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Acute kidney injury
Kasemsan A. MD
Epidemiology
5-7% of hospitalized patients
Up to 30% of patients in ICU
Harrison’s principle of Internal medicine 19 th ed.,2015
 Volume depletion
 Adverse effects of medications
 Obstruction of the urinary tract
Common causes of community-acquired AKI
 Sepsis
 Major surgical procedures
 Critical illness :heart or liver failure
 CI-AKI
 Nephrotoxic medication
Common causes of hospital-acquired AKI
Definition
Increased in SCr by ≥ 0.3 mg/dl (≥ 26.5 µmol/l) within 48 hour
Increased in SCr to ≥ 1.5 times baseline, which is known or
presumed to have occurred within the prior 7 days
Urine volume < 0.5 ml/kg/h for 6 hours.
KDIGO AKI,2012
Staging of AKI
KDIGO AKI,2012
Comparison of RIFLE and AKIN criteria
for diagnosis and classification of AKI
KDIGO AKI,2012
Non-oliguric and oliguric AKI
Oliguria
urine output < 400 ml/day
Non-oliguria
urine output > 400 ml / day
Anuria
urine output < 100 ml/day
Conceptual model of AKI
KDIGO AKI,2012
Novel biomarker for AKI
NGAL (Neutrophil Gelatinase- Associated Lipocalin)
KIM-1
IL-18
Cystatin C
L – type fatty acid binding protein (L-FABP)
KDIGO AKI,2012
KDIGO AKI,2012
Kashani K. Crit Care. 2013;6;17(1):R25.
IGFBP7 (insulin-like growth factor-binding protein 7)
TIMP-2 (tissue inhibitor of metalloproteinase-2)
Diagnosis : [TIMP-2]・[IGFBP7] > 0.3 (ng/ml)(2)/1,000
predicts moderate to severe AKI (stage 2-3) within 12 h
AKI : Urinary Biomarkers
Kashani K. Crit Care. 2013;6;17(1):R25.
Bihorac A. Am J Respir Crit Care Med. 2014;189(8):932-9.
Etiology & Pathophysiology
Harrison’s principle of Internal medicine 19 th ed.,2015
Comprehensive clinical nephrology 5th edition
Pathophysiology of prerenal azotemia
Intravascular
volume depletion
Reduced cardiac output
Systemic vasodilation
Renal vasoconstriction
Increased IAP
Renal blood flow = 20% of CO
Tubulo Glomerular Feedback [TGF]
Decreased perfusion pressureNSAID EffectRAAS Blockade effect
J G A buelo : NEJM 357:797-805, 2007
Pathophysiology of intrinsic renal azotemia
Glomerular Tubular
Interstitium
Vascular
Harrison’s principle of Internal medicine 19 th ed.,2015
Harrison’s principle of Internal medicine 19 th ed.,2015
Pathophysiology of acute tubular necrosis
Comprehensive clinical nephrology 5th edition
Tubular
effects
Comprehensive clinical nephrology 5th edition
Phase
of
ATN
Drugs
and
the
kidney
Comprehensive clinical nephrology 5th edition
Pathophysiology of acute interstitial nephritis
Acute declination in renal function
Inflammatory infiltrates and edema
within interstitium
Classic triads (only 10%)
Maculopapular rash
Peripheral eosinophila or
eosinophiluria
Arthralgias
Causes
Drugs e.g. Penicillins, cephalosporins,
NSAIDs, PPIs
Infection e.g. Pyelonephritis,
leptospirosis, Hantavirus
Autoimmune e.g. Sjogren syndrome,
sarcoidosis, SLE
Malignancy e.g. lymphoma, leukemia
Glomerular disease
Idiopathic e.g. TINU syndrome
Pathophysiology of postrenal azotemia
Increased intratubular pressure
Overcome glomerular filtration
pressure
Decreased GFR
Upper tract extrinsic causes
Lower tract causes
Upper tract intrinsic causes
Brenner and Rector’s The kidney 9th edition
Harrison’s principle of Internal medicine 19 th ed.,2015
Postrenal azotemia without
obstructive uropathy by ultrasound
Early obstruction
Intratubular obstruction
Volume depletion
Pre-existing small kidney
Trapped kidney (e.g. retroperitoneal fibrosis)
Diagnostic approach
History taking
Physical examination
Laboratory investigation
BUN,Creatinine
Urinalysis
Urine profile (urine electrolyte, urine creatinine, urine osmole)
Imaging
Kidney biopsy
Comprehensive clinical nephrology 5th edition
