acute kidney injury 2013
DESCRIPTION
Resident level lecture on AKITRANSCRIPT
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acute renal failure…from basics to the latest advances
Joel M. Topf, MDClinical Nephrologist
http://pbfluids.com
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the housemoment
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Dr. Haas invented the first dialysis machine designed for humans and in 1928 he treated 6 patients.
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Dr. Haas invented the first dialysis machine designed for humans and in 1928 he treated 6 patients.
All of them died.
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In 1943, Willem Kolff’s, working in Nazi occupied Netherlands created the second human dialysis machine from a washing machine, juice cans and sausage casings.
In 1943 he dialyzed his first patient, a young man with acute nephritis.
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In 1943, Willem Kolff’s, working in Nazi occupied Netherlands created the second human dialysis machine from a washing machine, juice cans and sausage casings.
In 1943 he dialyzed his first patient, a young man with acute nephritis.
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In 1943, Willem Kolff’s, working in Nazi occupied Netherlands created the second human dialysis machine from a washing machine, juice cans and sausage casings.
In 1943 he dialyzed his first patient, a young man with acute nephritis.
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In 1943, Willem Kolff’s, working in Nazi occupied Netherlands created the second human dialysis machine from a washing machine, juice cans and sausage casings.
In 1943 he dialyzed his first patient, a young man with acute nephritis.
Dr. Haas
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In 1943, Willem Kolff’s, working in Nazi occupied Netherlands created the second human dialysis machine from a washing machine, juice cans and sausage casings.
In 1943 he dialyzed his first patient, a young man with acute nephritis.
Dr. Haas0 for 22
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In 1943, Willem Kolff’s, working in Nazi occupied Netherlands created the second human dialysis machine from a washing machine, juice cans and sausage casings.
In 1943 he dialyzed his first patient, a young man with acute nephritis.
In 1945, a 67-year-old woman in uremic coma presented to Dr Kolff.
Dr. Haas0 for 22
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In 1943, Willem Kolff’s, working in Nazi occupied Netherlands created the second human dialysis machine from a washing machine, juice cans and sausage casings.
In 1943 he dialyzed his first patient, a young man with acute nephritis.
In 1945, a 67-year-old woman in uremic coma presented to Dr Kolff.
Dr. Haas
Regained consciousness after 11 hours of hemodialysis.
0 for 22
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0
20
40
60
80
Mo
rtality (%
)
75
45
Sepsis Other Causes
Mortality by Etiology
Commonly quoted mortality of 70% is for dialysis requiring ICU patients
For hospital acquired ARF: 20%
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Am J Med 2005 118, 827-832
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Patients with primary diagnosis of AKI have higher mortality when they are:
admitted on week-ends
admitted to smaller hospitals
James et al. Weekend Hospital Admission, Acute Kidney Injury, and Mortality. Journal of the American Society of Nephrology (2010) vol. 21 (5) pp. 845-851
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ICU associated AKI is characterized by a d e l a y b e t w e e n a d m i s s i o n a n d d e v e l o p m e n t o f acute renal injury
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R isk
I njury
F ailure
L oss of function
E nd-Stage Renal disease
rifle criteria for stratifying arf
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R isk
Increase in Cr of 1.5-2.0 X baseline or urine output < 0.5 mL/kg/hr for more than 6 hours.
I njury
F ailure
L oss of function
E nd-Stage Renal disease
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R isk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
I njury
increase in Cr 2-3 X baseline (loss of 50% of GFR) or urine output < 0.5 mL/kg/hr for more than 12 hours.
F ailure
L oss of function
E nd-Stage Renal disease
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R isk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
I njury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs
F ailure increase in Cr rises > 3X baseline Cr (loss of 75% of GFR) or an increase in serum creatinine greater than 4 mg/dL, or urine output < 0.3 mL/kg/hr for more than 24 hours or
anuria for more than 12 hours.
