Management

Diagnosis
Approach Considerations
The following studies are indicated in patients with oliguria:
 Urine analysis
 Blood urea nitrogen (BUN) and serum creatinine
 Serum sodium
 Serum potassium
 Serum phosphate and calcium
 Acid-base balance
 Complete blood count (CBC)
Additional laboratory studies should be performed as indicated. Decreased complement
levels (C3, C4) are characteristic of acute poststreptococcal glomerulonephritis but can
also be observed in lupus nephritis and membranoproliferative glomerulonephritis. A
suspected diagnosis of acute poststreptococcal glomerulonephritis can be confirmed by
detection of elevated antistreptococcal titers.
The presence of antinuclear antibodies is suggestive of lupus nephritis, and
antineutrophil cytoplasmic antibodies indicate vasculitis.

Imaging studies
Imaging studies in oliguria include the following:
 Renal ultrasonography
 Voiding cystourethrography - Indicated for suspected bladder outlet obstruction
 Radionuclide renal scanning - May be useful in the assessment of transplant
rejection and obstruction
 Chest radiography - May be indicated if pulmonary edema is suspected
 Echocardiography – May be useful in the presence of congestive heart failure

Methods to asses volume status in renal patient

Invasive or Static or Assess fluid

Method Comments
noninvasive dynamic responsiveness

Of limited value with

poor correlation with
Historical findings Noninvasive Static No
invasive pressure
measurements

Physical exam Noninvasive Static Yes Of limited value but

 Invasive or Static or Assess fluid
Method Comments
noninvasive dynamic responsiveness

serial examinations may

and
detect changes in organ
dynamic
perfusion

Requires use of
standardized measures
of vascular pedicle width
Chest radiograph Noninvasive Static No and cardiothoracic ratio.
Serial chest X-ray may be
helpful in determining
effects of fluid therapy

Central venous Poor correlation with

Invasive Static No
pressure fluid responsiveness

Pulmonary
Poor correlation with
capillary wedge Invasive Static No
fluid responsiveness
pressure

Single measures of
cardiac chamber volume
Echocardiogram Noninvasive Static No
hard to assess. Serial
measures may be helpful

Invasive (pulse
Stroke volume or Requires sedated,
oximeter
pulse pressure Dynamic Yes mechanically ventilated
method in
variation patient
noninvasive)

Esophageal Not useful for continuous

Invasive Dynamic Yes
doppler measurements

Vena cava
Noninvasive Dynamic Yes Body habitus dependent
diameter

Passive leg raising Noninvasive Dynamic Yes Unreliable with intra-

(bioreactance, abdominal hypertension
end-tidal CO2) 
 Invasive or Static or Assess fluid
Method Comments
noninvasive dynamic responsiveness

Invasive (FloTrac
or PiCCO or
LiDOO)