 Increased BUN
 Dehydration
 UGIB
 Steroid use
 Hypercatabolic state
 High protein diet
 Heart failure
 Outdated tetracycline
 Decreased BUN
 Liver disease
 Malnutrition
 Anabolic state
 Increased creatinine
 Large muscle bulk
 Rhabdomyolysis
 Reduced tubular secretion
 Trimethoprim
 Cimetidine
 Probenecid
 Creatine supplement
 Decreased creatinine
 Small muscle mass
 Aging
 Vegetarian
 Limb amputation
Pseudoazotemia
Prerenal
azotemia
vs
Acute
tubular
necrosis
Diagnostic index Prerenal AKI ATN
Urine Na (mEq/L) <20 >40
FENa (%) <1 >2
Renal failure index
(UNa/(Ucr/Pcr))
<1 >1
Urine sp.gr. >1.018 About 1.010
Urine osmolarity
(mOsm/kgH2O)
>500 About 300
Ucr/Pcr >40 <20
UUN/BUN >8 <3
BUN/Cr >20 <10-15
Urine sediment Hyaline casts Muddy brown casts
AKI with FENa < 1%
Prerenal
Extra-renal loss
Hepatorenal syndrome
Acute glomerulonephritis
TTP/HUS
Early urinary tract
obstruction
Acute tubular necrosis
Non-oliguric AKI
Contrasted induced
nephropathy
ACEIs/ARBs/NSAIDs
AKI in pregnancy
Sepsis
Extensive burn
Rhabdomyolysis
Hemolysis
Uric acid nephropathy
AKI with FENa > 2%
Classical ATN
Ischemic
Toxic
Acute interstitial nephritis
Acute renal artery
occlusion
Late urinary tract
obstruction
Prerenal AKI
Diuretics use
Mineralocorticoid deficiency
CKD
Alkalosis (bicarbonaturia)
Renal salt wasting
Diabetes mellitus
Harrison’s Internal medicine 19th edition
RBC
RBC cast
Muddy brown cast
WBC
WBC cast
Eosinophiluria
Hyaline cast
Broad waxy cast
Step to approach azotemia
Step 1: Exclude and correct pseudoazotemia
Step 2: Classification AKI, AKI on top CKD, CKD progression
Step 3: Finding postrenal AKI and correction
Step 4: Find and correct intrinsic renal causes of AKI
Step 5: Prerenal AKI vs ATN
Step 6: Dialysis if indicated
Adapted from KDIGO guidelines 2012
Step approach to AKI
Management
of
Acute kidney injury
KDIGO AKI,2012
Management of AKI
Specific treatment is not available for the majority of forms of AKI.
Supportive therapy to ameliorate derangements of fluid and
electrolyte homeostasis and prevent uremic complications.
Elimination of nephrotoxic agents (ACE inhibitors, ARBs,
NSAIDs, aminoglycoside, amphotericin B)
KDIGO AKI,2012
Management of AKI
Initiation of renal replacement therapy when indicated.
The ultimate goals of management are to prevent death,
facilitate recovery of kidney function, and minimize the risk of
CKD.
KDIGO AKI,2012
Hemodynamic monitoring and support for
prevention and management of AKI
In the absence of hemorrhagic shock, KDIGO 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)
KDIGO recommend the use of vasopressors in conjunction
with fluids in patients with vasomotor shock with or at risk for
AKI. (1C)
KDIGO AKI,2012
Hemodynamic monitoring and support for
prevention and management of AKI
KDIGO suggest using protocol-based management of
hemodynamic and oxygenation parameters to prevent
development or worsening of AKI in high-risk patients in the
perioperative setting (2C) or in patients with septic shock (2C).
KDIGO AKI,2012
Glycemic control and nutritional support
In critically ill patients, KDIGO suggest insulin therapy targeting
plasma glucose 110–149 mg/dl (6.1–8.3 mmol/l). (2C)
KDIGO suggest achieving a total energy intake of 20–30
kcal/kg/d in patients with any stage of AKI. (2C)
KDIGO suggest to avoid restriction of protein intake with the
aim of preventing or delaying initiation of RRT. (2D)
KDIGO AKI,2012
KDIGO suggest administering
0.8–1.0 g/kg/d of protein in noncatabolic AKI patients without
need for dialysis (2D)
1.0–1.5 g/kg/d in patients with AKI on RRT (2D)
Up to a maximum of 1.7 g/kg/d in patients on continuous renal
replacement therapy (CRRT) and in hypercatabolic patients.
