ACUTE KIDNEY INJURY

(AKI)

Prof DR Dr Haerani Rasyid,Mes, SpPD,KGH,SpGK

TIM GINJAL HIPERTENSI
UNHAS
2019
Learning Objectives
• Definitions and classification of AKI
• Epidemiology and clinical outcome
• Etiology and diagnosis
• Management of AKI
Definition
• Acute kidney injury (AKI)—or acute renal
failure (ARF), as it was previously termed—is
defined as an abrupt or rapid decline in renal
filtration function. This condition is usually
marked by :
1. a rise in serum creatinine concentration
2. creatinine levels may be normal, and the
only sign of a kidney injury may be
decreased urine production.
Definition (cont...)
According to KDIGO (Kidney Disease Improving
Global Outcome), AKI definition :
• Serum Cr↑by 1.5x baseline for 7 days OR
• Cr↑by ≥ 0.3 mg/dl for 48 hours OR
• Urine output < 0.5 ml/kg/hour for 6 hours
 KDIGO Classification of AKI ( 2012 )
Stage Serum creatinine Urine output
Stage Cr Criteria UOP Criteria
1 1.5-1.9× baseline <0.5 ml/kg/hr for 6-12 hrs
1OR Cr↑by 1.5-2x baseline or < 0.5 ml/kg/hr for
>0.3 mg/dL
Cr↑by0.3 mg/dl 6hr
<0.5 ml/kg/hr > 12 hrs
2 22-2.9×Cr↑by
baseline
2-3x < 0.5 ml/kg/hr for
12hr
3 33 timesCr↑by
baseline
more than 3x or <0.3
< 0.3 ml/kg/hr
ml/kg/hr for> 24 hrs
OR Cr↑by 0.5 if baseline >4mg/dl OR
24hr
increase in Cr to ≥4.0 mg/dL Anuria > for
Or anuria 12 12h
hrs
OR
Initiation of RRT
 RIFLE criteria for Acute Renal Dysfunction
GFR criteria Urine output criteria
Abrupt (1-7 days)
Decreased UO relative to
decrease (> 25%) in GFR
Risk Or Scr x 1.5
the fluid input
High Sensitivity
UO < 0.5/ml/kg/h x 6hr
Sustained (> 24 hrs)
Adjusted creat or UO < 0.5/ml/kg/h
Injury GFR decrease> 50% x 12 hr ??
or Scr x 2

Adjusted creat or GFR UO < .5/ml/kg/h

decrease > 75%
Failure x 24 hr High Specificity
Scr x 3 or Scr > 4mg%
When acute > 0.5mg%
Anuria x 12 hrs

Loss Irreversible ARF or

persistent ARF > 4 wks
ESRD > 3 months
ESRD
 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
Acute
Kidney
Injury

Prerenal Intrinsic Postrenal

AKI AKI AKI

Acute Acute Acute

Acute Intratubular
Tubular Interstitial Vascular
GN Obstruction
Necrosis Nephritis Syndromes
Pre-renal 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)
• 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)
• Severe renal vasoconstriction: Sepsis, drugs (nonsteroidal anti-
inflammatory agents, ß-adrenergic agonists), hepatorenal syndrome
• Mechanical occlusion of renal arteries: Thrombotic occlusion,
miscellaneous (emboli, trauma [e.g., angioplasty])
Renal AKI
• Tubule : ATN (sepsis, ischemic, toxins)
• Interstitium: AIN (Drug, infection, neoplasm)
• Glomerulus: AGN (primary, post-infectious,
rheumatologic, vasculitis, HUS/TTP)
• Vasculature:
– Atheroembolic dz, renal artery thromboembolism, renal artery
dissection, renal vein thrombosis

