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Acute Renal Failure
 Definition and Classification
 Epidemiology
 Pathophysiology and Etiology
• Prerenal ARF
• Intrinisic ARF
• Postrenal ARF
 Pharmacologic Management of ARF
 RRT in ARF
Definition
 MDRD
eGFR= 186 x Screatˉ ¹·¹⁵⁴ X Age ˉ⁰·²°³ X 1.21 [if black] X o.74 [if
female]
Undersetimates GFR in healthy people (when GFR >60 ml/min)
 Cockcroft-Gault formula
(140-Age) X Mass (In KG) X [o.85 if female]/72 X Serum Creat

The non-steady-state conditions that prevail in ARF preclude estimation of GFR using standard formulae derived from patients with chronic kidney disease.
RR= 2.4
RR= 4.15
RR=6.37
Shortcomings
 The assignement of corresponding changes in serum creat and changes
in urine output to the same strata is not based on evidence. The criteria
that results in the least favorable rifle strata to be used.
 The patient would progress from "risk" on day one to "injury" on day
two and "failure" on day three, even though the actual GFR has been
<10 mL/min over the entire period.
 It is impossible to calculate the change in serum creatinine in patients
who present with ARF but without a baseline measurement of the
serum creat. The authors of the RIFLE criteria suggest back-calculating
an estimated baseline creat using the four-variable MDRD equation,
assuming a baseline GFR of 75 mL/min per 1.73 m2 .
Diagnostic criteria
 Abrupt (within 48 hours) absolute increase in the serum creatinine
concentration of ≥ 0.3 mg/dL (26.4 micromol/L) from baseline.
 Or a percentage increase in the serum creatinine concentration of ≥ 50
percent.
 Or oliguria of less than 0.5 mL/kg per hour for more than six hours.
•The diagnostic criteria could be applied only after volume status had been
optimized
•Urinary tract obstruction needed to be excluded if oliguria was used as the sole
diagnostic criteria
Syndromes of acute renal failure
Prerenal ARF
Intravascular volume depletion
Decreased effective blood volume
Altered intrarenal hemodynamics
preglomerular (afferent) vasoconstriction
postglomerular (efferent) vasodilation
Intrinsic ARF
Acute tubular necrosis
ischemic
nephrotoxic
acute interstitial nephritis
acute glomerulonephritis
acute vascular syndromes
Postrenal ARF
Epidemiology of ARF
 The observed incidence, etiology, and outcomes of ARF are highly
dependent upon the populations studied and the definition of ARF
employed.
 The absence of centralized registries to track the incidence and
outcomes of patients with ARF has hindered our understanding of its
epidemiology.
The changing epidemiology of
acute renal failure
NATURE CLINICAL PRACTICE NEPHROLOGY
(2006) 2,364-377
Non -ICU
ICU
Key Points
 The absolute incidence of acute renal failure (ARF) has increased in the past
two decades, while the mortality rate has remained relatively static
 The lack of a standard definition of ARF complicates the process of identifying
the factors that underlie changes in epidemiology of this condition.
 Despite the use of different definitions in different studies, various factors that
have contributed to altered epidemiology of ARF in the past few decades have
been identified
 These factors include geographical site of disease onset (developed vs
developing countries; community vs hospital vs intensive care unit), patient
age, infections (HIV, malaria, leptospirosis and hantavirus), concomitant
illnesses (cardiopulmonary failure, hematooncological disease), and
interventions (hematopoietic progenitor cell and solid organ transplantation)
Prerenal Acute Renal Failure
 GFR is reduced as a result of hemodynamic disturbances
that decrease glomerular perfusion.
 The defining feature of prerenal ARF is the absence of
cellular injury and the normalization of renal function with
reversal of the altered hemodynamic factors.