L oss of function
E nd-Stage Renal disease
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R isk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
I njury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs
F ailure: Inc Cr > 200% or > 4 mg/dL or U.O. < 0.3 mL/kg/hr > 24 hrs or anuria for more than 12 hours
L oss of function persistent renal failure (i.e. need for dialysis) for more than 4
weeks.
E nd-Stage Renal disease
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R isk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
I njury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs
F ailure: Inc Cr > 200% or > 4 mg/dL or U.O. < 0.3 mL/kg/hr > 24 hrs or anuria for more than 12 hours
L oss of function: Need for dialysis for more than 4 weeks
E nd-Stage Renal disease persistent renal failure (i.e. need for dialysis) for more than 3
months.
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R isk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
I njury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs
F ailure: Inc Cr > 200% or > 4 mg/dL or U.O. < 0.3 mL/kg/hr > 24 hrs or anuria for more than 12 hours
L oss of function: Need for dialysis for more than 4 weeks
E nd-Stage Renal disease : Need for dialysis for more than 3 months
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nice criteria. do they work?
20,126 consecutive admissions to a university hospital Excluded kids Kidney transplant and
dialysis patients Patients admitted for <
24 hours Using RIFLE:
Risk 9.1% Injury 5.2% Failure 3.7%
Uchino S, Bellomo R, Goldsmith D. Crit Care Med 2006 Vol 34 1913-1917.
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nice criteria. do they work?
20,126 consecutive admissions to a university hospital Excluded kids Kidney transplant and
dialysis patients Patients admitted for <
24 hours Using RIFLE:
Risk 9.1% Injury 5.2% Failure 3.7%
No Renal failure82%
Failure4%
Injury5%
Risk9%
Uchino S, Bellomo R, Goldsmith D. Crit Care Med 2006 Vol 34 1913-1917.
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Hos
pita
l Mor
talit
y
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Hos
pita
l Mor
talit
y
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>3x
BL
Cr
Cr >
4
Hos
pita
l Mor
talit
y
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nice criteria. do they work in the icu?
University of Pittsburgh has 7 ICUs
5,383 patients Excluded dialysis
Subsequent admissions
Frequency of acute Kidney failure: No AKD 1,766
Risk 670
Injury 1,436
Failure 1,511Hoste E, Clermont G, Kersten A. Crit Care 2006 Vol 310
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nice criteria. do they work in the icu?
University of Pittsburgh has 7 ICUs
5,383 patients Excluded dialysis
Subsequent admissions
Frequency of acute Kidney failure: No AKD 1,766
Risk 670
Injury 1,436
Failure 1,511
No Renal failure33%
Failure28%
Injury27%
Risk12%
Hoste E, Clermont G, Kersten A. Crit Care 2006 Vol 310
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No AKI Risk Injury Failure0
5
10
15
20
25
30
RRTLOSICU LOSMortality
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No AKI Risk Injury Failure0
5
10
15
20
25
30
RRTLOSICU LOSMortality
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No AKI Risk Injury Failure0
5
10
15
20
25
30
RRTLOSICU LOSMortality
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AKIN criteria
refinement of RIFLE criteria smaller change in Cr 0.3 time constraint of 48 hours for the diagnosis of
AKI anyone requiring dialysis is stage 3 AKI
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RIFLE v AKIN
RIFLERIFLE
R Cr increased by 50-100%
I Cr increased by 100-200%
F Cr increased by more than 200% or Cr > 4
L Need for dialysis for > 4 weeks
E Need for dialysis for > 3 months
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RIFLE v AKIN
RIFLERIFLE
R Cr increased by 50-100%
I Cr increased by 100-200%
F Cr increased by more than 200% or Cr > 4
L
E
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RIFLE v AKIN
RIFLERIFLE AKINAKIN
R Cr increased by 50-100% 1 Cr increased by 0.3 or
50-100%
I Cr increased by 100-200% 2 Cr increased by
100-200%
F Cr increased by more than 200% or Cr > 4 3 Cr increased by more
than 200%, Cr > 4, or renal replacement therapyL
Cr increased by more than 200%, Cr > 4, or renal replacement therapy
E
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AKIN vs RIFLE120,123 critically ill patients in 57 ICUs in New Zealand and Australia
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AKIN vs RIFLE120,123 critically ill patients in 57 ICUs in New Zealand and Australia
64%
16%
14%6%
RIFLE
63%18%
10%9%
AKIN
NoneRisk / 1Injury / 2Failure / 3
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AKIN vs RIFLE120,123 critically ill patients in 57 ICUs in New Zealand and Australia
64%
16%
14%6%
RIFLE
63%18%
10%9%
AKIN
NoneRisk / 1Injury / 2Failure / 3
2.24
3.95
5.13
2.45
4.23
5.22
Risk / 1 Injury / 2Failure / 3
mortality odds ratio vs no AKI
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oliguria: sensitive or specific?