(2D)
KDIGO suggest providing nutrition preferentially via the enteral
route in patients with AKI. (2C)
KDIGO AKI,2012
Glycemic control and nutritional support
Use of diuretic in AKI
KDIGO recommend not using diuretics to prevent AKI. (1B)
Suggest not using diuretics to treat AKI, except in the
management of volume overload. (2C)
KDIGO AKI,2012
Vasodilator therapy
KDIGO recommend not using low-dose dopamine to prevent or
treat AKI. (1A)
Suggest not using fenoldopam to prevent or treat AKI. (2C)
Suggest not using atrial natriuretic peptide (ANP) to prevent
(2C) or treat (2B) AKI.
KDIGO AKI,2012
Growth factor intervention
KDIGO recommend not using recombinant human (rh) IGF-1 to
prevent or treat AKI. (1B)
KDIGO AKI,2012
Adenosine receptor antagonist
KDIGO suggest that a single dose of theophylline may be given
in neonates with severe perinatal asphyxia who are at high risk
of AKI. (2B)
KDIGO AKI,2012
Prevention of aminoglycoside and amphotericin
related AKI
KDIGO suggest not using aminoglycosides for the treatment of
infections unless no suitable, less nephrotoxic, therapeutic
alternatives are available. (2A)
KDIGO suggest that, in patients with normal kidney function in
steady state, aminoglycosides are administered as a single
dose daily rather than multiple-dose daily treatment regimens.
(2B)
KDIGO AKI,2012
KDIGO recommend monitoring aminoglycoside drug levels when
treatment with multiple daily dosing is used for more than 24 hours. (1A)
Suggest monitoring aminoglycoside drug levels when treatment with
single-daily dosing is used for more than 48 hours. (2C)
Suggest using topical or local applications of aminoglycosides (e.g.,
respiratory aerosols, instilled antibiotic beads), rather than i.v. application,
when feasible and suitable. (2B)
KDIGO AKI,2012
Prevention of aminoglycoside and amphotericin
related AKI
KDIGO suggest using lipid formulations of amphotericin B
rather than conventional formulations of amphotericin B. (2A)
In the treatment of systemic mycoses or parasitic infections,
KDIGO recommend using azole antifungal agents and/or the
echinocandins rather than conventional amphotericin B, if equal
therapeutic efficacy can be assumed. (1A)
KDIGO AKI,2012
Prevention of aminoglycoside and amphotericin
related AKI
Other method of prevention of AKI
in the critically ill
KDIGO suggest that off-pump coronary artery bypass graft
surgery not be selected solely for the purpose of reducing
perioperative AKI or need for RRT. (2C)
Suggest not using NAC to prevent AKI in critically ill patients
with hypotension. (2D)
KDIGO recommend not using oral or i.v. NAC for prevention of
postsurgical AKI. (1A)
KDIGO AKI,2012
Contrast induced AKI
Contrast induced AKI
Define and stage AKI after administration of intravascular
contrast media as per Recommendations (Not Graded)
In individuals who develop changes in kidney function after
administration of intravascular contrast media, evaluate for CI-
AKI as well as for other possible causes of AKI. (Not Graded)
KDIGO AKI,2012
Assess the risk for CI-AKI and, in particular, screen for pre-
existing impairment of kidney function in all patients who are
considered for a procedure that requires intravascular (i.v. or i.a.)
administration of iodinated contrast medium. (Not Graded)
Risk factors
Pre-existing CKD
Diabetes mellitus
Advanced CHF
High dose contrast media
Hemodynamic instability
KDIGO AKI,2012
Contrast induced AKI
Consider alternative imaging methods in patients at increased
risk for CI-AKI. (Not Graded)
KDIGO AKI,2012
Contrast induced AKI
Nonpharmacological prevention
strategies of CI-AKI
Use the lowest possible dose of contrast medium in patients at
risk for CI-AKI. (Not Graded)
KDIGO 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)
KDIGO AKI,2012
Pharmacological prevention
strategies of CI-AKI
KDIGO recommend i.v. volume expansion with either isotonic
sodium chloride or sodium bicarbonate solutions rather than no i.v.
