ACUTE RENAL FAILURE
Shahzad Qureshi M.D.
Division of Nephrology
Loyola University Medical Center
Define and review classification of ARF
Epidemiology of ARF
Measurement of kidney function
Pathophysiology of ARF
Management and treatment of ARF
Review clinical cases
What is ARF?
A) Increase in serum Creatinine 0.5mg/dL.
B) An increase in serum Creatinine of more
then 50% from baseline.
C) A reduction in the calculated Creatinine
Clearance of 50%
2004 ADQI group classification
Risk (R) -Increase Cr x1.5 or Decrease GFR x
25% or UO <0.5 ml/kg/hr x 6hrs
Injury (I)- Increase Cr x2.0 or Decrease GFR x
50% or UO <0.5 ml/kg/hr x 12hrs
Failure (F)- Increase Cr x3.0 or Decrease GFR
x75% or anuria x 12 hours
Loss (L)- Persistent ARF, complete loss of kidney
function x 4 weeks (needing RRT)
End Stage Kidney Disease (E)- Loss of kidney
function x 3 months
Measurement of Kidney
Serum creatinine is a reflection of creatinine
Creatinine production is determined by muscle
mass and must be interpreted with respect to pt’s
age, weight and sex.
Creatinine is filtered and secreted and tends to
over estimate GFR.
Certain diseases and medications interfere with
correlation between serum Cr and GFR. (i.e..
Acute glomerulonephritis, trimethoprim,
Serum Creatinine (cont.)
Cr Cx= (140 - age y)(weight kg)(0.85 if
female)/(72 X serum creatinine mol/L)
MDRD (Modified Diet and Renal Disease)
GFR, in mL/min per 1.73 mm2 = 186.3 X ((serum
creatinine) exp[-1.154]) X (Age exp[-0.203]) X
(0.742 if female) X (1.21 if African American)
Serum Creatinine (cont.)
None of the equations accurately determine
GFR in ARF. (Assume Cr is stable)
More accurate techniques involve nuclear
medicine studies and GFR scans.
New biochemical markers investigated (i.e..
5 % of hospitalized patients dev. ARF.
0.5% of these patients require dialysis.
20% of critical care admissions dev. ARF.
Hospital acquired ARF usually develops in
the setting of ICU secondary to multisystem
Causes of ARF in Hospitalized
CHF, volume depletion, sepsis
10% Urinary obstruction
4% Glomerulonephritis or vasculitis
Mortality rates range from 7-80% depending on
patients other co morbidities.
This rate has remained unchanged since the advent
of dialysis because of increasing age and co
Most common cause of death associated with ARF
are sepsis, cardiac failure and respiratory failure.
Mortality rates are lower for nonoliguric
(>400ml/day) then oliguric ARF (<400 ml/day).
1) As an adaptive response to severe volume
depletion and hypotension with structurally and
functionally intact nephrons. (Pre renal azotemia)
2) In response to cytoxic or ischemic insults to the
kidney with structural and functional damage.
(Intrinsic Renal failure)
3) With obstruction to passage of urine. (Post
Nausea? Vomiting? Diarrhea?
Hx of heart disease, liver disease,
previous renal disease, kidney stones,
Any recent illnesses?
Any edema, change in
Any new medications?
Any recent radiology studies?
– Mucus membranes, orthostatics
– JVD, rubs
– Decreased breath sounds
Rash (Allergic interstitial nephritis, Livedo reticularis)
Extremities (Skin turgor, Edema)
Workup for ARF
– Urine sediment (U/A): casts, cells, protein
– Urine electrolytes (UNa and UUN) and urine Cr to
– Urine osmolarity
– Urine protein
– Urine eosinophils
Kidney U/S - r/o hydronephrosis
A 75yo man, NH resident, with
Alzheimer’s dementia admitted for
aspiration pneumonia. BUN 50 and Cr 2.6
A. ATN from Abx
D. AIN from
Pre Renal Azotemia
Impaired renal blood flow as a result of true
intravascular depletion, decreased effective
circulating volume to the kidneys, or agents that
impair renal blood flow.