oliguria is a biomarker of ARF
Used in the definition of RIFLE and AKIN
How good is it at predicting AKICreatinine
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ICU patients and tracked hourly urine outputs
oliguria: <0.5 ml/kg/hr
primary outcome: how predictive was oliguria for subsequent AKI as defined by creatinine
239 patients, 723 days, 23 cases of hospital acquired AKI
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duration of oliguria AKI the next day No AKI next day
None 5 443
≥1 hour 18 257
≥2 hours 15 194
≥3 hours 13 125
≥4 hours 12 95
≥5 hours 7 75
≥6 hours 5 50
≥12 hours 4 9
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duration of oliguria AKI the next day No AKI next day
None 5 443
≥1 hour 18 257
≥2 hours 15 194
≥3 hours 13 125
≥4 hours 12 95
≥5 hours 7 75
≥6 hours 5 50
≥12 hours 4 9
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duration of oliguria AKI the next day No AKI next day
None 5 443
≥1 hour 18 257
≥2 hours 15 194
≥3 hours 13 125
≥4 hours 12 95
≥5 hours 7 75
≥6 hours 5 50
≥12 hours 4 9
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duration of oliguria AKI the next day No AKI next day
None 5 443
≥1 hour 18 257
≥2 hours 15 194
≥3 hours 13 125
≥4 hours 12 95
≥5 hours 7 75
≥6 hours 5 50
≥12 hours 4 9
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ICU associated AKI is characterized by a d e l a y b e t w e e n a d m i s s i o n a n d d e v e l o p m e n t o f acute renal injury
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4"days"
1"day"
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N=29,269
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N=29,269
AKI 1,738 (5.7%)
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N=29,269
AKI 1,738 (5.7%)
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T h i s d e l a y i n t h e development of AKI is an opportunity.
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T h i s d e l a y i n t h e development of AKI is an opportunity.
Often AKI is the result of a second hit. Don’t hit your patient.
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risk factors for AKI
CKD
Age >75
Peripheral vascular disease
Heart failure
Liver disease
Diabetes
Nephrotoxins NSAIDs
Aminoglycoseide
Hypotension Hypovolemia
Cardiac disease
Iatrogenic
Sepsis
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risk factors for AKI
CKD
Age >75
Peripheral vascular disease
Heart failure
Liver disease
Diabetes
Nephrotoxins NSAIDs
Aminoglycoseide
Hypotension Hypovolemia
Cardiac disease
Iatrogenic
Sepsis
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etiologies of arf
Seventy percent have concurrent oliguria
< 400 mL/day
< 0.5 mL/kg/hr in children
< 1 mL/kg/hr in infants
Complicates 5-7% of hospitalizations
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Community acquired49.7%
Hospital acquired50.3%
Hou SH, Bushinsky DA, Wish JB. Am J Med 1983; 74: 243-8.Nash K, Hafeez A, Hou S. Am J Kidney Dis. 2002; 39: 930-6.
Kaufman J, Dhakal M, Patel B, Et al. Am J Kidney Dis 1991; 17: 191-8.
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Hou SH, Bushinsky DA, Wish JB. Am J Med 1983; 74: 243-8.Nash K, Hafeez A, Hou S. Am J Kidney Dis. 2002; 39: 930-6.