volume expansion, in patients at increased risk for CI-AKI. (1A)
Recommend not using oral fluids alone in patients at increased risk
of CI-AKI. (1C)
KDIGO AKI,2012
KDIGO suggest using oral NAC together with i.v. isotonic
crystalloids in patients at increased risk of CI-AKI. (2D)
Suggest not using theophylline to prevent CI-AKI. (2C)
Recommend not using fenoldopam to prevent CI-AKI. (1B)
Pharmacological prevention
strategies of CI-AKI
KDIGO AKI,2012
Effects of hemodialysis
or hemofiltration
KDIGO suggest not using prophylactic intermittent
hemodialysis (IHD) or hemofiltration (HF) for contrast-media
removal in patients at increased risk for CI-AKI. (2C)
KDIGO AKI,2012
Indications for acute renal
replacement therapy
A : metabolic Acidosis
E : Electrolyte imbalance
I : Intoxication / Ingestion of toxic substance
O : fluid Overload that is refractory to diuretics
U : signs of Uremia
KDIGO AKI,2012
Mode of RRT
Conventional intermittent hemodialysis (IHD)
Sustained low-efficacy dialysis (SLED)
Continuous renal replacement therapy (CRRT)
Peritoneal dialysis(PD)
KDIGO AKI,2012
Vascular access for renal replacement
therapy in AKI
When choosing a vein for insertion of a dialysis catheter in
patients with AKI, consider these preferences (Not Graded):
First choice: right jugular vein
Second choice: femoral vein
Third choice: left jugular vein
Last choice: subclavian vein
KDIGO AKI,2012
AKI : TREATMENT
Specific Rx : Rx cause of AKI
Supportive Rx
1. Maintain hemodynamic and oxygenation
2. Monitor VS, I/O, BW
3. Monitor BUN, Cr, electrolyte,…
4. Discontinue all nephrotoxic agents
5. Nutrition : prefer enteral route
6. Total energy intake 20-30 kcal/kg/day
7. Protein intake g/kg/day
Non-catabolic 0.8-1.0
RRT 1.0-1.5
CRRT, Hypercatabolic up to a max. of 1.7
8. In critically ill patients : insulin therapy targeting PG 110-149 mg/dL
Take home messages
KDIGO AKI,2012
Brenner and Rector’s The kidney 9th edition
9. HypoNa : free water restriction < 1 L/day
10. Volume overload : salt restriction < 1.0-1.5 g/day, furosemide 200 mg iv bolus or 20 mg/h iv
11. Not using diuretics to enhance kidney function recovery or to reduce the duration or
frequency of RRT
12. Not using low-dose dopamine, fenoldopam, ANP, rh IGF-1
13. HyperK : K diet restriction, off ACEI & ARB & K-sparing diuretics, medical Rx
14. Metabolic acidosis : NaHCO3 if pH < 7.15
15. HypoCa : CaCO3 if symptomatic or NaHCO3 to be administered
16. HyperP : P diet restriction, P binders
17. HyperMg : avoid Mg-containing medications
18. Hyperuricemia : usually mild (< 15 mg/dL),if severe add allopurinol, or recombinant uricase
19. Check for changes of drug dosing
20. RRT when indicated
Take home messages
KDIGO AKI,2012
Brenner and Rector’s The kidney 9th edition
AKI for General practice

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AKI for General practice

  • 2. Epidemiology 5-7% of hospitalized patients Up to 30% of patients in ICU Harrison’s principle of Internal medicine 19 th ed.,2015  Volume depletion  Adverse effects of medications  Obstruction of the urinary tract Common causes of community-acquired AKI  Sepsis  Major surgical procedures  Critical illness :heart or liver failure  CI-AKI  Nephrotoxic medication Common causes of hospital-acquired AKI
  • 3. Definition Increased in SCr by ≥ 0.3 mg/dl (≥ 26.5 µmol/l) within 48 hour Increased in SCr to ≥ 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days Urine volume < 0.5 ml/kg/h for 6 hours. KDIGO AKI,2012
  • 5. Comparison of RIFLE and AKIN criteria for diagnosis and classification of AKI KDIGO AKI,2012
  • 6. Non-oliguric and oliguric AKI Oliguria urine output < 400 ml/day Non-oliguria urine output > 400 ml / day Anuria urine output < 100 ml/day
  • 7. Conceptual model of AKI KDIGO AKI,2012
  • 8. Novel biomarker for AKI NGAL (Neutrophil Gelatinase- Associated Lipocalin) KIM-1 IL-18 Cystatin C L – type fatty acid binding protein (L-FABP) KDIGO AKI,2012
  • 10. Kashani K. Crit Care. 2013;6;17(1):R25.
  • 11. IGFBP7 (insulin-like growth factor-binding protein 7) TIMP-2 (tissue inhibitor of metalloproteinase-2) Diagnosis : [TIMP-2]・[IGFBP7] > 0.3 (ng/ml)(2)/1,000 predicts moderate to severe AKI (stage 2-3) within 12 h AKI : Urinary Biomarkers Kashani K. Crit Care. 2013;6;17(1):R25. Bihorac A. Am J Respir Crit Care Med. 2014;189(8):932-9.