Intravascular volume
depletion
Altered intrarenal
hemodynamics
Etiologies of
Prerenal ARF
Decreased effective
arterial blood volume
Abdominal compartment
syndrome
Pathophsiology
OF PRERENAL ARF
Compensatory
mechanisms
Injury
Diagnosis of Prerenal ARF
 Hx
 P/E
 Urine sediment (usually normal, without cellular elements
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or abnormal casts, unless chronic kidney disease is present)
UNa< 15 meq/L (>20 in ATN)
U/Pcreat> 20 (<15 in ATN)
FeNa <1% (>1% in ATN)
UNa/K <1/4
BUN/creat >20
BUN/CREAT of >20 is typical, BUT is not specific to
prerenal ARF and may also be seen:
 Obstructive uropathy
 Gastrointestinal bleeding
 Other states associated with increased urea production.

FE Urea
 Patients on diuretics
 Prerenal azotemia due to vomiting on NG suctioning.
 FE Na may be low is sepsis, RCN, myoglobinuria,
nonoliguric ATN, acute GN, urinary tract obstruction
and renal allograft rejection
Significance of the fractional excretion of urea in the
differential diagnosis of acute renal failure
 102 patients were divided into three groups:
 Prerenal azotemia (N 50)
 Prerenal azotemia treated with diuretics (N 27)
 ATN (N 25)
Kidney International, Vol. 62 (2002), pp. 2223–2229
 FENa was low only in the patients with untreated plain
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prerenal azotemia while it was high in both the prerenal
with diuretics and the ATN groups.
FEUN was essentially identical in the two pre-renal
groups (27.9 2.4% vs. 24.5 2.3%), and very different
from the FEUN found in ATN (58.6 3.6%, P < 0.0001).
92% of the patients with prerenal azotemia had FENa
<1%.
48% of those patients with prerenal and diuretic therapy
had FENa <1%
89% of patients with prerenal azotemia and on diuretics
had a FEUN< 35%.
FE UREA
 Low FE urea <=35% is a more sensitive and specific
index than FE Na in differentiating between ARF due
to prerenal azotemia and that due to ATN, especially
if diuretics have been administered.
ARF Associated with ACE
Inhibitors and Angiotensin
Receptor Blockers
 Acute renal failure can develop acutely, when ACEI or ARB
therapy is initiated, or in patients receiving chronic
therapy, especially in patients with underlying CHF
 Predisposing factors:
• Advanced cardiac failure with low mean arterial pressure
• Volume depletion due to diuretic therapy
• The presence of renal vascular disease
• The concomitant use agents with vasoconstrictor effects
(NSAIDs, cyclooxygenase-2 inhibitors, cyclosporine, and
tacrolimus)
• CKD: The risk of ARF is higher in patients with chronic
kidney disease of any cause than in patients with normal
renal function
 Serum creatinine and electrolyte concentrations should be
measured before and 1 wk after initiating or changing the
dose of therapy
 An increase in serum creatinine of >0.5 mg/dl if the initial
serum creatinine is <2.0 mg/dl, or a rise of >1.0 mg/dl if
the baseline serum creatinine is >2.0 mg/dl, has been
suggested as a threshold for discontinuation of therapy
 The development of ARF should prompt an
evaluation for cardiac failure, hypotension, volume
depletion, use of a concomitant vasoconstrictive
agent, or renovascular disease.
Acute Renal Failure Associated with
NSAIDS
 Nonsteroidal anti-inflammatory drugs (NSAID)
agents inhibit the synthesis of vasodilatory
prostaglandins in the kidney.
 Risk factors:
Severe CHF
 Advanced liver disease
 Severe atherosclerotic vascular disease
 CKD

 Elderly patients are at increased risk due to the
increased prevalence of cardiac dysfunction, occult
renal vascular disease, and subclinical chronic
kidney disease.
Abdominal Compartment
Syndrome
 Unusual cause of decreased renal perfusion
associated with increased intra-abdominal
pressure
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Trauma patients who require massive volume resuscitation
Mechanical limitations of the abdominal wall (tight surgical
closures or scarring after burn injuries)
Medical etiologies that are characterized by intraabdominal
inflammation with fluid sequestration, such as bowel
obstruction, pancreatitis, and peritonitis.