Kaufman J, Dhakal M, Patel B, Et al. Am J Kidney Dis 1991; 17: 191-8.
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hospital acquired acute renal failure
Sepsis7%
Other2%
CHF4%
Unknown3%
Other7%
Obstruction2%
Hypotension11%
Volume Contraction21%
Post-Op15%
Contrast11%
Medication16%
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hospital acquired acute renal failure
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differentiation of prerenal from intrinsic renal disease
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Excreted Na
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Excreted NaFiltered Na
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Excreted NaFiltered Na
Fractional excretion of sodium:
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Excreted Na = Urine Na x Urine Volume
Calculating the Numerator
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Calculating the Denominator
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Calculating the Denominator
Filtered Na = Serum Na x GFR
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Calculating the Denominator
GFR = Urine Cr x Urine Volume Serum Cr
Filtered Na = Serum Na x GFR
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Calculating the Denominator
GFR = Urine Cr x Urine Volume Serum Cr
Filtered Na = Serum Na x GFR
Filtered Na = Serum Na x UrCr x UrVol Serum Cr
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Excreted NaFiltered Na
FENa =
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Excreted NaFiltered Na
FENa =
FENa =
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Excreted NaFiltered Na
FENa =
Urine Na x Urine VolumeFENa =
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Excreted NaFiltered Na
FENa =
Urine Na x Urine VolumeSerum Na x UrCr x Urine Volume Serum Cr
FENa =
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Excreted NaFiltered Na
FENa =
Urine Na x Urine VolumeSerum Na x UrCr x Urine Volume Serum Cr
FENa =
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Excreted NaFiltered Na
FENa =
Urine Na x Urine VolumeSerum Na x UrCr x Urine Volume Serum Cr
FENa =
Urine NaSerum Na x UrCr Serum Cr
FENa =
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Excreted NaFiltered Na
FENa =
Urine Na x Urine VolumeSerum Na x UrCr x Urine Volume Serum Cr
FENa =
Urine NaSerum Na x UrCr Serum Cr
FENa =
Urine Na x Serum CrSerum Na x UrCr
FENa =
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FENa the easy way
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FENa the easy way
FENa is a small number 0.1% to 3%
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FENa the easy way
FENa is a small number 0.1% to 3% So the calculation will be 0.001-0.03 prior to
converting to percent by X 100
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FENa the easy way
FENa is a small number 0.1% to 3% So the calculation will be 0.001-0.03 prior to
converting to percent by X 100 So make the fraction small by putting the small
numbers over the big numbers
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Sr Na
FENa the easy way
FENa is a small number 0.1% to 3% So the calculation will be 0.001-0.03 prior to
converting to percent by X 100 So make the fraction small by putting the small
numbers over the big numbers
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Sr Na
Sr Na
FENa the easy way
FENa is a small number 0.1% to 3% So the calculation will be 0.001-0.03 prior to
converting to percent by X 100 So make the fraction small by putting the small
numbers over the big numbers
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Sr Na Sr Cr
Sr Na
FENa the easy way
FENa is a small number 0.1% to 3% So the calculation will be 0.001-0.03 prior to
converting to percent by X 100 So make the fraction small by putting the small
numbers over the big numbers
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Sr Na Sr Cr
Sr Na
Sr Cr
FENa the easy way
FENa is a small number 0.1% to 3% So the calculation will be 0.001-0.03 prior to
converting to percent by X 100 So make the fraction small by putting the small
numbers over the big numbers
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Sr Na
Ur Na Sr Cr
Sr Na
Sr Cr
FENa the easy way
FENa is a small number 0.1% to 3% So the calculation will be 0.001-0.03 prior to
converting to percent by X 100 So make the fraction small by putting the small
numbers over the big numbers
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Sr Na
Ur Na Sr Cr
Sr Na
Sr Cr x Ur Na
FENa the easy way
FENa is a small number 0.1% to 3% So the calculation will be 0.001-0.03 prior to
converting to percent by X 100 So make the fraction small by putting the small
numbers over the big numbers
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Sr Na
Ur Na Ur Cr
Sr Cr
Sr Na
Sr Cr x Ur Na
FENa the easy way
FENa is a small number 0.1% to 3% So the calculation will be 0.001-0.03 prior to
converting to percent by X 100 So make the fraction small by putting the small
numbers over the big numbers
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Sr Na
Ur Na Ur Cr
Sr Cr
Sr Na
Sr Cr x Ur Na
x Ur CrFENa =
FENa the easy way
FENa is a small number 0.1% to 3% So the calculation will be 0.001-0.03 prior to
converting to percent by X 100 So make the fraction small by putting the small
numbers over the big numbers
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Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the filtered sodium
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serum Na x GFR x minutes in a day
urinary Na excretion
Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the filtered sodium
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Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the filtered sodium
140 x 0.1 x 1440
180
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Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the filtered sodium
20160
180
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Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the filtered sodium
0.8%
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Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the filtered sodium
0.8%
So does ATN cause the tubules to fail to reabsorb the 99%?