  • 12. Etiology & Pathophysiology Harrison’s principle of Internal medicine 19 th ed.,2015
  • 14. Pathophysiology of prerenal azotemia Intravascular volume depletion Reduced cardiac output Systemic vasodilation Renal vasoconstriction Increased IAP Renal blood flow = 20% of CO Tubulo Glomerular Feedback [TGF]
  • 15. Decreased perfusion pressureNSAID EffectRAAS Blockade effect J G A buelo : NEJM 357:797-805, 2007
  • 16. Pathophysiology of intrinsic renal azotemia Glomerular Tubular Interstitium Vascular Harrison’s principle of Internal medicine 19 th ed.,2015
  • 17. Harrison’s principle of Internal medicine 19 th ed.,2015
  • 18. Pathophysiology of acute tubular necrosis Comprehensive clinical nephrology 5th edition
  • 21.
  • 23. Pathophysiology of acute interstitial nephritis Acute declination in renal function Inflammatory infiltrates and edema within interstitium Classic triads (only 10%) Maculopapular rash Peripheral eosinophila or eosinophiluria Arthralgias Causes Drugs e.g. Penicillins, cephalosporins, NSAIDs, PPIs Infection e.g. Pyelonephritis, leptospirosis, Hantavirus Autoimmune e.g. Sjogren syndrome, sarcoidosis, SLE Malignancy e.g. lymphoma, leukemia Glomerular disease Idiopathic e.g. TINU syndrome
  • 24. Pathophysiology of postrenal azotemia Increased intratubular pressure Overcome glomerular filtration pressure Decreased GFR Upper tract extrinsic causes Lower tract causes Upper tract intrinsic causes Brenner and Rector’s The kidney 9th edition Harrison’s principle of Internal medicine 19 th ed.,2015
  • 25. Postrenal azotemia without obstructive uropathy by ultrasound Early obstruction Intratubular obstruction Volume depletion Pre-existing small kidney Trapped kidney (e.g. retroperitoneal fibrosis)
  • 26. Diagnostic approach History taking Physical examination Laboratory investigation BUN,Creatinine Urinalysis Urine profile (urine electrolyte, urine creatinine, urine osmole) Imaging Kidney biopsy Comprehensive clinical nephrology 5th edition
  • 27.  Increased BUN  Dehydration  UGIB  Steroid use  Hypercatabolic state  High protein diet  Heart failure  Outdated tetracycline  Decreased BUN  Liver disease  Malnutrition  Anabolic state  Increased creatinine  Large muscle bulk  Rhabdomyolysis  Reduced tubular secretion  Trimethoprim  Cimetidine  Probenecid  Creatine supplement  Decreased creatinine  Small muscle mass  Aging  Vegetarian  Limb amputation Pseudoazotemia
  • 28. Prerenal azotemia vs Acute tubular necrosis Diagnostic index Prerenal AKI ATN Urine Na (mEq/L) <20 >40 FENa (%) <1 >2 Renal failure index (UNa/(Ucr/Pcr)) <1 >1 Urine sp.gr. >1.018 About 1.010 Urine osmolarity (mOsm/kgH2O) >500 About 300 Ucr/Pcr >40 <20 UUN/BUN >8 <3 BUN/Cr >20 <10-15 Urine sediment Hyaline casts Muddy brown casts
  • 29. AKI with FENa < 1% Prerenal Extra-renal loss Hepatorenal syndrome Acute glomerulonephritis TTP/HUS Early urinary tract obstruction Acute tubular necrosis Non-oliguric AKI Contrasted induced nephropathy ACEIs/ARBs/NSAIDs AKI in pregnancy Sepsis Extensive burn Rhabdomyolysis Hemolysis Uric acid nephropathy
  • 30. AKI with FENa > 2% Classical ATN Ischemic Toxic Acute interstitial nephritis Acute renal artery occlusion Late urinary tract obstruction Prerenal AKI Diuretics use Mineralocorticoid deficiency CKD Alkalosis (bicarbonaturia) Renal salt wasting Diabetes mellitus
  • 32. RBC RBC cast Muddy brown cast WBC WBC cast Eosinophiluria Hyaline cast Broad waxy cast
  • 33. Step to approach azotemia Step 1: Exclude and correct pseudoazotemia Step 2: Classification AKI, AKI on top CKD, CKD progression Step 3: Finding postrenal AKI and correction Step 4: Find and correct intrinsic renal causes of AKI Step 5: Prerenal AKI vs ATN Step 6: Dialysis if indicated Adapted from KDIGO guidelines 2012 Step approach to AKI
  • 36. Management of AKI Specific treatment is not available for the majority of forms of AKI. Supportive therapy to ameliorate derangements of fluid and electrolyte homeostasis and prevent uremic complications. Elimination of nephrotoxic agents (ACE inhibitors, ARBs, NSAIDs, aminoglycoside, amphotericin B) KDIGO AKI,2012
