ACUTE KIDNEY INJURY

(AKI)

Haerani Rasyid
FK UNHAS
2016
DEFINITION
Acute kidney injury (AKI) : abrupt or rapid decline in
renal filtration function.
Usually marked by :
1. Rise in serum creatinine concentration
2. Decreased urine production.
 Classification
KDIGO (Kidney Disease Improving Global Outcome)
AKIN Classification of AKI
KDIGO CLASSIFICATION OF AKI ( 2012 )
Stage Serum creatinine Urine output

1 Stage
1.5-1.9 baselineCr Criteria <0.5UOP Criteria for 6-12 hrs
ml/kg/hr
OR
1>0.3 mg/dL
Crby 1.5-2x
baseline or Crby 0.3 < 0.5 ml/kg/hr for 6hr
mg/dl
<0.5 ml/kg/hr > 12 hrs
2 2-2.9 baseline
2 Crby 2-3x < 0.5 ml/kg/hr for 12hr
3 3 times baseline <0.3 ml/kg/hr > 24 hrs
3OR Crby more than 3x or Crby 0.5 OR
< 0.3 ml/kg/hr for 24hr
increase in Cr to
if baseline 4.0 mg/dL
>4mg/dl Anuria
Or anuria>for12
12hhrs
OR
Initiation of RRT

Source : KDIGO AKI Guideline. 2012.

AKIN CLASSIFICATION OF AKI
Stage Serum creatinine Urine output

1 Stage baselineCr Criteria

1.5-2 <0.5UOP Criteria for hrs
ml/kg/hr
OR
1>0.3 mg/dL
Crby 1.5-2x
baseline or Crby 0.3 < 0.5 ml/kg/hr for 6hr
mg/dl
<0.5 ml/kg/hr > 12 hrs
2 >2-3.0 baseline
2 Crby 2-3x < 0.5 ml/kg/hr for 12hr
3 >3x times baseline <0.3 ml/kg/hr > 24 hrs
3OR Crby more than 3x or Crby 0.5 OR
< 0.3 ml/kg/hr for 24hr
increase in Cr to
if baseline 4.0 mg/dL
>4mg/dl Anuria
Or anuriafor 12 hrs OR need
for 12h
OR for RRT
Need for RRT
EPIDEMIOLOGY

5-10% in hospitalized pts

70% in critically ill pts
5-6% ICU pts require RRT
(Renal Replacement Therapy)
CLASSIFICATION OF THE ETIOLOGIES OF AKI
CLASSIFICATION OF THE ETIOLOGIES OF AKI

Harrisons Ed.19th. Acute Kidney Injury. Sushrut S.W, Joseph V.B. 2015
Prerenal AKI

Renal AKI

Postrenal AKI
ETIOLOGI OF PRERENAL AKI
Decreased intravascular fluid volume
Extracellular fluid loss: burns, diarrhea, vomiting,
diuretics, salt-wasting renal disease, primary adrenal
insufficiency, gastrointestinal hemorrhage
Extracellular fluid sequestration: pancreatitis, burns,
crush, injury, nephrotic syndrome, malnutrition,
advanced liver disease
ETIOLOGI OF PRERENAL AKI
Decreased cardiac output
Myocardial dysfunction: MI, arrhythmias, ischemic heart
disease, cardiomyopathies, valvular disease, hypertensive
disease, severe cor pulmonale
Peripheral vasodilation
Drugs: antihypertensive agents
Sepsis,
Miscellaneous: adrenal cortical insufficiency,
hypermagnesemia, hypercapnia, hypoxia
ETIOLOGI OF PRERENAL AKI

Severe renal vasoconstriction

Sepsis
Drugs: nonsteroidal anti-inflammatory agents, -
adrenergic agonists.
Hepatorenal syndrome
Mechanical occlusion of renal arteries
Thrombotic occlusion
Miscellaneous: emboli, trauma (e.g., angioplasty)
 DIAGNOSIS OF PRERENAL AKI
Etiology Clinical Features
Prerenal History of poor fluid intake or fluid
azotemia loss (hemorrhage, diarrhea, vomiting,
sequestration into extravascular
space); NSAID/ACE-I/ARB; heart failure;
evidence of volume depletion (tachycardia,
absolute or postural hypotension,
low jugular venous pressure,
dry mucous membranes), decreased
effective circulatory volume (cirrhosis,
heart failure)
Laboratory Features
BUN/creatinine ratio above
20, FeNa
<1%, hyaline casts in urine
sediment,
urine specific gravity >1.018,
urine
osmolality >500 mOsm/kg
Comments
Low FeNa, high specific gravity and
osmolality may not be seen in the
setting of CKD, diuretic use; BUN
elevation out of proportion to creatinine
may alternatively indicate upper
GI bleed or increased catabolism.
Response to restoration of hemodynamics
is most diagnostic.

