ACUTE RENAL

FAILURE
.
DEFINITION:
Acute renal failure (ARF), also termed acute
renal insufficiency, is a clinical syndrome in
which a sudden deterioration in renal function
results in the inability of the kidneys to
maintain fluid and electrolyte homeostasis.
ARF occurs in 2-3% of children admitted to
pediatric tertiary care centers and in as many
as 8% of infants in neonatal intensive care
units.
A classification system has been proposed to
standardize the definition of acute kidney injury
in adults. These criteria of:
Risk, Injury, Failure, Loss, and End-stage renal
disease were given the acronym of RIFLE. A
modified RIFLE criteria (pRIFLE) has been
developed to characterize the pattern of acute
kidney injury in critically ill children.
PRIFLE CRITERIA
CRITERIA ESTIMATED CCI URINE OUTPUT

RISK eCCL decrease by 25% <0.5ml /kg/hr for 8

hrs
INJURY eCCL decrease by 50% <0.5ml/kg/hr for 16
hrs
FAILURE eCCL decrease by 75% <0.3ml/kg/hr for 24
hrs or anuric for 12
hrs

LOSS Persistent failure>4weeks

END-STAGE End-stage renal disease

(persistent failure>3
months)
PATHOGENESIS
ARF has been conventionally classified into 3
categories:
 Prerenal
 Intrinsic renal
 Postrenal
PRERENAL ARF
Prerenal ARF, also called prerenal azotemia, is
characterized by diminished effective circulating
arterial volume, which leads to inadequate renal
perfusion and a decreased GFR. Evidence of kidney
damage is absent.
COMMON CAUSES:
 dehydration
 sepsis
 hemorrhage
 severe hypoalbuminemia
 cardiac failure.
CAUSES
Haemorrhage

Dehydration

Cardiac failure
INTRINSIC RENAL ARF
Intrinsic renal ARF includes a variety of disorders
characterized by: renal parenchymal damage,
sustained hypoperfusion and ischemia.
CAUSES:
 Many forms of Glomerulonephritis, including
postinfectious glomerulonephritis, lupus nephritis,
Henoch-Schönlein purpura nephritis,
membranoproliferative glomerulonephritis, and anti-
glomerular basement membrane nephritis, can cause
ARF.
 Acute tubular necrosis (ATN).
 Acute interstitial nephritis.
 Tumor lysis syndrome.
POST RENAL ARF
Postrenal ARF includes a variety of disorders
characterized by obstruction of the urinary tract.
CAUSES:
In neonates and infants, congenital conditions such as
 posterior urethral valves.
 bilateral ureteropelvic junction obstruction
account for the majority.
 Other conditions such as urolithiasis.
 tumor (intra-abdominal or within the urinary tract).
 hemorrhagic cystitis.
 neurogenic bladder can cause ARF in older children
and adolescents.
Clinical manifestations
A carefully taken history is critical
in defining the cause of ARF.
 An infant with a 3-day history of vomiting and
diarrhea most likely has prerenal ARF
caused by volume depletion.
 A 6 yr old child with a recent pharyngitis who presents
with periorbital edema, hypertension, and gross
hematuria most likely has intrinsic ARF related to
acute postinfectious glomerulonephritis.
HENOCH-SCHONLEIN
PURPURA
 A neonate with a history of hydronephrosis on
prenatal ultrasound and a palpable bladder and
prostate most likely has congenital urinary tract
obstruction, suggesting post renal ARF.
 The physical examination must be thorough,
with careful attention to volume status.
1. Tachycardia, dry mucous membranes, and poor
peripheral perfusion suggest inadequate
circulating volume and the possibility of
prerenal ARF.
2. Peripheral edema and a cardiac gallop suggest
volume overload and the possibility of intrinsic
ARF from glomerulonephritis or ATN.
3. The presence of a rash and arthritis might
suggest systemic lupus erythematosus (SLE) or
Henoch-Schönlein purpural nephritis.
Palpable flank masses might suggest renal vein
thrombosis,tumors, cystic disease, or urinary
tract obstruction.
Lab findings
Laboratory abnormalities can include:
 Anemia (the anemia is usually dilutional or hemolytic) as
in SLE, renal vein thrombosis,HUS).
 Leukopenia (SLE, sepsis) .
 Thrombocytopenia (SLE, renal vein thrombosis, sepsis,
HUS).
 Hyponatremia (dilutional).
 Metabolic acidosis.
 Elevated serum concentrations of blood urea
nitrogen, creatinine, uric acid, potassium, and
phosphate (diminished renal function).
 Hypocalcemia (hyperphosphatemia).
 The serum C3 levels may be depressed and antibodies
in the serum to streptococcal, nuclear, neutrophilic
cytoplasmic or GBM antigens may be found.
 The presence of hematuria, proteinuria, and red
blood cell or granular urinary casts suggests
intrinsic ARF, in particular glomerular
disease.