  • 37. Management of AKI Initiation of renal replacement therapy when indicated. The ultimate goals of management are to prevent death, facilitate recovery of kidney function, and minimize the risk of CKD. KDIGO AKI,2012
  • 38. Hemodynamic monitoring and support for prevention and management of AKI In the absence of hemorrhagic shock, KDIGO 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) KDIGO recommend the use of vasopressors in conjunction with fluids in patients with vasomotor shock with or at risk for AKI. (1C) KDIGO AKI,2012
  • 39. Hemodynamic monitoring and support for prevention and management of AKI KDIGO suggest using protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting (2C) or in patients with septic shock (2C). KDIGO AKI,2012
  • 40. Glycemic control and nutritional support In critically ill patients, KDIGO suggest insulin therapy targeting plasma glucose 110–149 mg/dl (6.1–8.3 mmol/l). (2C) KDIGO suggest achieving a total energy intake of 20–30 kcal/kg/d in patients with any stage of AKI. (2C) KDIGO suggest to avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT. (2D) KDIGO AKI,2012
  • 41. KDIGO suggest administering 0.8–1.0 g/kg/d of protein in noncatabolic AKI patients without need for dialysis (2D) 1.0–1.5 g/kg/d in patients with AKI on RRT (2D) Up to a maximum of 1.7 g/kg/d in patients on continuous renal replacement therapy (CRRT) and in hypercatabolic patients. (2D) KDIGO suggest providing nutrition preferentially via the enteral route in patients with AKI. (2C) KDIGO AKI,2012 Glycemic control and nutritional support
  • 42. Use of diuretic in AKI KDIGO recommend not using diuretics to prevent AKI. (1B) Suggest not using diuretics to treat AKI, except in the management of volume overload. (2C) KDIGO AKI,2012
  • 43. Vasodilator therapy KDIGO recommend not using low-dose dopamine to prevent or treat AKI. (1A) Suggest not using fenoldopam to prevent or treat AKI. (2C) Suggest not using atrial natriuretic peptide (ANP) to prevent (2C) or treat (2B) AKI. KDIGO AKI,2012
  • 44. Growth factor intervention KDIGO recommend not using recombinant human (rh) IGF-1 to prevent or treat AKI. (1B) KDIGO AKI,2012
  • 45. Adenosine receptor antagonist KDIGO suggest that a single dose of theophylline may be given in neonates with severe perinatal asphyxia who are at high risk of AKI. (2B) KDIGO AKI,2012
  • 46. Prevention of aminoglycoside and amphotericin related AKI KDIGO suggest not using aminoglycosides for the treatment of infections unless no suitable, less nephrotoxic, therapeutic alternatives are available. (2A) KDIGO suggest that, in patients with normal kidney function in steady state, aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens. (2B) KDIGO AKI,2012
  • 47. KDIGO recommend monitoring aminoglycoside drug levels when treatment with multiple daily dosing is used for more than 24 hours. (1A) Suggest monitoring aminoglycoside drug levels when treatment with single-daily dosing is used for more than 48 hours. (2C) Suggest using topical or local applications of aminoglycosides (e.g., respiratory aerosols, instilled antibiotic beads), rather than i.v. application, when feasible and suitable. (2B) KDIGO AKI,2012 Prevention of aminoglycoside and amphotericin related AKI
  • 48. KDIGO suggest using lipid formulations of amphotericin B rather than conventional formulations of amphotericin B. (2A) In the treatment of systemic mycoses or parasitic infections, KDIGO recommend using azole antifungal agents and/or the echinocandins rather than conventional amphotericin B, if equal therapeutic efficacy can be assumed. (1A) KDIGO AKI,2012 Prevention of aminoglycoside and amphotericin related AKI
  • 49. Other method of prevention of AKI in the critically ill KDIGO suggest that off-pump coronary artery bypass graft surgery not be selected solely for the purpose of reducing perioperative AKI or need for RRT. (2C) Suggest not using NAC to prevent AKI in critically ill patients with hypotension. (2D) KDIGO recommend not using oral or i.v. NAC for prevention of postsurgical AKI. (1A) KDIGO AKI,2012
  • 51.