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Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the filtered sodium
0.8%
So does ATN cause the tubules to fail to reabsorb the 99%?
NO
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false positive FeNa
Contrast nephropathy Acute glomerulonephritis ATN with heart failure ATN with burns ATN with cirrhosis
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Contrast nephropathy Acute glomerulonephritis ATN with heart failure ATN with burns ATN with cirrhosis
Low FeNa not pre-renal
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Contrast nephropathy Acute glomerulonephritis ATN with heart failure ATN with burns ATN with cirrhosis
Low FeNa not pre-renal
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Contrast nephropathy Acute glomerulonephritis ATN with heart failure ATN with burns ATN with cirrhosis
Low FeNa not pre-renal
these are cases of ATN where the tubules effectively hold on to sodium
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Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the filtered sodium but now the GFR is 30 not 100
The fena reflects the behavior of the tubules that are undamaged. Tubules affected by ischemia have a GFR of zero.
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serum Na x GFR x minutes in a day
urinary Na excretion
Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the filtered sodium but now the GFR is 30 not 100
The fena reflects the behavior of the tubules that are undamaged. Tubules affected by ischemia have a GFR of zero.
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Why is the feNa high in ATN
140 x 0.03 x 1440
180
Normally tubules reabsorb 98-99% of the filtered sodium but now the GFR is 30 not 100
The fena reflects the behavior of the tubules that are undamaged. Tubules affected by ischemia have a GFR of zero.
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Why is the feNa high in ATN
6048
180
Normally tubules reabsorb 98-99% of the filtered sodium but now the GFR is 30 not 100
The fena reflects the behavior of the tubules that are undamaged. Tubules affected by ischemia have a GFR of zero.
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Why is the feNa high in ATN
2.9%
Normally tubules reabsorb 98-99% of the filtered sodium but now the GFR is 30 not 100
The fena reflects the behavior of the tubules that are undamaged. Tubules affected by ischemia have a GFR of zero.
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Acute renal success
GFR is normally 100 mL/min
Total plasma volume is only 3 liters
without massive fluid reabsorption, 30 minutes to filter all the plasma
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Acute renal success
GFR is normally 100 mL/min
Total plasma volume is only 3 liters
without massive fluid reabsorption, 30 minutes to filter all the plasma
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Acute renal success
GFR is normally 100 mL/min
Total plasma volume is only 3 liters
without massive fluid reabsorption, 30 minutes to filter all the plasma
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Acute renal success
GFR is normally 100 mL/min
Total plasma volume is only 3 liters
without massive fluid reabsorption, 30 minutes to filter all the plasma
Tubuloglomerular feedback
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Kaplan, Kohn. American J Nephrol, 1992; 12: 49-54.
fractional excretion of urea
Based on the physiologic increase in urea reabsorption with pre-renal azotemia
Normal FE Urea is 50-65% in well hydrated individuals
In prerenal azotemia this falls below 35% Not affected by diuretics
Sr Na
Sr Cr x Ur Na
x Ur CrFENa =
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Kaplan, Kohn. American J Nephrol, 1992; 12: 49-54.
