Acute Renal

Failure
By Dr Shanker Lal Permar
DCH Trainee

Acute renal failure (ARF)

Acute renal failure (ARF) 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 23% of children admitted to
pediatric tertiary care centers and in as
many as 8% of infants in the neonatal
intensive care unit.

PATHOGENESIS.
ARF has been conventionally classified into
3 categories: prerenal, intrinsic renal, and
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
glomerular filtration rate (GFR).
If the underlying cause of the renal
hypoperfusion is reversed promptly, renal
function returns to normal. If hypoperfusion
is sustained, intrinsic renal parenchyma
damage can develop.

PRERENAL Causes
Dehydration
Hemorrhage
Sepsis
Hypoalbuminemia
Cardiac

failure

Intrinsic renal ARF

Intrinsic

renal ARF includes a variety of

disorders characterized by renal
parenchymal damage, including sustained
hypoperfusion/ischemia.
Many forms of glomerulonephritis,
including postinfectious glomerulonephritis,
lupus nephritis, Henoch-Schnlein purpura
nephritis, membranoproliferative
glomerulonephritis, and antiglomerular
basement membrane nephritis, can cause
ARF.

INTRINSIC RENAL Cause

Glomerulonephritis
Postinfectious/poststreptococcal
Lupus erythematosus
Henoch-Schnlein purpura
Membranoproliferative
Antiglomerular basement membrane

Hemolytic-uremic

syndrome
Acute tubular necrosis
Cortical necrosis
Renal vein thrombosis
Rhabdomyolysis
Acute interstitial nephritis
Tumor infiltration
Tumor lysis syndrome

Postrenal ARF
Postrenal

ARF includes a variety

of disorders characterized by
obstruction of the urinary tract.
In neonates and infants,
congenital conditions such as
posterior urethral valves and
bilateral ureteropelvic junction
obstruction account for the
majority of cases of ARF.

POSTRENAL Causes
Posterior

urethral valves
Ureteropelvic junction obstruction
Ureterovesicular junction
obstruction
Ureterocele
Tumor
Urolithiasis
Hemorrhagic cystitis
Neurogenic bladder

CLINICAL MANIFESTATIONS
AND DIAGNOSIS.
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
depletionBut HUS must be consideration .
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. A
critically ill child with a history of protracted
hypotension and exposure to nephrotoxic
medications most likely has ATN.

CLINICAL MANIFESTATIONS AND

DIAGNOSIS (continue)
A

neonate with a history of hydronephrosis

on prenatal ultrasound and a palpable bladder
and prostate most likely has congenital
urinary tract obstruction, probably related to
posterior urethral valves.
The physical examination must be thorough,
with careful attention to volume status.
Tachycardia, dry mucous membranes, and
poor peripheral perfusion suggest inadequate
circulating volume and the possibility of
prerenal ARF. Peripheral edema, rales, and a
cardiac gallop suggest volume overload and
the possibility of intrinsic ARF from
glomerulonephritis or ATN.

CLINICAL MANIFESTATIONS AND

DIAGNOSIS (continue)
The

presence of a rash and

arthritis may suggest systemic
lupus erythematosus (SLE) or
Henoch-Schnlein purpura
nephritis. Palpable flank
masses may suggest renal vein
thrombosis, tumors, cystic
disease, or urinary tract
obstruction.

Investigation
Blood counts
May reveal low hemoglobin
concentration from blood loss or
haemolysis but is usually
dilutional from fluid overload.
Leukocytosis may reveal acute
infection.
Platelet counts may be low in
HUS , renal vein thrombosis, or
SLE.

Serum Electrolytes and

Osmolality
Serum

sodium is low and

potassium is high.
Also measure plasma osmolality
and compare it with urine
osmolality. If ratio of urine to
plasma osmolality is more than
1.1:1.0 then pre renal failure is
the possibility and if ratio is less
than this then renal cause is
likely.

Blood Urea and Creatinine

Both are raised due to diminished
renal function.
Serum clacium, phosphate,
alkaline phosphatese
Serum calcium is low and
phosphates is raised while alkaline
phosphates is normal which
distinguish it from rickets.