Sepsis- Sepsis, sepsis syndrome, or septic Positive culture from FeNa may be low (<1%), particularly
associate shock. Overt hypotension not always normally sterile early in the course, but is usually >1%
d AKI seen in mild to moderate AKI body fluid; urine sediment with osmolality <500 mOsm/kg
often
contains granular casts,
renal tubular
epithelial cell casts

Ischemia- Systemic hypotension, often superimposed Urine sediment often

associate upon sepsis and/or reasons contains granular
d AKI for limited renal reserve such as older casts, renal tubular epithelial
age, CKD cell
casts. FeNa typically >1%.
Prerenal AKI

Renal AKI

Postrenal AKI
ETIOLOGI OF RENAL AKI

Harrisons Ed.19th. Acute Kidney Injury. Sushrut S.W, Joseph V.B. 2015
 PATOPHYSIOLOGY OF RENAL AKI

Harrisons Ed.19th. Acute Kidney Injury. Sushrut S.W, Joseph V.B. 2015
 ACUTE TUBULAR NECROSIS (ATN)

Etiologi of ATN
Sepsis (48%) Direct toxic Injury (20%)
Exogenous
Radiocontrast
Ischemia (32%) Aminoglycosides
prolonged prerenal azotemia Vancomycin
Hypotension Amphotericin B
Cisplatin
hypovolemic shock Acyclovir
cardiopulmonary arrest Calcineurin inhibitors
cardiopulmonary bypass HIV meds (tenofovir)
Endogenous (pigment nephropathy)
Rhabdomyolysis
Hemolysis
PATOPHYSIOLOGI ACUTE TUBULAR NECROSIS
ACUTE TUBULAR NECROSIS
Index Prerenal Oliguric AKI (ATN)
Azotemia
BUN/PCr Ratio >20:1 10-15:1
Urine sodium (UNa), <20 >40
meq/L
Urine osmolality, >500 <400
mosmol/L H2O

-Fractional <1% >2%

excretion of sodium
(FENa)

-FEUrea <35% >35%

Response to volume Cr improves with IVF Cr wont improve much

Urinary Sediment Bland, Hyaline Muddy brown granular

casts, cellular debris,
tubular epithelial cells
 DIAGNOSIS OF RENAL AKI
Nephrotoxin-Associated AKI: Endogenous
Etiology Clinical Features Laboratory Features Comments
Rhabdomyolysis Traumatic crush injuries, seizures, Elevated myoglobin, creatine FeNa may be low (<1%)
immobilization kinase;
urine heme positive with few
red
blood cells

Hemolysis Recent blood transfusion with Anemia, elevated LDH, low FeNa may be low (<1%); evaluation
transfusion haptoglobin for
reaction transfusion reaction
Tumor lysis Recent chemotherapy Hyperphosphatemia,
hypocalcemia,
hyperuricemia

Multiple myeloma Age >60 years, constitutional Monoclonal spike in urine or Bone marrow or renal biopsy can be
symptoms, serum diagnostic
bone pain electrophoresis; low anion
gap; anemia
 DIAGNOSIS OF RENAL AKI
Nephrotoxin-Associated AKI: Exogenous
Etiology Clinical Features Laboratory Features Comments
Contrast Exposure to iodinated contrast Characteristic course is rise FeNa may be low (<1%)
nephropathy in SCr
within 12 d, peak within 35
d,
recovery within 7 d

Tubular injury Aminoglycoside antibiotics, cisplatin,
tenofovir, zoledronate, ethylene
glycol,
aristolochic acid, and melamine (to
name a few)
Urine sediment often Can be oliguric or nonoliguric
contains granular
casts, renal tubular epithelial
cell
casts. FeNa typically >1%.