Urine and blood studies are helpful in diagnosing
pre renal ARF.
Hyaline casts can be seen (Not an abnormal
Treat with fluid boluses or continuous IVF,
monitor urine output.
Intravascular volume depletion
– Vomiting, diarrhea
– “Third spacing”
Reduced Cardiac output
– Cardiogenic shock, CHF, tamponade, huge PE....
– Anaphylaxis, Antihypertensive drugs
- Hepatorenal syndrome
- ACE-I, NSAIDS
Urine Indices in ARF
Pre Renal Intrinsic ATN Post Renal
> 500 < 350 < 350
Na (meq/L) < 20 > 40 > 40
Bun/Cr (mg/dL) > 20:1 < 10:1 < 10:1
FENa < 1% >3% >3%
FEUrea <35% >55% >55%
Hyaline casts Brown, Bland
Acute Renal Failure
PR PR ATN
500 40 40
350 20 20
ATN ATN PR
UOsm (U/P)Cr UNa FENa
What is FENa
The fraction of filtered
sodium excreted in the
FeNa = (urine Na x plasma Cr)
(plasma Na x urine Cr)
ARF syndromes with Low
Pre renal ARF
Vasoconstriction Mediated Intrinsic Renal Failure
-Tacrolimus, cyclosporine, cocaine
- Hepatorenal syndrome
- Radiocontrast Injury
- Sepsis (early), burn injury
- Acute Glomerulonephritis
Calculating FeNa after pt has
Caution with calculating FeNa if pt has gotten Loop
Diuretics in past 24-48 h
Loop diuretics cause natriuresis (incr urinary Na excretion)
that raises U Na-even if pt is prerenal
So if FeNa>1%, you don’t know if this is because pt is
euvolemic or because Lasix increased the U Na
So helpful if FeNa still <1%, but not if FeNa >1%
1. Fractional Excretion of Lithium (endogenous)
2. Fractional Excretion of Uric Acid
3. Fractional Excretion of Urea
Nurse pages you and states your patient
has not urinated in 8 hours….
What do you want to do?”
• Examine pt: Dry? Septic (vasodilated)?
•Check I/Os (has pt been drinking?)
•Insert Foley and measure PVR
•Flush foley (sediment can obstruct outflow)
• Give IV BOLUS (250-500cc IVF), see if pt urinates
in next 30-60 min
–If pt urinates, then the pt was dry
–If pt doesn’t urinate, then pt’s either REALLY dry or in
•Check UA, urine lytes, urine osmolarity, BMP
•Consider Renal U/S if reasonable
Post Obstructive Uropathy
Occurs if both urinary outflow tracts are
obstructed or outflow tract of solitary kidney is
Patients with SUDDEN ONSET of anuria are
likely to have post obstructive uropathy.
Primary causes include BPH, prostate and cervical
cancer, stones, strictures and retroperitoneal
Bladder catheterization and Renal U/S to assess
Can have obstruction w/o hydronephrosis on U/S
Monitor for post obstructive diuresis, hemorrhagic
You evaluate a 60 yo man who undergoes fem-
pop bypass for severe PVD now with oliguria
and rapidly increasing BUN, Cr.
A. ATN Brown, “Muddy” casts
B. Acute glomerulonephritis
C. Contrast Induced Nephropathy
D. Post-Obstructive uropathy
Intrinsic Acute Renal Failure
1. Tubular (ATN)
2. Interstitial (AIN)
3. Glomerular (Glomerulonephritis)
Most common cause of ARF in hospitalized
Contrast and aminoglycosides most often
associated with nonischemic ATN.
1) Initiation phase- Renal injury lasting
hours to days.