End-expiratory Passive leg Requires 15-s end-

Dynamic Yes
occlusion raising expiratory occlusion

Not able to assess

Bioimpedance Noninvasive Static No
intravascular volume

Urine analysis
Careful examination of a freshly voided urine sample is a rapid and inexpensive way of
distinguishing prerenal from intrinsic renal failure.
In prerenal failure, a few hyaline and fine, granular casts may be observed with little
protein, heme, or red cells. Heme-positive urine in the absence of erythrocytes suggests
hemolysis or rhabdomyolysis.
In intrinsic renal failure, hematuria and proteinuria are prominent. Broad, brown,
granular casts are typically found in ischemic or toxic acute tubular necrosis, and red
cell casts are characteristically observed in acute glomerulonephritis. The urine in acute
interstitial nephritis shows white cells, especially eosinophils and white cell casts.
BUN and Serum Creatinine
In prerenal failure, elevation of BUN levels is marked and the BUN-to-creatinine ratio is
greater than 20. This reflects increased proximal tubular reabsorption of urea. The
hallmark of established acute kidney injury is a daily increase in serum creatinine levels
(0.5-1.5 mg/dL daily) and BUN levels (10-20 mg/dL daily).
Elevations in BUN levels can also result from steroid therapy, parenteral nutrition, GI
bleeding, and catabolic states. A spurious elevation in serum creatinine can be
encountered following the use of drugs that interfere with the tubular secretion of
creatinine (eg, trimethoprim, cimetidine) or drugs that provide chromogenic substrates
(eg, cephalosporins), which interfere with the Jaffé reaction for determination of serum
creatinine.
Although serum creatinine levels are the criterion standard for diagnosis of acute kidney
injury, they remain an unreliable indicator during acute changes in kidney function for
the following reasons:
 Serum creatinine levels can widely vary with age, gender, lean muscle mass,
muscle metabolism, and hydration status
 Serum creatinine levels may not change until about 50% of kidney function has
already been lost
 At lower rates of glomerular filtration, the increased amount of tubular secretion
of creatinine results in overestimation of renal function
 During acute changes in glomerular filtration, serum creatinine levels do not
accurately depict kidney function until steady-state equilibrium has been reached,
which may require several days
In the future, defining acute kidney injury by either a predictive biomarker of kidney
damage or a sensitive measure of decrease in kidney function may be possible.
Fortunately, the tools of modern science offer promising novel biomarkers for the early
diagnosis of acute kidney injury and its clinical outcomes. [14, 15] These biomarkers are
currently undergoing evaluation and validation and are not yet commercially available.

Serum Sodium
Hyponatremia is a common finding that is usually dilutional, secondary to fluid retention
and administration of hypotonic fluids.
Less common causes of hyponatremia include sodium depletion (hyponatremic
dehydration) and hyperglycemia (serum sodium concentration decreases by 1.6 mEq/L
for every 100 mg/dL increase in serum glucose above 100 mg/dL).
Occasionally, hypernatremia may complicate oliguric acute kidney injury and is usually
a result of excessive sodium administration (improper fluid administration or
overzealous sodium bicarbonate therapy).

Serum Potassium
Hyperkalemia is an important complication because of reduced glomerular filtration,
reduced tubular secretion, metabolic acidosis (each 0.1-unit reduction in arterial pH
raises serum potassium by 0.3 mEq/L), and associated catabolic state.
Hyperkalemia is most pronounced in patients with excessive endogenous potassium
production, which occurs in rhabdomyolysis, hemolysis, and tumor lysis syndrome.
Hyperkalemia represents a life-threatening emergency that must be promptly and
aggressively treated, primarily because of its depolarizing effect on cardiac conduction
pathways. Symptoms are nonspecific and may include malaise, nausea, and muscle
weakness. A high index of suspicion and frequent measurement of serum potassium
levels are therefore warranted in children with oliguric acute kidney injury.

Serum Phosphate and Calcium

Hyperphosphatemia and hypocalcemia frequently complicate oliguric acute kidney
injury. The phosphate excess is secondary to reduced renal excretion and can result in
hypocalcemia and calcium phosphate deposition in various tissues.
Hypocalcemia results from hyperphosphatemia-impaired GI calcium absorption
because of inadequate active vitamin D production by the kidney, skeletal resistance to
the calcemic action of parathyroid hormone, and coexistent hypoalbuminemia.
Determining ionized calcium levels is important because this unbound form of serum
calcium determines physiologic activity. Ionized calcium can be estimated by assuming
that 1 mg/dL of calcium is bound to 1 g/dL of albumin; thus, ionized calcium is the
difference between total calcium and serum albumin concentration.
Acidosis increases the fraction of total calcium in the ionized form; thus, overzealous
bicarbonate therapy can decrease ionized calcium. Severe hypocalcemia results in
tetany, seizures, and cardiac arrhythmias.