Interstitial Recent medication exposure; can Eosinophilia, sterile pyuria; Urine eosinophils have limited
nephritis have often diagnostic
fever, rash, arthralgias nonoliguric accuracy; systemic signs of
drug reaction often absent; kidney
biopsy may be helpful
 DIAGNOSIS OF RENAL AKI
Other Causes of Intrinsic AKI
Etiology Clinical Features Laboratory Features Comments
Glomerulonephriti Variable features include ANA, ANCA, AGBM Kidney biopsy may be necessary
s/vasculitis skin rash, arthralgias, sinusitis (AGBM antibody, hepatitis
disease), lung hemorrhage (AGBM, serologies, cryoglobulins,
ANCA, lupus), recent skin infection or blood culture,
pharyngitis (poststreptococcal) decreased complement
levels,
ASO titer (abnormalities of
these tests
depending on etiology)
Interstitial Nondrug-related causes include Eosinophilia, sterile pyuria; Urine eosinophils have limited
nephritis tubulointerstitial often diagnostic
nephritis-uveitis (TINU) nonoliguric accuracy; kidney biopsy may be
syndrome, Legionella infection necessary
 DIAGNOSIS OF RENAL AKI
Other Causes of Intrinsic AKI
Etiology Clinical Features Laboratory Comments
Features
TTP/HUS Neurologic abnormalities and/or AKI; Schistocytes on Typical HUS refers to AKI with a diarrheal
recent diarrheal illness; use of peripheral blood prodrome, often due to Shiga
calcineurin smear, elevated toxin released from Escherichia coli or
inhibitors; pregnancy or postpartum; LDH, anemia, other bacteria; atypical HUS is due
Spontaneous thrombocytopeni to inherited or acquired complement
a dysregulation. TTP-HUS refers to
sporadic cases in adults. Diagnosis
may involve screening for ADAMTS13
activity, Shiga toxinproducing E. coli,
genetic evaluation of complement
regulatory proteins, and kidney
biopsy.
Atheroembolic Recent manipulation of the aorta or Hypocomplement Skin or kidney biopsy can be diagnostic
disease other large vessels; may occur emia,
spontaneously eosinophiluria
or after anticoagulation; retinal (variable),
plaques, palpable purpura, livedo variable amounts
reticularis, GI bleed of
proteinuria
Prerenal AKI

Renal AKI

Postrenal AKI
 CLASSIFICATION OF POSTRENAL AKI

Level of obstruction
Upper tract (ureters)
Lower tract (bladder outlet or urethra)
Degree of obstruction
Partial vs. Completee
Anatomic lesion (unilateral vs. bilateral)
Functional
Duration (Acute vs Chronic)
Cause (Congenital vs Acquired)
UPPER TRACT OBSTRUCTION

Intrinsic: Extrinsic:
Nephrolithiasis Retroperitoneal or pelvic
Blood clot malignancy
Papillary necrosis Endometriosis/Prolapsed
Cancer uterus
Abdominal aortic aneurysm or
Iliac artery aneurysm
Retroperitoneal fibrosis
LOWER TRACT OBSTRUCTION

BPH or prostate cancer

Bladder cancer
Urethral strictures
Bladder stones
Blood clots
Functional obstruction as a result of neurogenic
bladder
 PATOPHYSIOLOGY OF POSTRENAL AKI