 The presence of white blood cells and white blood

cell casts, with low-grade hematuria and
proteinuria, suggests tubulointerstitial disease.

 Urinary eosinophils may be present in children

with drug-induced tubulointerstitial nephritis.
 Chest radiography may reveal cardiomegaly,
pulmonary congestion (fluid overload) or pleural
effusions.
 Renal ultrasonography can reveal hydronephrosis
and/or hydroureter, which suggest urinary tract
obstruction, or nephromegaly, suggesting intrinsic
renal disease.
 Renal biopsy can ultimately be required to determine
the precise cause of ARF in patients who do not have
clearly defined prerenal or postrenal ARF.
 Though serum creatinine is used to measure kidney
function, it is an insensitive and delayed measure of
decreased kidney function following acute kidney
injury.
 Other biomarkers under investigation include
changes in plasma neutrophil gelatinase-associated
lipocalin (NGAL) and cystatin C levels and urinary
changes in NGAL, interleukin-18 (IL-18), and
kidney injury molecule-1 (KIM-1).
Urine analysis, urine
chemistry and osmolality
in ARF
hypovulumia ATN Acute Glomerulo obstruction
iterstitial -nephritis
neohritis
sediment bland Broad, WBC, RBCs, RBC cast Bland or bloody
brownish eosinophills,
granular cast cell casts
protein None or low none or low Minimal but Increased > 100 low
may inc with mg/dl
NSAIDs
Urine <20 >3o >30 <20 <20 acute
sodium
(mEq/l)
Urine >400 <350 <350 >400 <350
osmolality
(mOsm/kg)
Fractional <1 >1 varies <1 <1 acute
excretion of
sodium (%)
>1 few days
treatment
Treatment of acute renal failure depends on the
underlying cause. Treatment may include:
 Hospitalization.
 Administration of intravenous (IV) fluids in large
volumes (to replace depleted blood volume).
 Diuretic therapy or medications (to increase urine
output).
 Close monitoring of important electrolytes such as
potassium, sodium, and calcium.
 Medications (to control blood pressure).
 Specific diet requirements.
TAKE CARE OF YOUR
KIDNEYS PLEASE!
SPECIFIC DIET REQUIREMENTS
In some cases, children may develop severe
electrolyte disturbances and toxic levels of certain
waste products normally eliminated by the
kidneys. Children may also develop fluid overload.
So in that case, Dialysis may be indicated.
Indications for dialysis
 Volume overload with evidence of hypertension and/or
pulmonary.
 Edema refractory to diuretic therapy.
 Persistent hyperkalemia.
 Severe metabolic acidosis unresponsive to medical
management.
 Neurologic symptoms (altered mental status, seizures).
 Blood urea nitrogen >100-150 mg/dL (or lower if
rapidly rising).
 Calcium:phosphorus imbalance, with hypocalcemic
tetany.
types
• Is useful in patients with relative stable
hemodynamic status. This highly efficient
process accomplishes both fluid and electrolyte
Intermittent removal in 3- to 4-hr session using a pump-
hemodialysis driven extracorporeal circuit and large central
venous catheter. Intermittent hemodialysis may
be performed 3 to 7 times per week based on
the patient’s fluid and elect.

• Is most commonly employed in neonates

Peritoneal and infants with ARF, although this
modality may be used in children and
dialysis adolescents of all ages.
HEMODIALYSIS
PERITONEAL DIALYSIS
 prognosis
The mortality rate in children with ARF
is variable and depends entirely on the
nature of the underlying disease
process rather than on the renal failure
itself.
 Children with ARF caused by a renal-limited
condition such as postinfectious glomerulonephritis
have a very low mortality rate (<1%).

 Those with ARF related to multiorgan failure have a

very high mortality rate (>90%).

 Recovery of renal function is likely after ARF resulting

from prerenal causes, HUS, ATN, acute interstitial
nephritis, or tumor lysis syndrome.

 Recovery of renal function is unusual when ARF

results from most types of rapidly progressive
glomerulonephritis, bilateral renal vein thrombosis, or
bilateral cortical necrosis.
KIDNEYS ARE LIFE!
THANKS