Clinical manifestations
 Respiratory compromise
 Decreased cardiac output
 Intestinal ischemia
 Hepatic dysfunction
 Oliguric renal failure
 The renal insufficiency results from decreased renal
perfusion and correlates with the severity of the increased
intraabdominal pressure.
 Oliguria develops when the intraabdominal pressure
exceeds 15 mmHg, with anuria developing at pressures >30
mmHg.
Diagnosis
 The diagnosis should be suspected in patients with a
tensely distended abdomen and progressive oliguria.
 Measurement of intraabdominal bladder pressure.
 Abdominal compartment syndrome can be excluded when
the bladder pressure is <10 mmHg and is virtually always
present if the pressure is >25 mmHg.
Treatment
Abdominal decompression:
 Paracentesis if massive ascites.
 Surgical decompression is required in the majority
of patients.
 Renal failure usually recovers promptly after relief
of the increased intraabdominal pressure
Postrenal Acute Renal Failure
Etiologies of Postrenal ARF
Intrinsic
Stone
Papillary necrosis
Blood clot
TCC
Extrinsic
Retroperitoneal fibrosis
Aortic aneurysm
Retroperitoneal or pelvic
malignancy
Lower tract obstruction
Urethral stricture
BPH
Prostate CA
TCC of bladder
Bladder stones
Blood clot
Fungus ball
Neurogenic bladder
Malpositioned catheter
Urine output?
 The obstruction:
 Complete
Anuria
Normal
InComplete
Polyuria
Fluctuating
Pathophysiology
 After the acute onset of obstruction, GFR declines
progressively, but it does not fall to zero.
 Factors that maintain GFR include continued salt and
water reabsorption along the nephron, dilatation of the
collecting system, and alterations in renal hemodynamics.
 Intratubular pressure rises acutely, but it begins to decline
within the first 4 to 8 h, returning to nearly normal by 24 h.
Ureteral
Pr
1- 2 H
2-5 H
Late phase
RBF
GFR
Complete obstruction
Recovery after relief of obstruction depends on:
 Severity
 Duration
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Less than 1 wk duration, recovery complete.
Little or no recovery after 12 wk.
Partial obstruction
The course after relief of partial obstruction is less predictable
 Depends on
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Severity
Duration
Presence of infection or preexisting renal disease.
 Relief of obstruction may be accompanied by a
post-obstructive diuresis;
 Excretion of salt and water retained during the
obstruction.
 Persistent salt-wasting and impaired urinary
concentrating ability .
Diagnosis
 Elderly male patients
 Measurement of a post-voiding residual bladder
volume, either by an bedside ultrasound bladder
scan or by placement of an indwelling bladder
catheter.
Diagnosis
 Ultrasonography
 Sensitivity and specificity are high
 Non diagnostic
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Early in the course of postrenal ARF.
Severe volume depletion.
Obstruction is due to retroperitoneal disease (e.g.,
retroperitoneal fibrosis, tumors, adenopathy) encasing the
ureter and preventing dilatation
Diagnosis
 Computed tomography
 Non-contrasted CT scanning may be particularly useful for
the identification of obstructing kidney stones
Intrinsic ARF
Etiology of Intrinsic ARF
Acute tubular necrosis
Ischemic
hypotension
hypovolemic shock
sepsis
cardiopulmonary arrest
cardiopulmonary bypass
Nephrotoxic
drug-induced
aminoglycosides
radiocontrast agents
amphotericin
cisplatinum
acetaminophen
pigment nephropathy
intravascular hemolysis
rhabdomyolysis
Acute interstitial nephritis
Dug-induced
penicillins
cephalosporins
sulfonamides
rifampin
dilantin
furosemide
non-steroidal antiinflammatory drugs
Infection-related
bacterial infection
viral infections
rickettsial disease
tuberculosis
Systemic diseases
systemic lupus
erythematosus
sarcoidosis
Sjögren syndrome
tubulointerstitial nephritis
and uveitis (TINU) syndrome
Malignancy
malignant infiltration of
interstitium
multiple myeloma
Idiopathic
Acute glomerulonephritis
poststreptococcal glomerulonephritis
postinfectious glomerulonephritis
endocarditis-associated
glomerulonephritis
systemic vasculitis
hemolytic uremic
syndrome/thrombotic thrombocytopenic
purpura
rapidly progressive glomerulonephritis
(RPGN)
Acute vascular syndromes
renal artery thromboembolism
renal artery dissection
renal vein thrombosis
atheroembolic disease
ATN
 Acute tubular necrosis is the most common form of
intrinsic ARF (85 %)
 Tubular injury
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Nephrotoxic (35%)
Ischemic (50%)
Multifactorial.
