ACUTE RENAL FAILURE

CASE REVIEW

S> 22/M
(+) abdominal pain, crampy x 3 days
(+) undocumented fever, body
malaise, anorexia
(+) 30 episodes of loose watery
stools, ½ -1 cup in amount per episode
(+) 20 episodes of vomiting in 2 days
 CASE REVIEW

S> PMHx:
(-) previous surgical operation
(-) DM, HPN, kidney disease
FMHx:
(+) kidney disease, father
PSHx:
3 pack years, alcoholic beverage
drinker 2x a month
 CASE REVIEW

O> 90/60 80 20 36.9

poor skin turgor
pale conjunctivae,
clear breath sounds,
normal rate, regular rhythm,
no murmurs
(+) Goldflamm, left
(-) edema, full and equal pulses
 CASE REVIEW

O> Urinalysis:
dark yellow/ cloudy/ acidic/ 1.020/
+++ protein/ ++ sugar/ many RBC/
0-2 casts/ moderate bacteria

Creatinine:
389 (9/27) 478 (10/1)
663 (9/30) 174 (10/4)
 CASE REVIEW

A> ARF secondary to dehydration

secondary to AGE

VS.

ARF secondary to sepsis secondary to

pyelonephritis vs. ascending cholangitis
 Acute Renal Failure

• Usually asymptomatic
• Recent rise in serum urea and creatinine
 Acute Renal Failure

• Rapid decline in GFR

• Retention of nitrogenous waste products
• Perturbation of ECF volume and
electrolyte and acid-base homeostasis
 Types of ARF

1. Pre-renal ARF

2. Intrinsic renal ARF

3. Postrenal ARF
 PRE-RENAL ARF

• Physiologic response to renal

hypoperfusion
• Rapidly reversible when reperfused
• Usually brought about by hypovolemia,
low cardiac output, systemic
vasodilatation and renal
vasoconstriction
 PRE-RENAL ARF

SUGGESTIVE CLINICAL FEATURES

1. Thirst
2. Orthostatic hypotension
3. Tachycardia
4. Low JVP
5. Dry mucosa or axilla
6. Weight loss
7. Decreased effective circulatory volume
 PRE-RENAL ARF

COORDINATED NEURAL
HYPOVOLEMIA
AND HUMORAL RESPONSES
(FALL IN MAP)
(B.V. AND B.P. RESTORED)

CONSTRICTION OF AFFERENT ARTERIOLAR

EFFERENT ARTERIOLES VASODILATATION
 INTRINSIC RENAL ARF

• Ischemia-induced injury to renal

parenchymal cells
• CAUSES
1. diseases of large renal vessels
2. diseases of the renal microcirculation
and glomeruli
3. tubulointerstitial diseases
 INTRINSIC RENAL
ARF

ISCHEMIC NEPHROTOXIC
 3 PHASES OF ISCHEMIC INTRINSIC ARF

• Initiation Phase
– Within hours to days of renal hypoperfusion
– GFR declines due to:
• ↓ glomerular ultrafiltration pressure due to the fall in renal
blood flow
• Obstructed flow of glomerular filtrate due to the casts
produced by necrotic debris from the ischemic tubule
epithelium
• Backleak of glomerular filtrate through injured tubular
epithelium
• Maintenance Phase
– 1-2 weeks from ischemic injury
– Renal cell injury is established, urine output
is lowest and uremic complications arise
– Mechanisms:
• Persistent intrarenal vasoconstriction and medullary
ischemia
• Congestion of medullary blood vessels
• Reperfusion injury induced by reactive oxygen species
from leukocytes or renal parenchymal cells
• Recovery Phase
– Characterized by repair and regeneration of
renal parenchymal cells, particularly tubule
epithelial cells
– GFR gradually returns to premorbid levels
 INTRINSIC RENAL ARF

SUGGESTIVE CLINICAL FEATURES

1. Recent hemorrhage
2. Hypotension
3. Surgery
 Nephrotoxic
Intrinsic
ARF

EXOGENOUS ENDOGENOUS
(Radiocontrast, cyclosporine, (Rhabdomyolysis, hemolysis,
antibiotics, chemotherapy, Uric acid, oxalate, plasma
acetaminophen, abortifacients) Cell dyscrasia)
Decreased “true” or “effective” circulatory volume

Activation of
Central
Baroceptors

Angiotensin II Norepinephrine AVP

 Vasoconstriction/ mesangial cell contraction

Reduced renal blood flow and GFR

Preferential constriction efferent arteriole

Prostaglandin synthesis

Autoregulation
 Reduced renal blood flow and GFR

Ischemic injury
to renal
parenchyma

If hypoperfusion
sufficient to overwhelm
renal autoregulatory
defenses

Endothelial Medullary Tubule epithelial cell injury

(proximal tubule and
dysfunction congestion thick ascending limb)
 Tubule epithelial
Endothelial Medullary
cell injury
Dysfunction congestion

Persistent medullary Tubule Backleak of

ischemia obstruction filtrate

Sustained reduction in GFR

Recovery of renal Regeneration of tubule

perfusion epithelium

Recovery of GFR
 Prerenal vs. Intrinsic Renal ARF
Diagnostic Index Prerenal Intrinsic
Fractional excretion of sodium (%) <1 >1
Urine sodium concentration (mmol/L) <10 >20
Urine creatinine to >40 <20
plasma creatinine ratio
Urine urea nitrogen to plasma urea nitrogen >8 <3
urea
Urine specific gravity >1.020 ≈ 1.010
Urine osmolality (mOsm/kg H2O) >500 ≈ 300
Plasma BUN/creatinine ratio >20 <10-15
Renal failure index <1 >1
Urinary sediment Hyaline casts Muddy brown
granular casts
 POST RENAL ARF

 Accounts for <5% of cases

 Requires either obstruction to urine flow
between the external urethral meatus and
bladder neck, bilateral ureteric obstruction
 (+) gradual distention of proximal ureter,
renal pelvis and calyces and a fall in GFR
 POST-RENAL ARF

SUGGESTIVE CLINICAL FEATURES

1. Abdominal or flank pain
2. Palpable bladder
 TREATMENT

Prerenal ARF (fluid replacement)

- pRBC (severe hypovolemia 2˚ hge)
- isotonic solution (mild to moderate hge
or plasma loss)
- hypotonic solution (GUT/GIT losses)

Intrinsic Renal ARF

- glucocorticoids, plasmapharesis,
aggressive control of MAP
 TREATMENT

INDICATIONS FOR DIALYSIS

- Clinical evidence of uremia
- Intractable intravascular volume
overload
- Hyperkalemia or severe acidosis
resistant to conservative measures
- Prophylactic dialysis when urea >100-
150 mg/dL or creatinine >8-10 mg/dL
 OUTCOME AND LONG-TERM PROGNOSIS

• Mortality rate: 50%

• Patients who survive an episode of ARF
recover sufficient renal function to live
normal lives
• 50% have subclinical impairment of
renal function or residual scarring on
renal biopsy
THANK YOU VERY MUCH! 