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Dr. Osama El-Shahat
Consultant Nephrologist
Head of Nephrology Department
New Mansoura General Hospital (international)
ISN Educational Ambassador
Objectives
Treatment
Non- dialytic support
Dialytic support
Diagnosis
Incidence
Mortality
Biomarkers
Definatinon
ARF AKI
ARF AKI
1802: Ischuria Renalis (William Heberden)
1909: Acute Bright’s Disease (William Osler)
W.W.I: War Nephritis
W.W.II: Acute Kidney Insufficiency (Bywaters &
Beall)
1951: Acute Renal Failure (Homer W. Smith)
2006 : Acute Kidney Injury (AKI Network)
 By AKI we actually mean “loss of small solute
clearance” (urea/creatinine increase in
blood)
 This implies loss of GFR
 So…clinically we actually mean
“acute decrease in GFR”
What do we mean by AKI?
Lameire N, Van BW, Vanholder R. Nat Clin Pract Nephrol 2006; 2: 364–377.
Can we do staging for AKI?
AKIN Classification
What is the advantages of RIFLE Criteria?
 Applying the RIFLE criteria revealed new insights.
 Firstly, the RIFLE classification is feasible and
fairly straightforward.
 Secondly, the patients categorized as RIFLE-F had a
far higher mortality than RIFLE-I and -R patients.
Max Bell et al; Nephrol Dial Transplant 2005 20:354 –360
Number of ARF Hospitalizations: 1979 to 2002
Rates per 1,000 persons
0.0
0.5
1.0
1.5
2.0
2.5
1980 1982 1984 1986 1988 1990 1992 1994 1996 1998 2000 2002
Source: National Center for Health Statistics, National Hospital Discharge Survey
Kidney International advance online publication , 1
May 2013
Mortality in AKI
Causes of AKI
Pre renal Intrinsic renal Post renal
Decrease in
effective
blood volume.
Arterial
occlusion
Or
stenosis.
Homodynamic
Form.
Vascular
Vasculitis.
Malignant
hypertension
Acute
Glomerulo
nephritis
Acute
Interstitial
nephritis
Acute
Tubular
necrosis
Ischemic. Nephrotoxic.
Obstruction
Of
Collecting
System
Or
Extra renal
drainage
Exogenous
Antibiotic
Radio contrast
cisplatin
Endogenous
Intra tubular pigment
Intra tubular protein.
Intra tubular crystal.
Causes of AKI
Post-OP, sepsis,
shock,multi-organ
failure 70%
Obstructive
uropathy 15%
Glomerulonephritis 5%
Nephrotoxic agents 10%
reduced blood flow
ischemia
acute tubular necrosis
Timing nephrology consultation
(Mehta,Am J Med 2002)
In-hospital mortality
Early
consult
Delayed
consult
P
40% 67% <0,001
 Early nephrologist involvement in patients with
AKI may reduce the risk of a further decrease in
kidney function.
Am J Kidney Dis. 2011;57(2):228-234
Kidney International (2013) 83, 901–908
Early Referral
Biomarkers are foot prints of actual
organ damage
 Creatinine Not A Biomarker
 The creatinine level is influenced by multiple non-
renal factors, such as age, gender, muscle mass, muscle
metabolism, diet, medications, and hydration status
 In AKI, the serum creatinine level can take several
hours or days to reach a new steady state and thus does
not reflect the actual decrease in GFR in the acute
setting
 Because of renal reserve, the serum creatinine level
may not rise until more than half of the kidney
function has been lost
Creatinine is late, or is it too late?
New urinary biomarkers for the early detection of
acute kidney disease
Han, Bonventre,Current Opin Crit Care 2004, 10:476–482
Neutrophil gelatinase associated lipocalin
Early detection of AKI by Cystatin C
Definition of AF
Area under the ROC
Day - 2 Day - 1 Day 0
≥ 50 % increase 0.82 0.97 0.99
≥ 100 % increase 0.92 0.98 0.98
≥ 200 % increase 0.97 0.99 0.99
•Changes in cystatin C were able to detect the onset of AKI
one to two days earlier than comparable changes in serum creatinine
1. RIFLE- R ( ≥ 50 % increase ): 1.5 ± 0.6 days earlier
2. RIFLE- I ( ≥ 100 % increase): 1.2 ± 0.9 days earlier
3. RIFLE- F ( ≥ 200 % increase): 1.0 ± 0.6 days earlier
Herget-Rosenthal et al, Kidney Int 2004, 66: 1115- 1122
Indications of Renal Biopsy
1
Urine
No cast
FENa<1%
Muddy
brown cast
FENa>1%
Red cell
cast
White cell
cast
eosinophil
Pre-renal
ATN Glomerular Interstitial
Biopsy
2. Unknown cause
3. Prolonged ATN
Loop diuretics in AKI
Diuretics, particularly high doses of loop diuretics, are frequently
administered to patients with acute renal failure. This is done in part
in an attempt to convert oliguric to nonoliguric acute renal failure.