  • 52. Contrast induced AKI Define and stage AKI after administration of intravascular contrast media as per Recommendations (Not Graded) In individuals who develop changes in kidney function after administration of intravascular contrast media, evaluate for CI- AKI as well as for other possible causes of AKI. (Not Graded) KDIGO AKI,2012
  • 53. Assess the risk for CI-AKI and, in particular, screen for pre- existing impairment of kidney function in all patients who are considered for a procedure that requires intravascular (i.v. or i.a.) administration of iodinated contrast medium. (Not Graded) Risk factors Pre-existing CKD Diabetes mellitus Advanced CHF High dose contrast media Hemodynamic instability KDIGO AKI,2012 Contrast induced AKI
  • 54. Consider alternative imaging methods in patients at increased risk for CI-AKI. (Not Graded) KDIGO AKI,2012 Contrast induced AKI
  • 55. Nonpharmacological prevention strategies of CI-AKI Use the lowest possible dose of contrast medium in patients at risk for CI-AKI. (Not Graded) KDIGO 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) KDIGO AKI,2012
  • 56. Pharmacological prevention strategies of CI-AKI KDIGO recommend i.v. volume expansion with either isotonic sodium chloride or sodium bicarbonate solutions rather than no i.v. volume expansion, in patients at increased risk for CI-AKI. (1A) Recommend not using oral fluids alone in patients at increased risk of CI-AKI. (1C) KDIGO AKI,2012
  • 57. KDIGO suggest using oral NAC together with i.v. isotonic crystalloids in patients at increased risk of CI-AKI. (2D) Suggest not using theophylline to prevent CI-AKI. (2C) Recommend not using fenoldopam to prevent CI-AKI. (1B) Pharmacological prevention strategies of CI-AKI KDIGO AKI,2012
  • 58. Effects of hemodialysis or hemofiltration KDIGO suggest not using prophylactic intermittent hemodialysis (IHD) or hemofiltration (HF) for contrast-media removal in patients at increased risk for CI-AKI. (2C) KDIGO AKI,2012
  • 59. Indications for acute renal replacement therapy A : metabolic Acidosis E : Electrolyte imbalance I : Intoxication / Ingestion of toxic substance O : fluid Overload that is refractory to diuretics U : signs of Uremia KDIGO AKI,2012
  • 60. Mode of RRT Conventional intermittent hemodialysis (IHD) Sustained low-efficacy dialysis (SLED) Continuous renal replacement therapy (CRRT) Peritoneal dialysis(PD) KDIGO AKI,2012
  • 61.
  • 62. Vascular access for renal replacement therapy in AKI When choosing a vein for insertion of a dialysis catheter in patients with AKI, consider these preferences (Not Graded): First choice: right jugular vein Second choice: femoral vein Third choice: left jugular vein Last choice: subclavian vein KDIGO AKI,2012
  • 63. AKI : TREATMENT Specific Rx : Rx cause of AKI Supportive Rx 1. Maintain hemodynamic and oxygenation 2. Monitor VS, I/O, BW 3. Monitor BUN, Cr, electrolyte,… 4. Discontinue all nephrotoxic agents 5. Nutrition : prefer enteral route 6. Total energy intake 20-30 kcal/kg/day 7. Protein intake g/kg/day Non-catabolic 0.8-1.0 RRT 1.0-1.5 CRRT, Hypercatabolic up to a max. of 1.7 8. In critically ill patients : insulin therapy targeting PG 110-149 mg/dL Take home messages KDIGO AKI,2012 Brenner and Rector’s The kidney 9th edition
