Management

Diagnosis
Approach Considerations
The following studies are indicated in patients with oliguria:

 Urinalysis
 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
Urinalysis
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 pCO 2 (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.