Acid-Base Balance
The impaired renal excretion of nonvolatile acids and decreased tubular reabsorption
and regeneration of bicarbonate results in metabolic acidosis with a high anion gap.
Severe acidosis can develop in children who are hypercatabolic (eg, shock, sepsis) or
who have inadequate respiratory compensation.
The last 2 digits of the arterial pH provide a bedside estimate of respiratory
compensation. Those numbers predict the partial pressure of carbon dioxide, or
pCO2 (eg, a patient with arterial pH of 7.25 has adequate respiratory compensation if
the arterial pCO2 is 25 ± 3 mm Hg).

Complete Blood Count

Anemia is a result of dilution and decreased erythropoiesis. Microangiopathic hemolytic
anemia with schistocytes and thrombocytopenia are indicative of hemolytic uremic
syndrome.
Patients with oliguria that is secondary to systemic lupus erythematosus may display
neutropenia and thrombocytopenia.
Eosinophilia is consistent with allergic interstitial nephritis. Prolonged acute kidney injury
can result in functional platelet disorders.

Renal Ultrasonography
Ultrasonography of the kidneys and bladder with Doppler flow studies is essential.
Exceptions may include children with unmistakable prerenal failure from dehydration
who promptly respond to fluid resuscitation or those with mild renal insufficiency
secondary to a nephrotoxin who respond to discontinuing the medication.
Ultrasonography provides important information regarding kidney size and echogenicity,
renal blood flow, collecting system, and bladder wall.
Children with acute intrinsic renal failure display echogenic kidneys that may be
enlarged. With prolonged renal failure, however, renal cortical necrosis may result in
decreased kidney size. Bilaterally small and scarred kidneys are indicative of chronic
renal disease. Congenital disorders, such as polycystic kidney disease and multicystic
 dysplasia, are easily detected. Calculi and tumors that can cause obstruction may also
be detected.
A Doppler study is critical in the evaluation of vascular obstruction. Hydronephrosis,
hydroureter, and a thickened bladder wall are consistent with an obstruction of the
bladder outlet or with one below that.

Electrocardiography
Electrocardiography is indicated if hyperkalemia is suspected or has been detected by
laboratory tests. The earliest sign is the appearance of tall peaked T waves.
Recognizing and treating hyperkalemia at this early stage is important.
Subsequent findings include the following:
 Prolongation of the PR interval
 Flattening of P waves
 Widening of QRS complexes
 ST segment changes
 Ventricular tachycardia
 Terminal ventricular fibrillation

Renal Biopsy
In general, kidney biopsy is not necessary in the initial evaluation; however, if prerenal
and postrenal causes have been ruled out and an intrinsic renal disease other than
prolonged ischemia, nephrotoxin, or postinfectious glomerulonephritis is suspected,
renal biopsy may be valuable in establishing diagnosis, guiding therapy, and providing
prognosis.
Histologic examination is especially valuable in the diagnosis and management of
transplant rejection, rapidly progressive glomerulonephritis, lupus nephritis, and
tubulointerstitial nephritis.
tubule cells, focal areas of proximal tubular dilatation and distal tubular casts, and areas
of cellular