Reduced GFR: underperfusion of glomeruli and

changes in the glomerular ultrafiltration coefficient
An initial period of hyperemia from afferent
arteriolar dilation is followed by intrarenal
vasoconstriction from the generation of angiotensin
II, thromboxane A2, vasopressin and a reduction in
NO production.
DIAGNOSIS OF POST RENAL AKI
Post Renal AKI
Etiology Clinical Features Laboratory Features Comments
History of kidney stones, No specific findings Imaging with computed
prostate other than AKI; tomography
disease, obstructed bladder may have pyuria or or ultrasound
catheter, hematuria
retroperitoneal or pelvic
neoplasm
COMPLICATIONS OF AKI
Intravascular overload
Electrolyte disturbance
Hyperkalemia (serum K+ >5.5 mEq/L)
Hyponatremia (serum Na+ < 135 mEq/L)
Hyperphosphatemia (serum phosphate concentration of >5.5 mg /dl)
Hypocalcemia (serum Ca++ < 8.5 mg/dl)
Hypercalcemia (serum Ca++ > 10.5 mg /dl)
Metabolic acidosis (arterial blood PH < 7.35)
Hyperuricemia
Bleeding tendency
Seizure
PREVENTION OF AKI
Renal AKI can be avoided: close attention to
cardiovascular function and intravascular volume in
high-risk patients (elderly & preexisting renal
insufficiency)
Aggressive restoration of intravascular volume
renal AKI after major surgery, trauma or burns.
Nephrotoxic: tailoring the dosage of potential
nephrotoxins to body size and GFR
MANAGEMENT OF AKI
Preliminary measures
Exclusion of reversible causes: Obstruction should be relived,
infection should be treated
Correction of prerenal factors: intravascular volume and
cardiac performance should be optimized
Maintenance of urine output: Loop diuretics may be usefully to
convert the oliguric form of ATN to the nonoliguric form.
High doses of loop diuretics such as Furosemide (up to 200
to 400 mg intravenously) may promote diuresis in patients who
fail to respond to conventional doses
MANAGEMENT OF PRERENAL AKI
Replacement fluids due to hypovolemia must be
tailored according to the composition of the lost fluid.
Severe hypovolemia due to hemorrhage should be
corrected with packed red blood cells
isotonic saline is usually appropriate replacement for
mild to moderate hemorrhage or plasma loss (e.g.,
burns, pancreatitis).
MANAGEMENT OF PRERENAL AKI
Hypotonic solutions (e.g., 0.45% saline): recommended as
initial replacement in patients with prerenal AKI due to
increased urinary or gastrointestinal fluid losses, although
isotonic saline may be more appropriate in severe cases.
Subsequent therapy should be based on measurements of
the volume and ionic content of excreted or drained fluids.
Serum potassium and acid-base status should be
monitored carefully.
MANAGEMENT OF RENAL AKI

No specific therapies for established renal AKI due to

ischemia or nephrotoxicity.
Focus on elimination of the causative hemodynamic
abnormality or toxin, avoidance of additional insults,
and prevention and treatment of complications.
Specific treatment of other causes: depends on the
underlying pathology.
MANAGEMENT OF POSTRENAL AKI
Requires close collaboration between nephrologist,
urologist and radiologist.
Obstruction of the urethra or bladder neck:
transurethral or suprapubic placement of a bladder
catheter
Ureteric obstruction: treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter.
CONSERVATIVE THERAPY

1. DIETARY MANAGEMENT
Protein 1.25 gm/kgBW to maintain nitrogen balance.
Restricting dietary protein 0.6 0.8 g/kg per day of
protein of high biologic value (i.e., rich in essential amino
acids) recommended in severe azotemia.
2. FLUID AND ELECTROLYTE MANAGEMENT
After hypovolemia corrected, total oral and intravenous
fluid administration = daily sensible losses (via urine,
stool, and NG tune o surgical drainage)+estimated IWL
(400500 ml/day).
Strict input output monitoring is
Hypervolemia: can usually be managed by restriction of
salt and water intake and diuretics.
 Hyperkalemia:
Restrict dietary K+ intake
Give calcium gluconate 10 ml of 10% solution over 5
minutes
Glucose solution 50 ml of 50 % glucose plus Insulin
10 units IV
Potassiumbinding ion exchange resin
Dialysis: therapy fails or the patient is very toxic
 Hyperphosphatemia: restriction of dietary phosphate
and by oral aluminum hydroxide or calcium carbonate,
which reduce gastrointestinal absorption of phosphate.
Hypocalcemia does not usually require treatment.
3. ACID BASE MANAGEMENT
Metabolic acidosis: treated if serum bicarbonate below
15 mmol/L or arterial pH falls below 7.2.
More severe acidosis is corrected by oral or intravenous
sodium bicarbonate.
Replacement estimates of bicarbonate deficit and
adjusted thereafter according to serum levels.
Complications of bicarbonate administration:
hypervolemia, metabolic alkalosis, hypocalcemia and
hypokalemia.
DIALYSIS / RENAL REPLACEMENT THERAPY (RRT)
Indications :
Oliguria/Anuria
Hyperammonemia
Hyperkalemia
Severe acidemia
Severe azotemia
Pulmonary Edema
Uremic complications
Severe electrolyte abnormalities
Drug overdose with a filterable toxin
Anasarca
Rhabdomyolysis
PROGNOSIS
Depend on severity of the underlying diseases and the
clinical setting
Morbidity and mortality: affected by the presence of
oliguria, GI bleeding, septicemia, metabolic acidosis
and neurologic abnormalities (oliguric > nonoliguric
patients).
Mortality rate: oliguric=50 %, nonoliguric= 26 %
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