Acute Kidney Injury

(AKI)
Dr. Atma Gunawan SpPD.KGH
 LEARNING OBJECTIVE:
After completing this module, the students be able
to:
• Explain the definitions of AKI
• Explain the risk factors associated with AKI
• Explain the pathophysiology of AKI
• Explain the complication of AKI
• Evaluation and management of AKI
 Incidence/Prevalence
• An incidence of 10-25%. Nearly 5% of people in hospital and as many as 15% of
critically ill people.
• Patients who are admitted with ARF on the ICU have an overall mortality of 23-
80%.
• Patients with ARF not requiring RRT have a mortality of 10–53%.
• Patients who develop ARF that requires RRT have a higher mortality of 57–80%.
• Of those patients with ARF who receive RRT and survive, only 5–30% require
long-term HD.
• The mortality of patients who are admitted to ICU with ARF, or who go on to
develop ARF, remains high.

Thadhani R, Pascual M, Bonventre JV. Acute renal failure. N Engl J Med 1996;334:1448-60.
Albright RC Jr. Acute renal failure: a practical update. Mayo Clin Proc 2001;76:67-74.
Singri N, Ahya SN, Levin ML. Acute renal failure. JAMA 2003;289: 747-51.
Hou SH, Bushinsky DA, Wish JB, et al. Hospital-acquired renal insufficiency: a prospective study. Am J Med 1983;74:243–248.
Brivet FG, Kleinknecht DJ, Loirat P, et al. Acute renal failure in intensive care units — causes, outcomes and prognostic factors of hospital
mortality: a prospective multicenter study. Crit Care Med 1996;24:192–198.
 Definitions

Acute Renal Failure

Acute Kidney Injury

 Definition AKI (Kidney Disease: Improving Global
Outcomes KDIGO 2012)

• AKI is defined as any of the following :

• Increase in SCr by ≥ 0.3 mg/dl within 48 hours; or
• Increase in SCr to ≥1.5 times baseline, which is
known or presumed to have occurred within the
prior 7 days; or
• Urine volume < 0.5 ml/kg/h for 6 hours
30

25

20 Mo rta lity
RRT
15
LOS
10 ICU LOS

0
No AKI Risk Injury Fa ilure
Principle causes of AKI
Causes of ARF in hospitalized pts
45% ATN
• Ischemia, Nephrotoxins
21% Prerenal
• CHF, volume depletion, sepsis
10% Urinary obstruction
4% Glomerulonephritis or vasculitis
2% AIN
1% Atheroemboli
Pathophysiology
 Pathophysiology of prerenal AKI
Hypovolemia
RAA-axis
RBF maintained
initially through:
- Local myenteric
reflex
- PG synthesis
- Actions of Ag II
Homeostatic goal:
Restore intravascular volume
and blood pressure to maintain
perfusion of essential organs
Decreased cardiac output
Systemic vasodilatation
Baroreceptor activation
Neurohormonal responses
Vasopressin Sympathetic
nervous system
Vasoconstriction
Mesangial cell contraction
Avid salt and water reabsorption
Reducing sweating
Thirst and salt appetite
Prerenal AKI
Dramatic reduction in renal Dramatic reduction in
Blood flow, glomerular filtration, splanchnic, skin, and
urine flow muskuloskeletal blood flow
 Glomerular Hypoperfusion
•  ECF volume

•  Effective volume (CHF,

sepsis, cirrhosis)

• Glomerular Hemodynamic:
– Vasoconstriction (pre glomerular) Contrast
CSA
• NSAID/ COX-2 inhibitor Ampho
• Contrast
• Amphotericin B
• Cyclosporine/ tacrolimus NSAID ACE-I
ARB
• Hypercalcemia
– Efferent vasodilatation
• ACE inhibitors/ ARBs
Intrarenal mechanisms for autoregulation of GFR
 Renal blood supply
– the kidneys receive 20-25% of the cardiac output
– vascular supply:
» renal arteries
» interlobar arteries
» arcuate arteries
» interlobular arteries
» afferent arterioles
» glomerular capillaries
» efferent arterioles
» peritubular capillaries
 2 3
4

1 7

8
Patophysiology ATN
Contribution of ‘back-Leakage’ of glomerular filtrate and
intratubule obstruction to Renal Failure in ATN