Treatment
Fluid Management
The major goal of fluid management is to restore and maintain normal intravascular
volume. Patients with oliguric acute kidney injury may present with hypovolemia,
euvolemia, or volume overload, and an estimation of fluid status is a prerequisite for
initial and ongoing therapy. This is accomplished by determination of input and output,
body weights, vital signs, skin turgor, capillary refill, peripheral edema, cardiopulmonary
examination, serum sodium, and fractional excretion of sodium (FENa).
Children with intravascular volume depletion require prompt and vigorous fluid
resuscitation. Initial therapy includes isotonic sodium chloride or lactated Ringer solution
at 20mL/kg over 30 minutes, which can be repeated twice if necessary. This therapy
should result in increased urine output within 4-6 hours. If oliguria persists (confirmed
with bladder catheterization), central venous monitoring may be required to guide
further management. Potassium administration is contraindicated until urine flow is
established.
Oliguria with volume overload requires fluid restriction and intravenous furosemide.
Failure to respond to furosemide suggests the presence of acute tubular necrosis rather
than renal hypoperfusion, and fluid removal by dialysis or hemofiltration may be
required, especially if signs of pulmonary edema are evident.
Potassium should be withheld until the oliguria improves and serum potassium levels
begin to fall.
Monitoring treatment progress
Input and output records, daily weights, physical examination, and serum sodium guide
ongoing therapy. When appropriate fluid therapy is administered, the body weight
should decrease by 0.5-1.0% daily as a result of caloric deprivation, and the serum
sodium concentration should remain steady. A more rapid weight loss and increasing
serum sodium indicate inadequate fluid replacement. An absence of weight loss with
decreasing serum sodium suggests excess free-water replacement.

Management of Hyperkalemia
In practice, the definitive therapy for significant hyperkalemia accompanying oliguric
acute kidney injury frequently includes dialysis. The other forms of therapy outlined in
this section serve primarily to tide over the crisis.
Serum potassium levels of 5.5-6.5 mEq/L should be treated by eliminating all sources of
potassium from the diet or IV fluids and administration of a cation exchange resin, such
as sodium polystyrene sulfonate (Kayexalate). Kayexalate requires several hours of
contact with the colonic mucosa to be effective, and the rectal route of administration is
preferred. Complications of this therapy include hypernatremia and constipation.
Emergency treatment of hyperkalemia is indicated when serum potassium exceeds
6.5mEq/L or if peaked T waves are present. In addition to Kayexalate, patients should
receive calcium gluconate (with continuous electrocardiographic monitoring) to
counteract the effects of hyperkalemia on the myocardium.
Uptake of potassium by cells can be stimulated by infusion of glucose and insulin or by
beta-agonists (albuterol by nebulizer). The efficacy and convenience of nebulized
albuterol has been well described in hemodialysis patients with hyperkalemia, but it can
cause tachycardia.
 Sodium bicarbonate, which also causes a rapid shift of potassium into cells, was the
drug of choice in the past. However, the current recommendation is to use this therapy
only in the concomitant presence of severe acidosis. Such therapy should be used with
caution because it can precipitate hypocalcemia and sodium overload.

Management of Other Electrolytes and Acid-Base Balance

The primary treatment for hyponatremia is free water restriction; however, a serum
sodium level of less than 120 mEq/L or accompanied central nervous system (CNS)
dysfunction may require 3% sodium chloride infusion.
The management of hyperphosphatemia includes dietary restriction and oral phosphate
binders (calcium carbonate or calcium acetate). Hypocalcemia usually responds to the
oral calcium salts used for control of hyperphosphatemia but may require 10% calcium
gluconate infusion if severe.
Mild metabolic acidosis is treated with oral sodium bicarbonate or sodium citrate.
Severe acidosis (pH < 7.2), especially in the presence of hyperkalemia, requires IV
bicarbonate therapy. Recognize that bicarbonate therapy requires adequate ventilation
(to excrete the carbon dioxide produced) to be effective, and it may precipitate
hypocalcemia and hypernatremia. Patients who cannot tolerate a large sodium load (eg,
those with congestive heart failure) may be treated in an ICU setting with IV
tromethamine (THAM), with provision of adequate ventilatory support pending institution
of dialysis.

Management of Hypertension
Mild hypertension usually responds to salt restriction and diuretics. Moderate,
asymptomatic hypertension is most commonly treated with oral or sublingual calcium
channel blockers or with IV hydralazine.
For patients with hypertensive encephalopathy, treatment may require continuous
sodium nitroprusside infusion with monitoring of thiocyanate levels. Because
nitroprusside therapy requires careful drip calculations and administration, other
immediate alternatives include a nicardipine drip or labetalol. Once the hypertensive
crisis has been controlled, oral long-acting agents can be initiated.