However, a retrospective observational report found that the use of
diuretics in this setting may increase the risk of death and no
recovery of renal function.
3.4.1: We recommend not using diuretics to prevent AKI. (1B )
3.4.2: We suggest not using diuretics to treat AKI, except in the
management of volume overload. (2C )
There is insufficient evidence that the low-dose dopamine
improves survival or obviates the need for dialysis in persons with
acute renal failure. The routine use of low-dose dopamine should be
discouraged until a prospective, randomized, placebo-controlled trial
establishes its safety and efficacy.
Is the administration of dopamine associated with adverse or
favorable outcomes in acute renal failure? Auriculin Anaritide
Acute Renal Failure Study Group.
Low Dose Dopamine in AKI
3.5.1: We recommend not using low-dose dopamine to prevent or
treat AKI. (1A)
IV Fluids in AKI
3.1.1: In the absence of hemorrhagic shock, we
suggest using isotonic crystalloids rather than
colloids (albumin or starches) as initial
management for expansion of intravascular
volume in patients at risk for AKI or with AKI.
(2B)
Contrast Induced AKI
isotonic sodiumwith eitherexpansionvolume.i.v:We recommend4.4.1
. volume expansion,i.v, rather than nochloride or sodium bicarbonate solutions
)A1AKI. (-in patients at increased risk for CI
or)IHD(hemodialysisnot using prophylactic intermittent:We suggest4.5.1
hemofiltration (HF) for contrast-media removal in patients at increased risk for
)C2AKI. (-CI
, incrystalloidsisotonic.i.vwithtogether,NACoral:We suggest using4.4.3
)D2AKI. (-patients at increased risk of CI
4.3.2:We recommend using either iso-osmolar or low-osmolar iodinated
contrast media, rather than high-osmolar iodinated contrast media in patients
at increased risk of CI-AKI. (1B)
Bicarbonate or Saline
Among the large
randomized trials there
was no evidence of benefit
for hydration with sodium
bicarbonate compared
with sodium chloride for
the prevention of CI-AKI.
Contrast Induced AKI
Stage-based management
General Principles
Stage 1 (Risk)
Risk for more severe AKI
Monitor (prevent
progression)
Stage 2 (Injury)
Risk of AKI-related
mortality/morbidity high
Conservative therapy)
Stage 3 (Failure)
Highest risk of death
Consider RRT
Avoid subclavian catheters if possible
Discontinue all nephrotoxic agents when possible
Consider invasive diagnostic workup
Consider Renal Replacement Therapy
1 2 3
Non-invasive diagnostic workup
Ensure volume status and perfusion pressure
Check for changes in drug dosing
AKI Stage
Consider functional hemodynamic monitoring
Monitoring Serum creatinine and urine output
Consider ICU admission
Avoid hyperglycemia
Consider alternatives to radiocontrast procedures
Indications for RRT in critically ill AKI patients
Renal Indications
Life-threatening indications
Hyperkalemia
Metabolic Acidosis
Pulmonary edema
Uremic omplications
Dialysis Interventions forTreatment of AKI
 5.1.1: Initiate RRT emergently when life-threatening
changes in fluid, electrolyte, and acid-base balance
exist.(Not Graded)
 5.1.2: Consider the broader clinical context, the presence
of conditions that can be modified with RRT, and trends
of laboratory tests—rather than single BUN and
creatinine thresholds alone—when making the decision
to start RRT. (Not Graded)
Conclusions
Early detection and treatment of AKI may improve
outcomes.
Even a minor acute reduction in kidney function has
an adverse prognosis.