  • 64. 9. HypoNa : free water restriction < 1 L/day 10. Volume overload : salt restriction < 1.0-1.5 g/day, furosemide 200 mg iv bolus or 20 mg/h iv 11. Not using diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT 12. Not using low-dose dopamine, fenoldopam, ANP, rh IGF-1 13. HyperK : K diet restriction, off ACEI & ARB & K-sparing diuretics, medical Rx 14. Metabolic acidosis : NaHCO3 if pH < 7.15 15. HypoCa : CaCO3 if symptomatic or NaHCO3 to be administered 16. HyperP : P diet restriction, P binders 17. HyperMg : avoid Mg-containing medications 18. Hyperuricemia : usually mild (< 15 mg/dL),if severe add allopurinol, or recombinant uricase 19. Check for changes of drug dosing 20. RRT when indicated Take home messages KDIGO AKI,2012 Brenner and Rector’s The kidney 9th edition

Editor's Notes

  1. เนื่องจากการกำหนดนิยามของARF แตกต่างกัน ADQI (Acute Dialysis Quality Initiative) จึงกำหนดนิยามใหม่ให้เป็นมาตรฐานโดยใช้คำว่า. “ Acute Kidney Injury (AKI) ” โดย AKI หมายถึงSpectrum ของโรคที่มีการลดลงของหน้าที่ของไตอย่างเฉียบพลันซึ่งอาจจะเป็นผลจากการเปลี่ยนแปลงหน้าที่หรือการเปลี่ยนแปลงโครงสร้างของไตก็ได้ จะวินิจฉัยว่าเป็น AKI เมื่อมีการเพิ่มขึ้นของค่า Creatinin ในซีรั่มมากกว่า0.5มก/ดลหรือร้อยละ150จากค่าตั้งต้นหรือปริมาณปัสสาวะน้อยกว่า0.5มล/กก/ชม และการเปลี่ยนแปลงของค่า Creatinin ต้องมีหลักฐานว่าเกิดภายใน 48 ชั่วโมง( รณิษา รัตนะรัต. 2553:477-478) อดีตการวินิจฉัย ARF หรือ AKI ใช้ระดับของ Creatinin ในเลือดและปริมาณปัสสาวะ ปัจจุบันมีการปรับปรุงเกณฑ์โดย Acute Kidney Injury Network(AKIN) ที่เรียกว่า modified RIFLE หรือ AKIN Criteria ดังนี้ 1. Neutrophil Gelatinase Associated Lipocalin (NGAL) ซึ่งตรวจได้ทั้งในเลือดและปัสสาวะ NGAL พบได้ในเซลล์และอวัยวะหลายชนิดของร่างกายได้แก่เซลล์เม็ดเลือดขาวชนิด Neutrophil และเซลล์ epithelium ต่างๆรวมทั้งเซลล์ท่อไตส่วนต้นด้วย แม้ว่าจะพบได้ในเซลล์หลายชนิดแต่พบว่า NGAL ในร่างกายและปัสสาวะจะเพิ่มขึ้นอย่างชัดเจนหลังการเกิดอันตรายต่อเซลล์ท่อไต ( tubular injury) และก่อนการเพิ่มขึ้นของ Cr เช่น NGAL สูงขึ้นเพียง2ชั่วโมงหลังการผ่าตัด 2. Cystacin C ถูกสร้างโดยเซลล์ที่มีนิวเคลียสทุกเซลล์และถูกกรองออกมาจากโกลเมอรูลัสที่ไตอย่างอิสระ ตรวจพบได้ในเลือดและปัสสาวะ ระดับของ Cystacin C ไม่ขึ้นกับเพศ เชื้อชาติ มวลกล้ามเนื้อเหมือน Cr 3. Kidney injury molecule-1 (KIM-1) KIM-1 เป็นTransmembrane glycoprotein แสดงเมื่อเซลล์ท่อไตส่วนต้นได้รับอันตรายจากการขาดเลือดหรือได้รับสารที่เป็นอันตรายต่อไต สามารถตรวจได้ในปัสสาวะ 4. Interleukin-18(IL-18) เป็น Proinflammatory cytokine สร้างมากขึ้นในภาวะการอักเสบของร่างกาย เมื่อไตได้รับอันตราย ท่อไตสร้าง IL-18 และมีส่วนหนึ่งที่ขับออกทางไปทางปัสสาวะและสามารถตรวจวัดได้ ค่า IL-18 สามารถวินิจฉัยได้เร็วกว่าการใช้Cr 24-48 ชั่วโมง 5. L-type fatty acid blinding protein (L-FABP) L-FABP เกี่ยวข้องกับขบวนการในการเพิ่มกรดไขมันเข้าเซลล์ของตับและไตและเร่งการ เมตาบอลิซึมของกรดไขมันด้วย ซึ่งเป็นการป้องกันการเพิ่มขึ้นของการออกซิเดชั่นของ Free fatty acid ในร่างกายซึ่งจะทำให้เกิดภาวะOxidative stress ดังนั้นบทบาทของ L-FABP จึงเป็นantioxidant ของเซลล์ การเพิ่มขึ้นของ L-FABP ในเลือดและปัสสาวะจึงเกี่ยวข้องกับภาวะที่มีอันตรายต่อไตด้วย มีการศึกษาพบว่าการตรวจ urine L-FABP นั้นมีความไวในการวินิจฉัยภาวะ contrast induced nephropathy กว่า ซีรั่ม Cr และสามารวินิจฉัยภาวะ AKI ในผู้ป่วย sepsisได้แต่ยังช้ากว่าNGAL