2) Maintenance phase- Lasts days to
weeks. GFR and U.O at lowest.
3) Recovery Phase- Postacute tubular necrosis
diuresis. Can still exp. uremia and hypovolemia as
tubular function not completely restored.
Tubular-Cell Injury and Repair in Ischemic Acute Renal Failure.
Thadhani, R. et al. N Engl J Med 1996;334:1448-1460
Reverse underlying causes and correct fluid
and electrolyte balances
Treatment is supportive.
Drugs such as mannitol, loop diuretics,
dopamine and CCB successful in promoting
diuresis in animals but not in humans.
Dialysis as needed (IHD vs. CRRT)
60yo woman with h/o OA has labs
drawn BUN=24, Cr 1.8. U/A reveals
20 WBC, no bacteria. What is the cause
A. Pre renal azotemia
secondary to UTI
B. ATN secondary to
C. AIN secondary to
Acute Interstitial Nephritis
70% Drug hypersensitivity
30% Antibiotics: PCNs (Methicillin), Cephalosporins,
Strep, Legionella, CMV, other bact/viruses
6% Autoimmune Dz (Sarcoid, Tubulointerstitial
AIN from Drugs
Renal damage is NOT dose-dependent
May take wks after initial exposure to drug
Up to 18 mos to get AIN from NSAIDS!
But only 3-5 d to develop AIN after second exposure to drug
Serum Eosinophilia (23%)
Maculopapular rash (15%)
Bland sediment or WBCs, sterile pyuria most commonly seen
WBC Casts are common
Urine eosinophils on Wright’s or Hansel’s Stain
- Also see urine eos in RPGN, renal atheroemboli...
Treatment is to remove offending agents. Most patients recover complete
kidney function w/I one year.
You evaluate a 32yo woman with oliguria, hematuria
and rapidly increasing BUN/Cr a few days after
experiencing a viral URI. U/A reveals…
C. Acute interstitial
D. Pre renal Azotemia
1° Disorders - Minimal Change Disease
- Membranous Nephropathy
2° Disorders- DM
- Hepatitis B
Can have normal serum creatinine (Not
Usually do NOT see RBC casts
Type 1: Anti-GBM dz (Anti GBM Ab positive)
- Goodpasture’s Disease
Type 2: Immune complex (Low compliment, elevated ESR)
IgA nephropathy (Normal Compliment levels)
Type 3: Pauci-immune (ANCA positive, assoc with vasculitis)
Proteinuria (1-2grams usually)
Treatment varies based on underlying disease
68y/o male with baseline Cr=1.2 underwent
angiogram 3 days prior for ACS. Now pt has
Cr=2.0 and blanching rash.
A. Renal Artery Stenosis
B. Contrast-Induced Nephropathy
C. Abdominal Aortic Aneurysm
D. Cholesterol Atheroemboli
Renal Atheroembolic Dz
1% of Cardiac caths: atheromatous debris scraped from the
aortic wall will embolize
– Skin (Livedo Reticularis, Purple toes)
– Renal (ARF)
– Gut (Mesenteric ischemia)
Cr will NOT improve with IVF
Diagnosis of exclusion: will NOT show up on MRI or
Renal U/S; WILL show up on renal bx
You are called to evaluate a 45
y/o female in the ER admitted
for heart palpatations. BUN 80,
Cr 3.0, Potassium 6.5
What do you do?
Treatment of Hyperkalemia
Glucose and Insulin
Cation-exchange resins (Kayexalate)
You admit the pt to telemetry and give
You recheck labs 4h later and BUN=105,
Cr=4.0, K=7.0. Suddenly the pt starts to
Acute Indications for Dialysis
Ingestion of drugs/Ischemia
An excess in the blood of urea, creatinine and other
nitrogenous end products with signs and symptoms listed .
– Fatigue, weakness
Mental status change
– Uremic encephalopathy
– Anorexia, early satiety, N/V,