 Profound ischemic injury may result in bilateral
cortical necrosis.
Prerenal
Prolonged
hypoperfusion
ATN
Ischemic ATN
Medical
Surgical
Cardiogenic shock
Sepsis
Burns
Severe volume
depletion
Cardiac
Vascular
Nephrotoxic ATN
Exogenous
• RCN
• Aminoglycosides
• Others meds
Endogenous
• Heme pigment (rhabdo, or massive
intavascular hemolysis)
Clinical course
Initiation
Maintenance
Recovery
Pathogenesis of ATN
Intrarenal
vasoconstrition
ATN
Intratubular
obstruction
Reduction in
Kf
Backleak of
glomerular
filtrate
Recovery from Ischemic Injury
In contrast to the heart and brain, where ischemic injury
results in permanent cell loss, the kidney is able to
completely restore its structure and function after acute
ischemic or toxic injury.
 The recovery from tubular necrosis involves the
dedifferentiation and proliferation of remaining viable
tubular epithelial cells followed by reestablishment of
cellular polarity, normal histologic appearance, and
physiologic function.
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Under normal circumstances, renal tubular cells in vivo are
quiescent and do not divide in response to growth factors.
After ischemic or toxic injury, alterations in gene
expression are observed that are similar to those induced in
vitro by growth factors.
Multiple growth factors, including (IGF-1), (EGF), and
(HGF), and their receptors are upregulated during the
regenerative process after renal injury
Administration of exogenous IGF-1, EGF, or HGF to
experimental animals after ischemic or toxic renal injury
accelerates renal regeneration.
Concern has been raised, that growth factors may also have
a deleterious effect, augmenting tubulointerstitial injury
and fibrosis.
Short-term Outcomes
 The outcome of ATN is highly dependent on the
severity of comorbid conditions.
 Uncomplicated ATN is associated with mortality
rates of 7 to 23%
 Mortality of ATN in postoperative or critically ill
patients with multisystem organ failure is high as
50 to 80%.
 Mortality rates increases with the number of failed
organ systems
Long-term Outcomes
 Long-term outcomes of patients who survive are
good.
 Of a population of 979 critically ill patients with
ARF who required RRT (predominately patients
with ATN), in-hospital mortality was 69%.
 Patients who survived to hospital discharge, 6mo survival was 77%, 1-yr survival was 69%, and
5-yr survival was 50%
 59% of surviving patients had no residual renal
insufficiency, and only 10% required chronic
dialysis therapy.
Long term outcomes in ARF in patients treated with continuous RRT. Am J Kidney
Dis, 2002
Radiocontratst Nephropathy
 Contrast media induced nephropathy (CMIN) is the
third highest cause of hospital-acquired acute renal
failure.
 In nearly half of these patients, CMIN occurred
during cardiac diagnostic or interventional
procedures such as percutaneous coronary
intervention.