Urine Examination
Urine

may be obtained by chatheterization

and examined for osmolality, urinary
sodium and microscopy.
If urine sodium is more than 20 mEq/l, then
intrinsic renal faliure is likely and if this is
less than 10 mEq/l, then pre-renal faliure is
likely.
Urine microscopy may reveal pus cells ( in
case of infection), RBCs ( in case of renal
stone, glomerulonephritis). Red cell or white
cell casts suggest the possibility of intrisic
renal disease.

C3 Complement level
C3 may be low in post-streptococcal
and membrano-proliferative
glomerulo-nephritis, SLE and shunt
nephritis.
Metabolic acidosis ( ABGs)
Metabolic acidosis is present.
Abdominal ultrasound
If will reveal the renal size,
structural defects, stones,
polycystic kidneys or renal
dilatation.

Plain X-ray abdomen

It may reveal the renal size stones
or spinal obnormalities.
Intra-venous Pyelogram (IVP)
IVP is necessary to document
structural defects before surgery.
Micturating Cysto-urethrogram
(MCUG)
MCU is necessary for posterior
urethral valves and to
demonstraete vesico-ureteric
reflux.

X-ray Chest
It may reveal cardiomegaly and
pulmonary congestion from fluid overload.
Renal Scan
DTPA (diethylene-triamine penta-acetic
acid) scan with 99Tc helps in diagnosing
obstructive uropathy or structural defects.
DMSA ( di-mercapto-succinic acid) scan
reveals functional renal cortex in reflux
nephropathy and renal scarring.

Renal Biopsy
It

may rarely be necessary for

ultimate diagnosis of a
glomerulonephritis.

Urinalysis, Urine Chemistries, and

Osmolality in Acute Renal Failure
HYPOVOLEMIA

ACUTE
TUBULAR
NECROSIS

ACUTE
INTERSTITIAL
NEPHRITIS

GLOMERULONE
PHRITIS

OBSTRUCTION

Sediment

Bland

Broad, brownish
granular casts

White blood cells,

eosinophils,
cellular casts

Red blood cells,

red blood cell casts

Bland or bloody

Protein

None or low

None or low

Minimal but may

be increased with
NSAIDs

Increased, >100
mg/dL

Low

Urine
sodium, mEq/L[*]

<20

>30

>30

<20

<20 (acute)

>40 (few days

Urine osmolality
mOsm/kg

>400

<350

<350

>400

<350

Fractional
excretion of
sodium%

<1

>1

Varies

<1

<1 (acute)

>1 (few days)

MEDICAL MANAGEMENT.
General Management
Establish a secure IV line.
Draw blood samples for necessary
investigations.
Collect urine sample. Catheterize if
bladder is palapable otherwise attach
urine bag.
Record blood pressure ( one hourly if it
is high four hour if it is normally).

MEDICAL MANAGEMENT
(continue)
Careful

intake and out put record.

Daily weight measurement .
Urea, creatinine, serum electrolytes, and
blood gases are estimated daily.
Frequent ECG monitoring to detect
hyperkalememia on time.
In estblished renal faliure, total fluied given
per day is 400ml fluid/m2/day ( insensible
losses) + output ( losses in urine, stool,
vomiting)

MEDICAL MANAGEMENT (continue)

In

infants 15ml/kg fluid plus output (losses in

urine, stool vomiting)
Increase fluids by 10% for each one degree
centigrade in temperature
In general, glucose-containing solution (1025%) without electrolytes are used as
maintenance fluids.

Management of complications
Hyperkalemia
hyperkalemia (serum potassium level
>6 mEq/L) may lead to cardiac
arrhythmia, cardiac arrest, and death.
Exogenous sources of potassium
(dietary, intravenous fluids, total
parenteral nutrition) should be
eliminated.
(Kayexalate), 1 g/kg, should be given
orally or by retention enema.

