ACUTE RENAL FAILURE
Definition :a rapid decline in renal function .with
an increase in serum creatinine level ( a relative
increase of 50 % or an absolute increase of 0.5
to 1.0 mg /dl ).
*ARF may be oliguric ,anuric ,or nonoliguric
.Severe ARF may occur without a reduction in
urine output ( nonoliguric ARF ).
Wt. gain and edema are the most common
clinical findings in patients with ARF.This is due
to a positive water and sodium balance.
*Characterized by azotemia (elevated BUN
and Cr )
A.Elevated BUN is also seen with
catabolic drugs (e.g. steroids ) ,GI / soft
tissue bleeding , and dietary protein intake
.
B.Elevated Cr is also seen with increased
muscle breakdown and various drugs.The
baseline Cr levelvaries propotionately with
muscle mass
Cirrhosis , hepatorenal syndrome.
_In patients with decreased renal perfusion ,NSAIDs
,ACE inhibitors ,and cyclosporin can precipitate
prerenal failure .
PATHOPHYSIOLOGY
Renal blood flow decreases enough to lower the
GFR which leads to decreased clearance of
metabolites (BUN ,Cr ,uremic toxin ).
Because the renal parenchyma is undamaged
,tubular function ( and therefore the
concentrating ability )is preserved.Therefore the
kidney responds apprpopriately ,conserving as
much sodium and water as possible.
This form of ARF is reversible on restoration of
blood flow ,but if hypoperfusion persists ,
ischemia results and can lead to acute tubular
necrosis (ATN )
LABORATORY FINDINGS
*Oliguria –always found in prerenal failure ( this is
to preserve volume ) .
*Increased BUN to serum Cr ratio (>20 :1 is the
classic ratio ) – because kidney can absorb urea.
*Increased urine osmolality ( >500 mOsm/kg H2O )because the kidney is also able to reabsorb
water.
*Decreased urine Na (<20 mEq /L FENa <1% )
because the Na is avidly reabsorbed .
*Increased urine / plasma Cr ratio (>40 :1 ) –
because much of the filtrate is reabsorbed ( but
not the creatinine )
* Bland urine sediment .
INTRINSIC RENAL FAILURE
A.Kidney tissue is damaged such that the
glomerular filtration and tubular function
are significantly impaired.The kidneys are
unable to concentrate urine effectively.
CAUSES
1.Tubular disease (ATN ) –can be caused by
ischemia ( most common cause ) ,nephrotoxins.
2.Glomerular disease( acute glomerulonephritis
GN )- e.g. Goodpastuer s syndrome ,Wegener s
granulomatosis , poststreptococcal GN, lupus .
3.Vasculardisease – e.g. renal artery occlusion
,TTP ,HUS .
4.Interstitial disease –e.g. allergic interstitial
nephritis ,often due to a hypersensitivity reaction
to medications
LABORATORY FINDINGS
*Decreased BUN – to serum Cr ratio (<20 :1 )in
comparison with prerenal failure.Both BUN and
Cr levels are still elevated , but less urea is
reabsorbed than in prerenal failure.
*Increased urine Na (>40 mEq /Lwith FENa
>2% to 3% ) – because Na is poorly reabsorbed
*Decreased urine osmolality ( <350 mosm /kg
H2O) – because renal water reabsorption is
impaired.
*Decreased urine – plasma Cr ratio ( <20 :2 ) –
because filtrate can not be reabsorbed
POST RENAL FAILURE
A.Least common cause of ARF.
B.Obstruction of urinary tract with intact kidney )
causes increased tubular pressure ( urine
produced can not be excreted ) , which leads to
decreased GFR . Blood supply and renal
parenchyma are intact .
C.Renal function is restored if obstruction is
relieved before the kidneys are damaged .
D.Postrenal obstruction , if untreated ,can lead to
ATN .
CAUSES
*Urethral obstruction secondary to enlarged
prostate (BPH ) is the most common cause .
Obstruction of the solitary kidney.
*Nephrolithiasis
*Obstructing neoplasm ( prostate , cervix ,
bladder )
*Retroperitoneal fibrosis.
* Ureteral obstruction is an uncommon cause
because the obstruction must be bilateral to
cause renal failure .
CAUSES OF ATN
*ISCHEMIC ARF
-Secondary to severe decline in renal blood flow as in shock ,
hemorrhage , sepsis ,DIC ,heart failure.
_Ischemia results in death of tubular cells.
*NEPHROTOXICARF
_Injury secondary to substances that directly injure renal parenchyma
and result in cell death .
_Causes include antibiotics ( aminoglycosides ) ,radiocontrast agents ,
NSAIDs( especially in the setting of CHF .), poisons myoglobinuria (
from muscle damage ,rhabdomyolysis , sternuous exercise ) ,
hemoglobinuria 9 from hemolysis ), chemothreapeutic drugs
(cisplatin ) , and kappa and gamma chains produced in multiple
myeloma .