Dialysis
The general goal of dialysis is to remove endogenous and exogenous toxins and to
maintain the fluid, electrolyte, and acid-base balance until renal function returns. The
indications for acute dialysis are not absolute, and the decision to use this modality
depends on the rapidity of onset, duration, and severity of the abnormality to be
corrected. Common indications include the following:
 Fluid overload that is unresponsive to diuretics or a hindrance to adequate
nutrition
 Symptomatic acid-base imbalance, electrolyte imbalance, or both (especially
hyperkalemia) that is unresponsive to nondialytic management
 Refractory hypertension
 Symptomatic uremia (CNS symptoms, pericarditis, pleuritis)
The choice between hemodialysis, peritoneal dialysis, and continuous venovenous
hemodialysis (CVVH) depends on the overall clinical condition, the availability of
technique, the etiology of the renal failure, institutional preferences, and specific
indications or contraindications.
Peritoneal dialysis
In general, peritoneal dialysis is a gentler continuous method that was a more preferred
technique in children in the past. It is not the treatment of choice for acute, severe fluid
overload or hyperkalemia, however, because the onset of action is slower. Specific
contraindications include abdominal wall defects, bowel distention, perforation or
adhesions, and communications between the chest and abdominal cavities.
Hemodialysis
Hemodialysis requires vascular access, heparinization, a large extracorporeal blood
volume, and skilled personnel, but it has the advantage of rapid correction of fluid,
electrolyte, and acid-base imbalances. This therapy may be difficult to accomplish in
hypotensive patients with multiorgan damage
CVVH
CVVH has emerged as an alternative therapy for children who require fluid removal in
an unstable, critically ill setting. The major advantage of these techniques is in their
potential ability to remove fluid, even in a hypotensive child in whom hemodialysis may
be contraindicated and peritoneal dialysis may be inefficient. However, patients require
the presence of trained personnel and specialized equipment that are available only at
select tertiary care centers.

Management of Urologic Obstruction

Patients with oliguria secondary to obstruction frequently require urologic care. The site
of obstruction determines the primary therapy.
Obstruction of the bladder neck due to posterior urethral valves should be immediately
relieved by gentle insertion of a fine urethral catheter. Foley catheters should not be
used because the balloon may become lodged in the dilated prostatic urethra, resulting
in incomplete bladder emptying.
The subsequent management of choice is endoscopic ablation of the valves. A
temporary cutaneous vesicostomy may be required in a small infant whose urethra may
not accept an endoscope or when hydronephrosis and renal function do not improve
after catheterization.
Relief of obstruction is often followed by postobstructive diuresis. The resultant polyuria,
hypokalemia, and hyponatremia should be managed with vigorous fluid replacement
guided by frequent determinations of urinary flow rate, urinary electrolytes, and serum
electrolytes.

Diet
Children with oliguric acute kidney injury are frequently in a highly catabolic state;
therefore, aggressive nutritional support is important. Adequate calories should be
provided to allow for maintenance requirements, and supplements should be provided
to combat excessive catabolism. Children should be administered at least 150% of
maintenance caloric intake and at least 3 g/kg/d of daily protein intake.
Protein of high biologic value should be administered in amounts that are sufficient to
maintain neutral nitrogen balance, reflected by steady BUN levels.
Oral feeding is the preferred route. Infants should be placed on a low-phosphorus
formula (Similac PM 60/40), and older children should be fed a low-phosphorus/low-
potassium diet.
Additional calories may be supplied by fortifying foods with Polycose and medium-chain
triglycerides.
Children who are nauseous or anorexic may benefit from enteral feedings. If these are
not possible, central IV hyperalimentation may be used to deliver concentrated dextrose
(25%) and lipids (20%).
If adequate nutrition cannot be achieved because of fluid restriction, early institution of
ultrafiltration or dialysis should be considered.