fractional excretion of urea
Based on the physiologic increase in urea reabsorption with pre-renal azotemia
Normal FE Urea is 50-65% in well hydrated individuals
In prerenal azotemia this falls below 35% Not affected by diuretics
Sr Urea
Sr Cr x Ur Urea
x Ur CrFEurea =
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Kaplan, Kohn. American J Nephrol, 1992; 12: 49-54.
fractional excretion of urea
Based on the physiologic increase in urea reabsorption with pre-renal azotemia
Normal FE Urea is 50-65% in well hydrated individuals
In prerenal azotemia this falls below 35% Not affected by diuretics
Sr Urea
Sr Cr x Ur Urea
x Ur CrFEurea =
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Carvounis, Sabeeha, Nisar, Et al. Kidney Int, 2002 Vol 62. p 2223-2229
FEurea in the differential diagnosis of atn
102 patients with ARF
Gold standard was consultants full analysis and retrospective analysis of response to treatment.
Divided the cases into: ATN
Prerenal without diuretic
Prerenal treated with diuretics
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0
25
50
75
100
Sensitivity (%
)
92
50
91 90
Pre-Renal, No diuretics Pre-Renal, Diuretics
FENaFEUrea
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FENa
FEUrea
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outcomes
Nephrology Dialysis Transplantation 23 2235-41, 2008Clin J Am Soc Nephrol 3: 881-886, 2008
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outcomes
Nephrology Dialysis Transplantation 23 2235-41, 2008Clin J Am Soc Nephrol 3: 881-886, 2008
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outcomes
Nephrology Dialysis Transplantation 23 2235-41, 2008Clin J Am Soc Nephrol 3: 881-886, 2008
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Acute kidney injury as a cause of CKD
3,679 diabetic veterans baseline creatinine 1.1, average age 61 primary outcome: development of CKD 4 secondary outcome: all-cause mortality
1,822 hospitalized 530 developed AKI at least once
88% AKIN 1
12% AKIN 2, 3
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39,805 Kaiser Permanente Hospitalized 1996-2003 all had pre-hospitalization GFR <45 among those who developed ARF (50%
increase in Cr and dialysis) 26% died in the hospital among survivors:
GFR 30-44 42% required permanent dialysis within a month of discharge
GFR 15-29 63% required permanent dialysis within a month of discharge
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26%
5%
20%
49%
ARF in hospital
Death in Hosp Died after d/c Alive, No dialysis ESRD
5%4%
90%
2%
No ARF in hospital
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34.7%
27.6%28.4%
45.2%
14.4%
77.0%
Death during Hospital
ESRD after D/C
GFR 30-44 GFR 15-29 GFR <15
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even the lucky ones, not so lucky
Survivors of ARF, not dialysis dependent
No ARF
dial
ysis
-free
sur
viva
l
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used to be...No dialysis. No foul.