Hunting AKI in ICU….use a RIFLE .
Early referral will improve outcome in AKI
Aki  sudan 2017 (1)

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Aki sudan 2017 (1)

  • 1. Dr. Osama El-Shahat Consultant Nephrologist Head of Nephrology Department New Mansoura General Hospital (international) ISN Educational Ambassador
  • 2. Objectives Treatment Non- dialytic support Dialytic support Diagnosis Incidence Mortality Biomarkers Definatinon ARF AKI
  • 3. ARF AKI 1802: Ischuria Renalis (William Heberden) 1909: Acute Bright’s Disease (William Osler) W.W.I: War Nephritis W.W.II: Acute Kidney Insufficiency (Bywaters & Beall) 1951: Acute Renal Failure (Homer W. Smith) 2006 : Acute Kidney Injury (AKI Network)
  • 4.  By AKI we actually mean “loss of small solute clearance” (urea/creatinine increase in blood)  This implies loss of GFR  So…clinically we actually mean “acute decrease in GFR” What do we mean by AKI?
  • 5. Lameire N, Van BW, Vanholder R. Nat Clin Pract Nephrol 2006; 2: 364–377. Can we do staging for AKI?
  • 7. What is the advantages of RIFLE Criteria?  Applying the RIFLE criteria revealed new insights.  Firstly, the RIFLE classification is feasible and fairly straightforward.  Secondly, the patients categorized as RIFLE-F had a far higher mortality than RIFLE-I and -R patients. Max Bell et al; Nephrol Dial Transplant 2005 20:354 –360
  • 8. Number of ARF Hospitalizations: 1979 to 2002 Rates per 1,000 persons 0.0 0.5 1.0 1.5 2.0 2.5 1980 1982 1984 1986 1988 1990 1992 1994 1996 1998 2000 2002 Source: National Center for Health Statistics, National Hospital Discharge Survey
  • 9. Kidney International advance online publication , 1 May 2013 Mortality in AKI
  • 10. Causes of AKI Pre renal Intrinsic renal Post renal Decrease in effective blood volume. Arterial occlusion Or stenosis. Homodynamic Form. Vascular Vasculitis. Malignant hypertension Acute Glomerulo nephritis Acute Interstitial nephritis Acute Tubular necrosis Ischemic. Nephrotoxic. Obstruction Of Collecting System Or Extra renal drainage Exogenous Antibiotic Radio contrast cisplatin Endogenous Intra tubular pigment Intra tubular protein. Intra tubular crystal.
  • 11. Causes of AKI Post-OP, sepsis, shock,multi-organ failure 70% Obstructive uropathy 15% Glomerulonephritis 5% Nephrotoxic agents 10% reduced blood flow ischemia acute tubular necrosis
  • 12. Timing nephrology consultation (Mehta,Am J Med 2002) In-hospital mortality Early consult Delayed consult P 40% 67% <0,001  Early nephrologist involvement in patients with AKI may reduce the risk of a further decrease in kidney function. Am J Kidney Dis. 2011;57(2):228-234
  • 13. Kidney International (2013) 83, 901–908 Early Referral
  • 14. Biomarkers are foot prints of actual organ damage  Creatinine Not A Biomarker  The creatinine level is influenced by multiple non- renal factors, such as age, gender, muscle mass, muscle metabolism, diet, medications, and hydration status  In AKI, the serum creatinine level can take several hours or days to reach a new steady state and thus does not reflect the actual decrease in GFR in the acute setting  Because of renal reserve, the serum creatinine level may not rise until more than half of the kidney function has been lost
  • 15. Creatinine is late, or is it too late?