CHF
Large
volume of
contrast
NSAIDs or
ACEI
DM
Baseline
renal
insufficiency
Risk
factors
Volume
depletion
ARF:increase in serum creat of>50 % above baseline or >1
mg/dl if baseline>2 mg/dl
 Normal baseline creat
negilgible risk
 Mild to moderate CKD
5-10 % risk
 Mild to moderate CKD + DM
10- 40 %
 Advanced renal insufficiency
>50 % risk
Pathogenesis
 Haemodynamic alterations and
tubuloglomerular feedback
 The injection of CM induces early, rapid renal
vasodilatation followed by prolonged vasoconstriction, with
an increase in intrarenal vascular resistances, a reduction of
total renal blood flow (RBF) and a decrease in glomerular
filtration rate (GFR).
 Conversely, the effect on the extrarenal vasculature is
transient vasoconstriction that precedes a stable decrease
in vascular peripheral resistances.
 The resulting renal ischaemia due to these haemodynamic
effects is, in part, responsible for nephropathy
 Endothelial dysfunction
 Vasoactive mediators
 Free radicals and reperfusion damage
 Haemorheological factors
 Tubular toxicity and immunological mechanisms
Treatment
 The best treatment of contrast-induced renal failure is
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prevention.
The use, if clinically possible, of ultrasonography,
magnetic resonance imaging or CT scanning without
radiocontrast agents, particularly in high-risk patients.
The use of lower doses of contrast and avoidance of
repetitive studies that are closely spaced (within 48 to 72
hours).
Avoidance of volume depletion or nonsteroidal
antiinflammatory drugs, both of which can increase renal
vasoconstriction.
The use of low or iso-osmolal nonionic contrast agents.
Treatment
 The administration of Intravenous Saline.
Isotonic saline at a rate of 1 mL/kg per hour, begun at
least two and preferably 6 to 12 hours prior to the
procedure, and continuing for 6 to 12 hours after
contrast administration.
 The administration of the antioxidant Acetylcysteine.
Dose of 600 to 1200 mg orally twice daily,
administered the day before and the day of the
procedure, based upon its potential for benefit and
low toxicity and cost.
Treatment
 Routine hemofiltration or hemodialysis for the
prevention of contrast nephropathy in patients with
stage 3 and 4 CKD is not recommended.
 More data are needed in stage 5 CKD (Prophylactic
use of hemodialysis in patients with stage 5 CKD, can
be considered,provided that a functioning access is
already available)
Extracorporeal blood purification therapies for prevention of radiocontrast-induced
nephropathy: a systematic review. Am J Kidney Dis 2006; 48:361.
Renal protection for coronary angiography in advanced renal failure patients by prophylactic
hemodialysis. A randomized controlled trial. J Am Coll Cardiol 2007; 50:1015.
Treatment
 There is no indication for prophylactic dialysis for
the prevention of volume overload in dialysisdependent patients.
Treatment
 Therapies with Limited Evidence
 Calcium Channel Blockers
 Diuretics
 Atrial Natriuretic Peptide (ANP)
 Endothelin (ET) Antagonists
 Prostaglandin E1
 ACE Inhibitors
 The high-osmolal contrast media (osmolality
1500–1800 mOsm/kg) are first generation agents.
 Low-osmolal contrast media still have an increased
osmolality compared with plasma (600–850
mOsm/kg),
 The newest nonionic radiocontrast agents have a
lower osmolality, 290 mOsm/kg, iso-osmolal to
plasma
 In high-risk patient populations (patientswith
underlying renal insufficiency and diabetes), both
low-osmolar and iso-osmolar contrasts tend to
reduce the risk of contrast nephropathy as
compared to the high-osmolar compounds.
 The volume of contrast administered to the patien
also appears to correlate with the incidence of
nephrotoxicity.
 In patients who undergo only diagnostic coronary
procedures, the volume of dye (approximately 100
mL) is considerably less than in patients who
undergo interventional procedures (approximately
250-300 mL).
Heme pigment-induced acute tubular necrosis
 Myoglobinuria: rhabdomyolysis.
 Hemoglobinuria: intravascular hemolysis.
Rhabdomyolysis
 The release of muscle cell contents as the result of
traumatic or nontraumatic injury of skeletal muscle
 Physical findings may consist of
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Tender, “doughy” muscles
Edema
weakness
Compartmental compression symptoms with signs and
symptoms of neurovascular compromise may develop,
necessitating the need for emergent fasciotomy.