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Acute renal failure is a risk factor for progression of CKDAcute renal failure is a risk factor for progression of CKD
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therapy
Internist management
Patient empowerment
Renal replacement therapy
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risk factors for AKI
CKD
Age >75
Peripheral vascular disease
Heart failure
Liver disease
Diabetes
Nephrotoxins NSAIDs
Aminoglycoseide
Hypotension Hypovolemia
Cardiac disease
Iatrogenic
Sepsis
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risk factors for AKI
CKD
Age >75
Peripheral vascular disease
Heart failure
Liver disease
Diabetes
Nephrotoxins NSAIDs
Aminoglycoseide
Hypotension Hypovolemia
Cardiac disease
Iatrogenic
Sepsis
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Internist management
Monitor I’s and O’s, daily weights
Frequent labs BMP, phosphorous,
albumin, U/A
Consult nephrology
Avoid hypotension
Dose adjust for renal failure
Follow-up after d/c for high risk of CKD
Avoid Iodinated contrast Aminoglycosides ACEi/ARB
Thoughtful fluid management
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risk factors for AKI
CKD
Age >75
Peripheral vascular disease
Heart failure
Liver disease
Diabetes
Nephrotoxins NSAIDs
Aminoglycoseide
Hypotension Hypovolemia
Cardiac disease
Iatrogenic
Sepsis
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risk factors for AKI
CKD
Age >75
Peripheral vascular disease
Heart failure
Liver disease
Diabetes
Nephrotoxins NSAIDs
Aminoglycoseide
Hypotension Hypovolemia
Cardiac disease
Iatrogenic
Sepsis
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Patient empowerment
talk to patients about what to do if they become acutely ill
increase fluid intake
decrease diuretics
monitor blood pressure
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renal replacement therapy
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Dialysate
1405.8
10817
76
7.8
1452
11035
0
0
Conventional Dialysis: combination of diffusive and convective Clearance
1405.8
10817
67
3.8
BloodUltra-filtrate
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Dialysate
1405.8
10817
76
7.8
1452
11035
0
0
Conventional Dialysis: combination of diffusive and convective Clearance
1405.8
10817
67
3.8
BloodUltra-filtrate
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1365.8
10817
67
3.8
Isolated Ultrafiltration: CHF SolutionsMinimal clearance
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1365.8
10817
67
3.8
1365.8
10817
67
3.8
Isolated Ultrafiltration: CHF SolutionsMinimal clearance
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1365.8
10817
67
3.8
1365.8
10817
67
3.8
80 mmol KIsolated Ultrafiltration: CHF SolutionsMinimal clearance
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1365.8
10817
67
3.8
1365.8
10817
67
3.8
80 mmol K5.8 mmol/L
Isolated Ultrafiltration: CHF SolutionsMinimal clearance
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1365.8
10817
67
3.8
1365.8
10817
67
3.8
80 mmol K5.8 mmol/L
= 13.8 litersIsolated Ultrafiltration: CHF SolutionsMinimal clearance
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Ultrafilter 3+ liters/hour
Replace all ultrafiltratewith sterile fluid at idealplasma concentrations
1365.8
10817
67
3.8
140 2
10830
0
0
CVVHConvective clearance
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Ultrafilter 3+ liters/hour
Replace all ultrafiltratewith sterile fluid at idealplasma concentrations
1365.8
10817
67
3.8
140 4
10830
0
0
CVVHConvective clearance
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Post-filter replacement fluid
CVVHConvective clearance
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Pre-filter replacement fluid
CVVHConvective clearance
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CVVHDFConvective and Diffusive
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high dose dialysissu
rviva
l
Severity of illness (CCARF Score)
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high dose dialysissu
rviva
l
Severity of illness (CCARF Score)
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high dose dialysissu
rviva
l
Severity of illness (CCARF Score)
Low dose
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high dose dialysissu
rviva
l
Severity of illness (CCARF Score)
High dose
Low dose
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high dose dialysissu
rviva
l
Severity of illness (CCARF Score)
High dose
Low dose
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high dose dialysissu
rviva
l
Severity of illness (CCARF Score)
High dose
Low dose
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high dose dialysissu
rviva
l
Severity of illness (CCARF Score)
High dose
Low dose
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Ronco’s landmark dialysis dose study
425 patients with dialysis dependent acute renal failure were randomized to one of three doses of CVVH
20 mL/kg/hr of effluent
35 mL/kg/hr
45 mL/kg/hr
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20 mL/kg/hr
35 mL/kg/hr
45 mL/kg/hr
Ronco C, Bellomo R, Hormea P, Et al. Lancet 2000; 355: 26-30.
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Ronco 425 CVVH 20/h vs. 35-45 ml/kg/h*
Bouman 106 CVVH 20ml/kg/h* vs. 48 ml/kg/h
Schiffl 160 Alternate day vs. daily hemodialysis
Saudan 206 CVVH 25 ml/kg/h vs. CVVHDF 42 ml/kg/h
Total (fixed effects)
Total (random effects)
1 10Odds ratio
Study n treatment groups
*For purposes of analysis the two high-dose arms in Ronco were combined, as were the two low-dose arms in Bouman. If these groups are removed the odds ratio is unchanged (1.94; P <0.001).