Brener & Rector; saunders. The Kindey 4th Ed

Investigations
 CKD or acute renal failure ?
CKD ARF
Marker renal function GFR < 70 Creatinine ↑ 1.5 x
ml/min,urinalysis,imaging baseline; oliguria,anuria
Time 3 months Within 7 days
Onset Gradual Sudenly
Urine output Prolong oliguria Little or no
Increasing creatinine Stable, slowly Daily
Anemia, hypertension Commonly Unusual
Hyperphosphate Common Rare
Hypocalcemia Common Rare
Imaging (USG) Small, density cortex ↑ Normal
 History & Examination
• History - Pre-existing medical conditions (Blood loss, Hematuria
(Calculi), BPH)
• Episodes of hypotension, Nephrotoxic agents
• Current volume status
– Skin turgor, mucous membranes, oedema, lung bases, heart sounds,
central pressures, blood pressure
• Chest: Rales (3rd space)
• Abdomen: Ascites (3rd space) Distended bladder (obstruction)
• GU: Prostatic enlargement/Pelvic mass (Obstruction)
• Extremities: Color/temperature (↓perfusion)
• Signs of systemic disease: Fever (Sepsis), rashes, anaemia
Biomarkers

Late detections
 Factors that affect serum creatinine concentration
Factor Effect on Mechanism
serum
creatinine
Kidney Increase Decreased GFR(increase is blunted by increased
Disease tubular secretion of creatinine and by reduced
creatinine generation)

Reduced Decrease Reduced creatinine generation (common in children,

muscle mass women, and older and malnourished patients)

Ingestion of Increase Transient increase in creatinine generation (increase

cooked meat may be blunted by transient increase in GFR)

Cimetidine, Increase Inhibition of tubular creatinine secretion

trimethoprim

Ketoacidosis Increase Positive interference with picric acid assay for

creatinine
 Investigation the causes AKI

Acute Kideny Injury

Prerenal
Postrenal
Uosm > 5000 mosm/kg
Uosm: variable
Una < 20meq/L
Intrinsic Renal Diseases Una: low early, high late
FEna < 1%
FEna: variable
Microscopy - bland
Microscopy - bland

ATN Acute Interstitial Nephritis Acute Glomerulonephritis

Uosm ~ 300 mosm/kg Uosm: variable, ~300 mosm.kg Uosm: variable (>400 in early GN)
Una > 40meq/L Una > 40 meq/L Una: variable (<20meq/l in early GN)
FEna > 2% FEna > 2% FEna: variable, <1% in early GN
Microscopy – dark pigment Microscopy – leukocytes, Microscopy – hematuria, proteinuria
(granular) cast erythrocyts, leukocyte casts Erythrocyte casts (dysmorphic)
Fractional excretion of
sodium:

Excreted Na
Filtered Na
Management
 Management Principles

• Determine exact diagnosis

• Remove offending agent/Treat causes
• Treat complications (i.e. Hyperkalemia, acidosis, lung edema)
• Reverse oliguria/Improve renal blood flow :
- correction of intravascular volume
- adequate hydration : fluid intake 30-40 cc/kgBW/day
- diuretics : furosemide
• Remove nephrotoxins, dose-adjust medications
• Provide nutrition (low K, low P)
 Treat causes
• Postrenal factor : correction obstruction (BPH, stones,
insertion dower catheter
• Prerenal factor : hydration until euvolemic or CVP 8-14
cmH20, treat heart failure, treat ascites and
hypoalbumin.
• Treat underlying sepsis
• Stop nephrotoxic drugs
 Volume Management

• Restrict fluid and sodium. Fluid intake : urine

volume + 500 cc
• Diuretics may be used to increase the urinary
volume . Target Urine output 0.5-1.0ml/kg/hour
• In severe cases of volume overload, furosemide
may be given as a bolus (200 mg) followed by an
intravenous drip (10–40 mg/h), with or without a
thiazide diuretic.
 Hyperkalemia

• Immediate antagonism of the cardiac effects of

• Hyperkalemia : 10 ml of 10% calcium gluconate IV).
• Rapid reduction in plasma K+ concentration by
• redistribution into cells : 10 units of IV regular insulin
followed immediately by 50 mL of 40% dextrose).
• Correction acidosis
• Β2-agonists nebulizer or IV ,most commonly albuterol.
• Restricting dietary K+ intake.
 Proposed Criteria for the Initiation of RRT in
Critically ill Patients
Oliguria (urine output< 500 ml/24 hrs)
Anuria (urine output< 100 ml/24 hrs)
Hyperkalemia ([K+]>6.5 mmol/liter)
Severe acidemia (pH<7.1)
Azotemia ([urea]> 85 mg/dL)
Clinically significant organ (especially lung) edema
Uremic encephalopathy
Uremic neuropathy/myopathy
Severe dysnatremia ([Na]>160 or<115 mmol/liter)

( KI 1998, R. Belloma and C. Ronco)

 Renal Replacement Therapy
• Intermittent hemodialysis (IHD)
• Continuous veno-venous hemofiltration (CVVH)
• CVV hemodialysis (CVVHD)
• CVV hemodiafiltration (CVVHDF)
• Slow low efficiency dialysis (SLED)
• Peritoneal dialysis (PD)
• Slow continuous ultrafiltration (SCUF)
Renal replacement therapy
Natural History of AKI
wassalam