The majority of cases of rhabdomyolysis are nontraumatic
Alcohol abuse
Massive muscle compression from immobilization in drug induced coma
Drug-induced
Seizures
Occlusive peripheral vascular disease.
Combination therapy with itraconazole, simvastatin, and cyclosporine
Conversion from one fibric acid to another, or from one statin-fibrate combination
to another
Detergent ingestion
Hemolysis
 Transfusion reactions due to ABO incompatible blood are
probably the most frequently encountered hemolytic
processes that can lead to acute renal failure.
 Severe acute hemolytic episodes in patients with glucose-6-
phosphate dehydrogenase deficiency.
Laboratory abnormalities
-Deposition in muscles
-Decreased responsiveness to PTH
-Impaired Vit D metabolism
Haptoglobin
Hypovolemia and High AG acidosis
 The urine may have a low FENa despite tubular
injury.
 Positive dipstick test for heme pigment without
red blood cells on microscopic exam should
suggest myoglobinuria.
 Heme-pigmented granular casts.
 Plasma is normal color in myoglobinuria and red
brown in hemoglobinuria
Treatment
 IVF
 Isotonic saline at 1 to 2 liters per hour
 Fluids are titrated to maintain a urine output of 200
to 300 mL/hour
 Continue until the urine discoloration clears, and
plasma creatine kinase decreases to less than 5,000
to 10,000 U/L (or there is cessation of hemolysis), or
symptomatic fluid overload develops.
Treatment
 Alkalinization.
 Mannitol diuresis.
Acute Interstitial Nephritis
Acute interstitial nephritis (AIN) is a syndrome of ARF
associated with an inflammatory infiltrate involving
the renal interstitium
Drug hypersensitivity
 Penicillin
 NSAIDs
 Cephalosporin
 Phenytoin
 Sulfonamide
 Furosemide
 Fluoroquinolone
 Thiazide diuretics
 Rifampin
 Allopurinol
 Alpha interferon
 Cimetidine
 Omeprazole
Others
Bacterial
• Streptococcus
• Staphylococcus
• Diphteria
• Mycoplasma
• Legionella
Viral
• CMV
• EBV
• Rubeola
• HIV
• Hantaan
Others
• Tuberculosis
• Rickettsia
• Leptospirosis
Systemic
Diseases
• Sjogren’s
• SLE
• Sarcoidosis
• Polyangiitis
Methicillin induced AIN
Renal symptoms typically develop 2 to 3 weeks after
the initiation of treatment:
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Hematuria
Pyuria with white blood cell casts
Proteinuria < 1g/d (can be nephrotic with NSAIDs)
Renal failure in 50% of patients
Extrarenal manifestations:
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Fever in 80%
Eosinophilia in 80%
Rash in 25%
Other kinetics
 Within 2 to 3 days after rechallenge with a drug with
previous sensitisation
 De novo in response to a med previoulsy tolerated
medication
 Renal failure is the most prominent feature
 Develops within 3 wk of initiation of drug therapy
in 80%
 Hematuria and pyuria each are present in only
50% of patients.
 Extrarenal manifestations, including fever,
maculo-papular rash, arthralgias, and eosinophilia
are each present in fewer than 50%
 All of them together in <5%
Eosinophiluria
Diagnostic value is poor.
Other conditions associated with
Eosinophiluria
 Prostatitis
 RPGN
 Bladder Cancer
 Renal Atheroembolic disease
Eosinophiluria
 PPV for AIN of only 50 %.
 NPV of 90%?
 Thus, the presence of eosinophiluria is not strongly
predictive of a diagnosis of AIN; however, its
absence is useful in excluding the diagnosis.