  • 16. New urinary biomarkers for the early detection of acute kidney disease Han, Bonventre,Current Opin Crit Care 2004, 10:476–482 Neutrophil gelatinase associated lipocalin
  • 17. Early detection of AKI by Cystatin C Definition of AF Area under the ROC Day - 2 Day - 1 Day 0 ≥ 50 % increase 0.82 0.97 0.99 ≥ 100 % increase 0.92 0.98 0.98 ≥ 200 % increase 0.97 0.99 0.99 •Changes in cystatin C were able to detect the onset of AKI one to two days earlier than comparable changes in serum creatinine 1. RIFLE- R ( ≥ 50 % increase ): 1.5 ± 0.6 days earlier 2. RIFLE- I ( ≥ 100 % increase): 1.2 ± 0.9 days earlier 3. RIFLE- F ( ≥ 200 % increase): 1.0 ± 0.6 days earlier Herget-Rosenthal et al, Kidney Int 2004, 66: 1115- 1122
  • 18. Indications of Renal Biopsy 1 Urine No cast FENa<1% Muddy brown cast FENa>1% Red cell cast White cell cast eosinophil Pre-renal ATN Glomerular Interstitial Biopsy 2. Unknown cause 3. Prolonged ATN
  • 19. Loop diuretics in AKI Diuretics, particularly high doses of loop diuretics, are frequently administered to patients with acute renal failure. This is done in part in an attempt to convert oliguric to nonoliguric acute renal failure. However, a retrospective observational report found that the use of diuretics in this setting may increase the risk of death and no recovery of renal function. 3.4.1: We recommend not using diuretics to prevent AKI. (1B ) 3.4.2: We suggest not using diuretics to treat AKI, except in the management of volume overload. (2C )
  • 20. There is insufficient evidence that the low-dose dopamine improves survival or obviates the need for dialysis in persons with acute renal failure. The routine use of low-dose dopamine should be discouraged until a prospective, randomized, placebo-controlled trial establishes its safety and efficacy. Is the administration of dopamine associated with adverse or favorable outcomes in acute renal failure? Auriculin Anaritide Acute Renal Failure Study Group. Low Dose Dopamine in AKI 3.5.1: We recommend not using low-dose dopamine to prevent or treat AKI. (1A)
  • 21. IV Fluids in AKI 3.1.1: In the absence of hemorrhagic shock, we suggest using isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume in patients at risk for AKI or with AKI. (2B)
  • 22. Contrast Induced AKI isotonic sodiumwith eitherexpansionvolume.i.v:We recommend4.4.1 . volume expansion,i.v, rather than nochloride or sodium bicarbonate solutions )A1AKI. (-in patients at increased risk for CI or)IHD(hemodialysisnot using prophylactic intermittent:We suggest4.5.1 hemofiltration (HF) for contrast-media removal in patients at increased risk for )C2AKI. (-CI , incrystalloidsisotonic.i.vwithtogether,NACoral:We suggest using4.4.3 )D2AKI. (-patients at increased risk of CI 4.3.2:We recommend using either iso-osmolar or low-osmolar iodinated contrast media, rather than high-osmolar iodinated contrast media in patients at increased risk of CI-AKI. (1B)
  • 23. Bicarbonate or Saline Among the large randomized trials there was no evidence of benefit for hydration with sodium bicarbonate compared with sodium chloride for the prevention of CI-AKI. Contrast Induced AKI
  • 24. Stage-based management General Principles Stage 1 (Risk) Risk for more severe AKI Monitor (prevent progression) Stage 2 (Injury) Risk of AKI-related mortality/morbidity high Conservative therapy) Stage 3 (Failure) Highest risk of death Consider RRT Avoid subclavian catheters if possible Discontinue all nephrotoxic agents when possible Consider invasive diagnostic workup Consider Renal Replacement Therapy 1 2 3 Non-invasive diagnostic workup Ensure volume status and perfusion pressure Check for changes in drug dosing AKI Stage Consider functional hemodynamic monitoring Monitoring Serum creatinine and urine output Consider ICU admission Avoid hyperglycemia Consider alternatives to radiocontrast procedures
  • 25. Indications for RRT in critically ill AKI patients Renal Indications Life-threatening indications Hyperkalemia Metabolic Acidosis Pulmonary edema Uremic omplications
  • 26. Dialysis Interventions forTreatment of AKI  5.1.1: Initiate RRT emergently when life-threatening changes in fluid, electrolyte, and acid-base balance exist.(Not Graded)  5.1.2: Consider the broader clinical context, the presence of conditions that can be modified with RRT, and trends of laboratory tests—rather than single BUN and creatinine thresholds alone—when making the decision to start RRT. (Not Graded)
  • 27. Conclusions Early detection and treatment of AKI may improve outcomes. Even a minor acute reduction in kidney function has an adverse prognosis. Hunting AKI in ICU….use a RIFLE . Early referral will improve outcome in AKI