.
–
–
–
–
–
–
–
–
Appropriate volume resuscitation
resuscitation..
Renal dosing of potentially toxic meds
To estimate GFR
When appropriate follow serum drug levels for
dosage adjustment
adjustment..
Use of NSAIDS, ACR, ARBs, diuretics should be
used sparingly in patients who are hypovolemic or
have renovascular disease.
disease.
Allopurinol / IVFs use in patients high risk for TLS
TLS..
Ethanol for EG toxicity / NAC for tylenol toxicity.
toxicity.
Alkalinization of urine : to prevent MTX toxicity.
toxicity.
Treatment of ARF
•
•
•
•
•
•
•
Eliminate the toxic insult
Hemodynamic support
Respiratory support
Fluid management
Electrolyte management
Medication dose adjustment
Dialysis
More prevention
prevention of ARF
• Diminish risk of nosocomial infection
– conservative use of IV catheters
– judicious use of antibiotics
– hand
hand--washing
• Prevention of nephrotoxicity
– avoid/reduce nephrotoxins
– IV NS
– N-acetylcysteine,
acetylcysteine, sodium bicarbonate
– correct hypokalemia
hypokalemia,, hypomagnesemia
– correct/treat other systemic diseases
• Pharmacology
– avoid overlapping nephrotoxins
– follow drug levels closely
• Attention to fluid status
– Regular weights, I & O
JASN 9(4):710-718, 1998
14
PrePre
-renal disease
Intrinsic renal Disease
• Intravenious fluid
fluid:: keep in mind where
the loss is coming from and administer
fluids accordingly
accordingly..
Inotropes,
p ,
preload
p
/
afterafter
f
-load
• Inotropes
reduction, anti
anti--arrythmics
arrythmics,, mechanical
aids in CHF
CHF..
• Large volume paracentesis:
paracentesis: to decrease
intra--abdominal pressure and increase
intra
venous return from the kidneys.
kidneys.
• Intrinsic renal disease:
disease: NO SPECFIC
REVERSING THERAPIES FOR ISCHEMIC
AND NEPHROTOXIC DISEASE.
DISEASE. SUPPORTIVE
CARE..
CARE
• Follow electrolytes
electrolytes.. Avoid further insult
insult..
• GN
GN:: may respond to steroids, alkylating
agents, plasmapheresis.
plasmapheresis.
• AIN
AIN:: glucocorticoids may be of use
use..
• Malignant HTN:
HTN: control of blood pressure
pressure..
• Scleroderma: HTN and ARF may responsive to
ACE.
PostPost
-renal treatment
Predictors of dialysis in ARF
• Oliguria:
•
•
•
•
Foley catheter
Nephrostomy tube
Stenting
5% will develop a salt wasting diuresis.
diuresis.
– <400cc/24hr 85% will require dialysis
– >400cc/24hr 30
30--40% will require dialysis
•
•
•
•
•
•
Mechanical ventilation
Acute myocardial infarction
Arrhythmia
Hypoalbuminemia
ICU stay
Multi
Multi--system organ failure
JASN 9(4):692-698, 1998
Arch IM 160:1309-1313, 2000
15
Contrast-induced renal
Contrastfailure
Dialysis needs
• A : acidosis (l
(life
ife--threatening
threatening))
• E : electrolyte abnormalities
• I : intoxication (methanol, ethylene
glycol,
glycol isopropanol
isopropanol,, theophylline
theophylline,, lithium,
lithium
salicylates))
salicylates
• O : volume overload
• U : uremia ((pericarditis
pericarditis,, seizures,
encephalopathy)
•
•
•
•
Risk is 40% for patient with diabetes
Oliguria and other symptoms develop in 24 hrs
Prevention:
N-acetylcystine 600 mg po bid x 2d (1 before and day
of)
– Give 0.45% NS iv 1 ml/kg/h 12 hrs before and after
– Contrast nephropathy( defined as >0.5 mg/dl
increase)-increase)
21% of controls and 2% of NN-acetylcysteine group
Tepel, NEJM, 2000.
16