Renal biopsy
 Failure to improve after discontinuation of potential
offending drug
 If the potential offending drug is critical for therapy
 If immunosupressive therapy is considered
Treatment
 Supportive
 Dicontinue offending drug
 Prednisone 1mg/kg/d for 4 weeks
Controversial
Rcommended if biopsy proven AIN and who have persistent renal
failure 1 week after DC the offending medication
 ?adjunct cyclophosphamide
Hepatorenal syndrome
 ARF in HRS results from profound renal
vasoconstriction in the setting of histologically
normal kidneys.
 Although many of the features of HRS resemble
prerenal azotemia, the defining feature is a lack of
improvement in renal function with volume
expansion.
 Recovery of renal function is usually observed after
restoration of hepatic function after liver
transplantation
Type I HRS
• Doubling of the serum creatinine
concentration to a level of >2.5 mg/dl, or a
reduction of the creatinine clearance by 50%
or more to a value of <20 ml/min, over a
duration of <2 wk
• Develops in hospitalized patients
• In 2/3 an inciting events is identified
Type II HRS
• Moderate and stable reduction in GFR
• Insidious onset and slow progression of
renal insufficiency in the setting of
refractory ascites
• Better prognosis
Diagnostic criteria
 Chronic or acute hepatic disease with advanced hepatic failure and
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portal hypertension
A plasma creatinine concentration above 1.5 mg/dL (133 µmol/L)
that progresses over days to weeks.
The absence of any other apparent cause for the renal disease,
including shock, ongoing bacterial infection, current or recent
treatment with nephrotoxic drugs, and the absence of
ultrasonographic evidence of obstruction or parenchymal renal
disease.
Urine red cell excretion of less than 50 cells/HPF and protein
excretion less than 500 mg/day.
Lack of improvement in renal function after volume expansion with
intravenous albumin (1 g/kg of body weight per day up to 100
g/day) for at least two days and withdrawal of diuretics.
Urine Na<10
Treatment
 Management of underlying cause
 Stop diuretics
 Low salt diet and free water restriction if
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hyponatremia
Midodrine + Octreotide + Albumin
Terlipressin + Albumin
RRT
TIPS
 The management of patients with acute renal failure
or acute kidney injury (AKI) is principally
supportive, with renal replacement therapy (RRT)
indicated in patients with severe kidney injury.
Treatment of ARF
Prevention
 Renal hypoperfusion is a predisposing factor to the
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development of renal failure.
Optimizing vascular hemodynamics to ensure adequate
renal perfusion is a fundamental principle in avoiding renal
failure.
Avoidance or discontinuation of drugs that increase renal
vaso-constriction, such as NSAID and selective COX-2
inhibitors.
Potentially nephrotoxic medications should be avoided,
particularly in high-risk patients, whenever possible.
Using alternative imaging techniques such as MRI scanning
should be considered in patients at high risk for contrast .
Pharmacologic Treatment of Acute Renal Failure
 Dopamine
 Loop diuretics
 ANP
 Thyroxine
 IGF-1
Indications for RRT
 Refractory fluid overload
 Hyperkalemia (plasma potassium concentration
>6.5 meq/L) or rapidly rising potassium levels
 Metabolic acidosis (pH less than 7.1)
 Signs of uremia, such as pericarditis, neuropathy, or
an otherwise unexplained decline in mental status
Timing of initiation of RRT
 It is not possible to specify a specific duration of
renal injury or level of azotemia at which RRT should
be optimally initiated.
 It is unproven whether initiation of earlier or
prophylactic dialysis offers any clinical or survival
benefit.
 The optimal timing for initiation of RRT in patients
with AKI will require an adequately powered
prospective randomized trial.
 Adequate design of such a trial is limited by the
current inability to quickly prospectively identify
patients with early AKI who will have protracted
renal injury and eventually require RRT.
 Initiation of dialysis prior to the development of
symptoms and signs of renal failure due to AKI is
recommended.
 Current data do not support the superiority of either
CRRT or IHD.
Learning objectives
 Understanding the limitations of serum creat
 Formulation of a DDx
 Understanding of the pathophysiology of ARF
 Prevention of ARF
THANK YOU