• Intratubular Obstruction
– myoglobin, hemoglobin, myeloma light chains,
uric acid, tumor lysis, drugs (bactrim, indinavir,
acyclovir, foscarnet, oxalate in ethylene glycol toxicity)
Renal AKI – Acute Tubular Necrosis
• ATN - Acute Tubular Necrosis
– Usually occurs after an ischemic event or exposure to nephrotoxic
agents.
– Look for muddy brown casts and FeNa>2%
• Direct toxic Injury (20%)
• Sepsis (48%) – Exogenous
• Radiocontrast
• Ischemia (32%) • Aminoglycosides
– prolonged prerenal azotemia • Vancomycin
• Amphotericin B
– Hypotension • Cisplatin
– hypovolemic shock • Acyclovir
– cardiopulmonary arrest • Calcineurin inhibitors
• HIV meds (tenofovir)
– cardiopulmonary bypass .
– Endogenous (pigment nephropathy)
• Rhabdomyolysis
• Hemolysis
Renal AKI – Acute Tubular Necrosis
Index Prerenal Oliguric AKI
Azotemia (ATN)
BUN/PCr Ratio >20:1 10-15:1
Urine sodium <20 >40
(UNa), meq/L
Urine osmolality, >500 <400
mosmol/L H2O

-Fractional <1% >2%

excretion of
sodium <35% >35%
-FEUrea
Response to Cr improves with Cr won’t improve
volume IVF much

Urinary Bland, Hyaline Muddy brown

Sediment granular casts,
cellular debris,
tubular epithelial
cells
Post-renal AKI
• Classification
– 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)
Post-renal AKI
• Etiology: 1) Upper Tract Obstruction
Intrinsic:  Extrinsic:
• Nephrolithiasis • Retroperitoneal or pelvic
• Blood clot malignancy
• Papillary necrosis • Endometriosis/Prolapsed
uterus
• Cancer
• Abdominal aortic aneurysm
or Iliac artery aneurysm
• Retroperitoneal fibrosis
Post-renal AKI
• Etiology: 2) Lower Tract Obstruction

– BPH or prostate cancer

– Bladder cancer
– Urethral strictures
– Bladder stones
– Blood clots
– Functional obstruction as a result of
neurogenic bladder
Post-renal AKI
• Etiology: 2) Lower Tract Obstruction

– BPH or prostate cancer

– Bladder cancer
– Urethral strictures
– Bladder stones
– Blood clots
– Functional obstruction as a result of
neurogenic bladder
Patophysiology
• Damage is caused mostly by renal perfusion
problems and tubular dysfunction
• Usual causes
– Hypo-perfusion and ischemia
– Toxin mediated
– Inflammation
Patophysiology (cont...)
Patophysiology
Renin Angiotensin Axis
Diagnosis
– Anamnesa: Detailed history
– Lab : Monitor serum Cr for at risk patients, BMP,
UA, Uosm, Ucr, Una (Urine Urea if on diuretics)
– Make sure I/Os are recorded correctly
– Ultrasound
• Structural anomalies – polycystic, obstruction, etc.
Management
Electrolyte management
– Sodium
• Hyponatremia – fluid restriction first, 3% NaCl if AMS or
seizing
– Potassium
• Calcium/Bicarb/Glucose/Insulin/Kayexalate
• Hemodialysis
Management
Nutrition management
– Initially very catabolic
– Goals:
• Adequate calories
• Protein depend on catabolism
• Low K and Phosf (depend on result of laboratory)
• Decreased fluid intake
Management
Renal Replacement Therapy
• Peritoneal Dialysis
• Acute Intermittent Hemodialysis
• Continuous Hemofiltration
– CAVH
– SCUF
– CVVH, CVVHD
– And others….
Management
Indications for RRT :
– Oliguria/Anuria
– Hyperammonemia
– Hyperkalemia
– Severe acidemia
– Severe azotemia
– Pulmonary Edema
– Uremic complications
– Severe electrolyte abnormalities
– Drug overdose with a filterable toxin
– Anasarca
– Rhabdomyolysis
THANK YOU...