Acute Renal Failure

Dr Wong Mun Hoe

MBBS (IMU) M.Med (UM)
Internal Medicine
So True, So False?
 Outline
• Definitions – Acute Renal Failure (ARF) and
Acute Kidney Injury (AKI)
• Etiology
• Pathogenesis
• Investigations
• Management
 Acute Renal Failure (ARF)
• What does it mean?
• A clinical syndrome characterized by
an abrupt decline in GFR and
accumulation of nitrogenous waste
products
 Lack of urine = ARF?
• Urine volume can be normal (non-
oliguric)
• Decreased (oliguric less than 400mls/24
hours)
• Absent (less than 100mls/ 24 hours)
 ARF to AKI
• There is lack of standard definition for acute renal failure.

• Therefore a group of experts have gathered around to form

the ACUTE DIALYSIS QUALITY INITIATIVE group (ADQI)

• Measuring creatinine and urine output

• The group has developed and published a set of consensus

criteria for classifying acute renal failure in 2002. New
terminology ACUTE KIDNEY INJURY (AKI) was introduced.

• ACUTE KIDNEY INJURY NETWORK (AKIN)

RIFLE Criteria
RIFLE vs AKIN
 Incidence of AKI
• Hospital admission : 2-7%

• ICU admission : 5-25%

• ICU admission with AKI requiring dialysis : 4%

• Commonest cause for AKI - SEPSIS

 Acute Kidney
Injury

Pre- Post-
Intrinsic
Renal Renal

Acute
Tubulo-
Glomerular Tubular
interstitial Necrosis
 Pre-Renal
Lack of blood supply to the kidneys:
• Inadequate blood volume
- massive blood loss eg trauma/ post
surgery
- massive loss of fluids
eg diarrhea, excessive use of diuretics
severe burns
• Adequate blood volume but poor cardiac
output
- cardiogenic shock, large pericardial effusion
 Pre-Renal
Decreased effective blood volume:

• Nephrotic Syndrome
• Cirrhosis of the liver

Afferent arteriolar vasoconstriction

• Drugs (NSAIDs, cyclosporine, amphotericin B,

noradrenaline)
• Hepatorenal Syndrome
• Radiocontrast agents,
 Pre-Renal
Efferent arteriolar vasodilatation
• ACE-I, ARB

Systemic vasodilatation
• Sepsis
• Anaphylaxis
• Anesthetics
• Drug overdose
 Renal
• Blood supply to the Kidney is adequate
• No outflow tract obstruction
• Cause of ARF lies within the kidney
– Interstium
– Glomeruli
– Tubules
 Renal
Interstium Acute Interstitial
Nephritis

Glomeruli  Acute
Glomerulonephritis

Tubules Acute Tubular

Necrosis
 Acute Interstitial Nephritis
• Drug induced • Infection related
– Penicillins – Bacterial
– Cephalosporins – Viral
– Sulfonamides – Rickettsial
– Rifampin – Tuberculosis
– Phenytoin
– Frusemide • Systemic diseases
– NSAIDs – SLE
• Malignancy – Sarcoidosis
• Idiopathic – Sjogrens syndrome
 Drug induced acute interstitial nephritis

•Fever
•Eosinophilia
•Rash
Renal biopsy
Inflammatory cells
including
Eosinophils in the
interstitium
Urine examination
shows
Eosinophils
 Glomerular
• Usually RPGN
- pauci immune eg wegener’s
granulomatosis
- Linear immune complex deposition eg
Good pasture’s syndrome
- Granular immune complex deposition eg
lupus nephritis, post infectious
CRESCENTIC GN
Pathologic diagnosis
extracapillary cell
proliferation within
Bowman space

The clinical manifestation

is the Rapidly Progressive
Glomerulonephritis (RPGN):
- active urine sediments
- rapid rise in s.creatinine
- poor response to treatment

Many different aetiologies

 Urinary abnormalities in Acute
Glomerulonephritis
Urinary casts –
RBC casts
Dysmorphic rbcs
 Acute Tubular Necrosis
• Acute tubular necrosis
- common cause of Acute renal
failure in surgical / ICU setting
- due to Ischaemic or toxins