Management of
complications(continue)
Calcium

gluconate 10% solution, 1.0

mL/kg IV, over 35 min
Sodium bicarbonate, 12 mEq/kg IV, over
510 min
Regular insulin, 0.1 U/kg, with glucose
50% solution, 1 mL/kg, over 1 hr
-adrenergic receptor agonist such as
salbutamol given by nibulization also
acutely lower potassiom level.

Management of complications(continue)

Metabolic Acidosis
metabolic acidosis is common in ARF
because of retention of hydrogen ions,
phosphate, and sulfate, but it rarely requires
treatment. If acidosis is severe (arterial pH
<7.15; serum bicarbonate <8 mEq/L) or
contributes to hyperkalemia, treatment is
required. The acidosis should be corrected
partially by the intravenous route, generally
giving enough bicarbonate to raise the
arterial pH to 7.20 (which approximates a
serum bicarbonate level of 12 mEq/L).

Management of
complications(continue)
Hypocalcaemia
Hypocalcaemia is primarily treated by
lowering the serum phosphorus level.
Calcium should not be given intravenously,
except in cases of tetany, to avoid
deposition of calcium salts into tissues.
Patients should be instructed to follow a low
phosphorus diet, and phosphate binders
should be orally administered to bind any
ingested phosphate and increase
gastrointestinal phosphate excretion.

Management of complications(continue)

Hyponatremia
Hyponatremia is most commonly a dilutional
disturbance that must be corrected by fluid
restriction rather than sodium chloride
administration. Administration of hypertonic (3%)
saline should be limited to those patients with
symptomatic hyponatremia (seizures, lethargy) or
those with a serum sodium level <120 mEq/L.
Acute correction of the serum sodium to 125
mEq/L (mmol/L) should be accomplished using the
following formula:
mEq/l of sodium required=0.6 weight (kg) (125serum sodium ,mEq/l)

Management of complications(continue)
Hypertension
Hypertension is a common complication in
acute renal failure as a result of volume
overload, primary renal disease, or both.
Nifedipine or diazoxide are used in acute
hypertension. In severe hypertension,
contonius IV infusion or sodium nitroprusside is
given. For chorionic hypertension , propranolol
or captopril is given.

Management of complications(continue)
Seizures
This is rare complication due to primary
renal disease, uremia, hyponatremia,
hypocalcemia, and hypertension.
Diazepam is the drugs of choice to control
such seizures.

Management of complications(continue)

Infection
Childrenwith

acute renal failure

are susceptible to infections
following bladder catheterization
or peritoneal dialysis.
Broad-spectrum antibiotic should
be used and nephrotoxic drugs
should be avoided.

Management of complications(continue)

Anemia
The anemia of ARF is generally mild (hemoglobin 910
g/dL) and primarily results from volume expansion
(hemodilution). Children with HUS, SLE, active bleeding,
or prolonged ARF may require transfusion of packed red
blood cells if their hemoglobin level falls below 7 g/dL.
In hypervolemic patients, blood transfusion carries the
risk of further volume expansion, which may precipitate
hypertension, heart failure, and pulmonary edema.
Slow (46 hr) transfusion with packed red blood cells
(10 mL/kg) diminishes the risk of hypervolemia. The use
of fresh, washed red blood cells minimizes the risk of
hyperkalemia. In the presence of severe hypervolemia
or hyperkalemia, blood transfusions are most safely
administered during dialysis/ultrafiltration.

Management of complications(continue)

Gastrointestinal
Bleeding
This

may be prevented
by giving calcium
carbonate antacids, or IV
cimetidine . (510mg/kg/12hour)

Management of complications(continue)
DIALYSIS.
Indications for dialysis in ARF include the
following:
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 greater than 100150
mg/dL (or lower if rapidly rising).
Calcium/phosphorus imbalance, with
hypocalcemic tetany

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%).

PROGNOSIS ( continue)
The prognosis for recovery of renal function
depends on the disorder that precipitated ARF.
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.
Medical management may be necessary for a
prolonged period to treat the sequelae of ARF,
including chronic renal insufficiency,
hypertension, renal tubular acidosis, and
urinary concentrating defect.

Thank
You
The End