Kellum J. Nature Clin Practice Nephrol 2007 3: 128-9.
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Ronco 425 CVVH 20/h vs. 35-45 ml/kg/h*
Bouman 106 CVVH 20ml/kg/h* vs. 48 ml/kg/h
Schiffl 160 Alternate day vs. daily hemodialysis
Saudan 206 CVVH 25 ml/kg/h vs. CVVHDF 42 ml/kg/h
Total (fixed effects)
Total (random effects)
1 10Odds ratio
Study n treatment groups
*For purposes of analysis the two high-dose arms in Ronco were combined, as were the two low-dose arms in Bouman. If these groups are removed the odds ratio is unchanged (1.94; P <0.001).
Kellum J. Nature Clin Practice Nephrol 2007 3: 128-9.
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ATN trial
US trial Prospective randomized, multi-center trial
27 institutions primarily veterans hospitals
Dose finding study, modality agnostic Conventional
dialysis SLED
CVVH CVVHD
CVVHDF
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interventions
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endpoint
Primary Endpoint: All-cause mortality at day 60.
Secondary endpoints: In-hospital death Recovery of renal function (CrCl>20)
defined as complete if Cr was <0.5 over the baseline
Duration of renal replacement therapy Dialysis free at 60 days Duration of ICU stay Return to previous home at day 60
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results
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results
563 enrolled in standard care561 randomized to intensive therapy
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60% sepsis
80% vented
Apache II score 26 predicted mortality 55%
BUN at initiation of RRT 65
half in the MICU half in the SICU
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This report currently should be viewed as the definitive study defining dialysis dosing in critically ill patients with AKI
H. David Hume
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…the patient dies from multi-organ failure while in exquisite electrolyte
& fluid balance.
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Fluid balance?
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Fluid balance?
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Patients stratified by net fluid gain from admission to initiation of CRT
Fluid in – fluid outICU admit weight X 100
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longer ICU stay
higher mortality
more multi-organ dysfunction
more likely to be intubated
more inotropes
more sepsis
higher PRISM score
More fluid. More sick.
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Worse fluid overload severity remained independently associated with mortality (OR, 1.03; 95% CI, 1.01-1.05). The relationship was satisfactorily linear and the OR suggests a
3% increase in mortality for each 1% increase in degree of fluid overload at CRRT initiation.
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80 kg adult Is and Os: 2,400 mL in (100 mL/hr) and
1,600 mL of urine (67 mL/hr) Positive balance of 800 mL. If after 3 days the
patient becomes oliguric with 200 mL of urine output for two days (2,200 mL positive per day) before initiating CRT.
That patient would be up 6,800 mL or 8% of bodyweight
24% increase in mortality compared to someone with matched ins and outs
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observational data from SOAP study of ICU care in Europe
198 ICUs 24 countries 147 patients 1120 had AKI ARF defined as a Cr >3.5 or urine output <
500 mL
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Moreover, this would suggest that prevention or management of fluid overload is evolving as a primary trigger/indicator for e x t r a - c o r p o re a l fl u i d remova l , and th is may be independent of dose delivery or solute clearance.
Critical Care 2008, 12:169
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summary
Prognosis is grim We have two validated, consensus definitions
R isk I njury F ailure L oss of function E srd
Outpatient and inpatient acquired ARF differ in etiology
Hospital acquired disease is your fault
AKIN Stage 1 Stage 2 Stage 3
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summary
FE of Urea is a validated way to separate pre-renal from AKI even in the presence of diuretics
Use of high dose dialysis regardless of methodology offers no survival benefit
Do not fluid overload your patient Dopamine doesn’t work
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Acute kidney injury is not a specialist’s emergency; it is seen commonly in acute medicine and, as such, it is essential that all physicians have the confidence and ski l ls to identify and manage it.
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Done