• Massive losses of blood •Drugs eg Aminoglycosides

volume •Toxins such as heavy
• Any prolonged and severe Metals
cause of renal hypoperfusion • Myoglobinuria
 Acute Tubular Necrosis
• The term acute tubular necrosis refers to the
histology seen in this condition following
severe ischaemia or exposure to nephrotoxins
• Acute tubular epithelial necrosis during the
acute phase of the illness
• Evidence of tubular cell regeneration during
recovery
 Acute Tubular Necrosis
• Damage mainly occurs in the outer medullary
segment (S3 segment of proximal tubule and
thick ascending limb of loop of Henle)
- lower basal blood flow
- higher oxygen requirement
 Pre-Renal or Renal?
• BUN : creatinine > 20 :1 in pre renal AKI due to
enhanced reabsorption of urea
• Fractional excretion of sodium (FENa)=
(Una/Pna) / ( Ucr/P cr) x 100
*usually < 1% in pre renal
*but can be affected by use of diuretics and co
existing liver disease.
 Post Renal
• The blood supply to the kidneys is normal
and the kidneys are normal
• The cause is obstruction of the urinary
outflow tracts
– Obstruction of both ureters – rare occurrence
– Obstruction of ureteric orifices – Ca bladder, Ca
Cervix
– Obstruction of urethra – Prostatomegaly,
Uretheral stricture
Renal calculi
 Post Renal

NORMAL HYDRONEPHROSIS
 Etiology of Post Renal AKI
• Upper tract obstruction • Lower track obstruction
• Intrinsic – Benign prostatic
– Nephrolithiasis hypertrophy
– Papillary necrosis – Prostate cancer
– Blood clot – Transitional cell carcinoma
– Transitional cell cancer – Urethral stricture
– Bladder stones
• Extrinsic – Blood clot
– Retroperitoneal/pelvic
malignancy – Neurogenic bladder
– Retroperitoneal fibrosis
– Endometriosis
– Abdominal aortic
anuerysm
 Approach to Renal Failure
• Determine that there is renal failure
– Detailed history
– Blood tests
– Urine output
• What is the cause?
– Acute vs chronic
– Pre-renal, renal, post renal
• When cause is established, institute
appropriate treatment
 Is it renal failure?
• Elevated serum urea and creatinine

• Oliguria/ anuria
 What is the cause?
• Post renal  obstructive; exclude with u/s
KUB

• Pre-renal  hypotension (from sepsis,

dehydration ,cardiac failure, blood loss)

• Renal  ATN, DRUGS, glomerulonephritis

 Investigations
• Urine
• Blood
• X-rays (KUB)
• Ultrasound Kidney Ureter bladder (KUB)
• Intravenous urography
• CT urethrogram (CTU)
• Renal Biopsy
 Urine
• Microscopy
– Casts
• RED - suggest glomerulonephritis/vasculitis
• WHITE - a tubulointerstitial disease or acute
pyelonephritis
– Red and white cells
– crystals
• Urinalysis
– Specific gravity, Protein, Glucose, Ketones, Nitrite,
pH
 Blood
• Urea (BUN), Creatinine (Ratio of Urea:
creatinine 10-15:1)
• Blood gasses
• Calcium/Phosphate
X-rays
 Ultrasound KUB
• Exclude obstructive uropathy
• Polycystic kidneys
IVU
• Investigate unexplained
haematuria
• Injection of IV contrast
• KUB X-rays taken
• Contraindicated in
obstructive uropathy!
Complications
What does this ECG show?

Tall, Symmetrical, Tented T Waves

HYPERKALEMIA
 Metabolic acidosis
• Severe acidosis may impair cardiac
contractility  reduce cardiac output  more
tissue hypoxia  worsen lactic acidosis
• NaHCO3 infusion NOT indicated in all cases 
may cause more problems eg
• Pulmonary edema (esp in anuric patients)
• Hypernatremia
• Metabolic alkalosis
 Metabolic acidosis
• Primary aim of therapy  reversal of
underlying disease

• NaHCO3 only used in severe metabolic

acidosis eg pH <7.1
• BUT… benefit not proven in clinical trials
 Acute pulmonary edema
• Breathless
• Raised JVP
• Bibasal crepitations
 Renal Replacement Therapy (RRT)
• Volume overload not responding to
diuretic
• Hyperkalemia (K+ >6.5 or rising)
• Severe metabolic acidosis
• Symptomatic uremia (pericarditis,
encephalopathy, bleeding dyscrasia,
nausea, vomiting, pruritus)
• Uremia (BUN >100)
Method : intermittent HD or continuous RRT (CRRT)
 Summary
• Definitions – Acute Renal Failure (ARF) and
Acute Kidney Injury (AKI)
• Etiology
• Pathogenesis
• Investigations
• Management
So True, So False?
Thank You
New dialysis patients, Malaysia 1980
to 2003.
Patients dialyzing in Malaysia on
December 31, 1980 to 2003