COURSE OF ATN
* Onset (insult )
*OLIGURIC PHASE
-Azotemia and uremia – average length 10 to 14 days
-urine output <400 -500 ml/day
*DIURETIC PHASE
-Begins when urine output is > 500 ml /day
*High urine output due to the following : fluid overload ( excretion of
retained salt , water ,other solutes that were retained during the
oliguric phase ) ,osmotic diuresis due to retained solutes during
the oliguric phase ; tubular cell damage ( delayed recovery of
epithelial cell function relative to GFR B)
*RECOVERY PHASE :recovery of tubular function .
DIAGNOSIS
1.BLOOD TESTS
A.Elevation in BUN and Cr levels
B.Electrolytes (K ,Ca ,PO4 ), albumin levels , CBC with
differential.
2.URINALYSIS
a.A dipstick test positive for protein ( 3+ ,4+ )suggests intrinsic
renal failure due to glomerular insult.
B.Microscopic examination of the urine sediment is very helpful.
*Hyaline casts are devoid of contents ( in prerenal failure )
RBC casts indicate glomerular disease.
* WBC casts indicate renal parenchymal inflammation.
*Fatty casts indicate nephrotic syndrome
3.URINE CHEMISTRY – to distinguish between
different forms of ARF .
A. Urine Na , Cr , and osmolality : Urine Na depends
on dietary intake.
B.FENa : collect urine and plasma electrolytes
simultaneously .
Values below <1% suggests prerenal failure.
*Values above >2% to 3% suggest ATN .
* FENa is most useful if oilguria is present .
4.Urine culture and sensitivity –if
infection is suspected .
5.RENAL ULTRASOUND
*Useful for evaluating kidney size and for excluding
urinary tract obstruction ( i.e postrenal failure ) –
presence of bilateral hydronephrosis or hydroureter.
*Order for most patients with ARF – unless the cause
of the ARF is obvious and is not postrenal.
6.CT scan ( abdomen and pelvis ) -may be helpful in
some cases ; usully done if renal ultrasound shows
an abnormality such as hydronephrosis.
7.Renal biopsy – useful occasionally if there is
suspicion of acute GN or acute allergic interstitial
nephritis.
8.Renal arteriography – to evaluate for possible
renal artery occlusion ; should be performed only if
specific therapy will make a difference.
COMPLICATIONS
1.ECF volume expansion and resulting pulmonary
edema – treat with diuretic (furosemide ).If there is no
response within 2 hours , consider dialysis.
2.Metabolic
A.Hyperkalemia – due to decreased excretion of K
and the movement of potassium from the ICF to ECF
due to tissue destruction and acidosis.
B Metabolic acidosis ( with increased anion gap )due to decreased excretion of hydrogen ions; if
severe ( below 16 mEq /L) ,correct with sodium
bicarbonate.
C.Hypocalcemia –loss of ability to form active Vit. D
and rapid development of PTH resistance.
d.Hyponatremia may occur if water intake is greater than body
losses , or if a volume depleted patient consumes excessive
hypotonic solutions. (hypernatremia may also be seen in
hypovolemic states )
E.Hyperphosphatemia .
F.Hyperuricemia
3.Uremia –Toxic end products of metabolism accumulate(
especially from protein metabolism )
4.Infection
*Acommon and serious complication of ARF ( occurs in 50% to 60
% of cases ). The cause is probably multifactorial , but uremia
itself is thought to impair immune functions .
*Exampls include pneumonia , UTI ,wound infection ,and sepsis .
TREATMENT
1.General measures
A.Avoid medications that decrease renal blood flow(
NSAIDs) and /or that are nephrotoxic (e.g.
aminoglycosides , radiocontrast agents )
B.Adjust the medication dosages for the level of the
renal function .
C.Correct fluid imbalance
*If the patient is volume depleted .
, give IV fluids .However, many patients with ARF are
volume overloaded ( especially if they are oliguric or
anuric ) , so diuresis may be necessary.
*The goal is to strike a balance beteween correcting
volume deficits and avoiding volume overload ( while
maintaining adequate urine output )
*Monitor fluid balance by daily weight
measurements ( most accurate estimate
) and fluid –output records.
D.Correct electrolytes disturbances if
present.
E.Optimize cardiac output. BP should be
approximately 120 to 140 /80 to 90.
F.Order dialysis if symptomatic uremia
,intractable acidemia , hyperkalemia , or
volume overload develop.
2.Prerenal failure
A.Treat the underlying disorder.
B.Give NS to maintain euvolemia and restore
BP- do not give patients with edema or
ascites. Stopping antihypertensive
medications may be necessary.
C.Eliminate any offending agents ( ACE
inhibitors ,NSAIDs ).
D.If the patient is unstable , Swan –Ganz
monitoring is indicated for accurate
assessment of intravascular volume.
3.Intrinsic
A.Once ATN develops , therapy is
supportive.Eliminate the cause /offending
agents.
B.If the patient is oliguric , a trial of furesomide
may help to increase urine output.This
improves fluid balance.
4.Postrenal – A bladder catheter may be
inserted to decompress the urinary tract.
Consider urology consultation.