AUTHOR AND EDITOR INFORMATION

Section 1 of 8  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• References

INTRODUCTION

Section 2 of 8  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• References

Background

Oliguria is defined as a urine output that is less than 1 mL/kg/h in infants, less than 0.5 mL/kg/h in children, and less than 400 mL/d in adults. It is one of the clinical hallmarks of renal failure. At onset, oliguria is frequently acute, it is often the earliest sign of impaired renal function, and it poses a diagnostic and management challenge to the clinician. In most clinical situations, acute oliguria is reversible and does not result in intrinsic renal failure. However, identification and timely treatment of reversible causes is crucial because the therapeutic window may be small.

Pathophysiology

Oliguria may result from 3 broad pathophysiologic processes: prerenal, intrinsic renal, and postrenal mechanisms.

Prerenal insufficiency is a functional response of structurally normal kidneys to hypoperfusion. Globally, prerenal insufficiency accounts for approximately 70% of community-acquired cases of acute renal failure (ARF) and up to 60% of hospital-acquired cases. The early phase of renal compensation for reduced perfusion includes autoregulatory maintenance of glomerular filtration rate via afferent arteriolar dilatation (induced by myogenic responses, tubuloglomerular feedback, and prostaglandins) and via efferent arteriolar constriction (mediated by angiotensin II).

The early phase also includes enhanced tubular reabsorption of salt and water (stimulated by the renin-angiotensin-aldosterone system and sympathetic nervous system). Rapid reversibility of oliguria following timely reestablishment of renal perfusion is an important characteristic and is the usual scenario in prerenal insufficiency. For example, oliguria in infants and children is most commonly secondary to dehydration, and it reverses without renal injury if the dehydration is corrected. However, prolonged renal hypoperfusion can result in a deleterious shift from compensation to decompensation.

This decompensation phase is characterized by excessive stimulation of the sympathetic and renin-angiotensin systems, with resultant profound renal vasoconstriction and ischemic renal injury. Iatrogenic interference with renal autoregulation by administration of vasoconstrictors (eg, cyclosporine, tacrolimus), inhibitors of prostaglandin synthesis (eg, nonsteroidal anti-inflammatory drugs), or angiotensin-converting enzyme (ACE) inhibitors can precipitate oliguric ARF in individuals with reduced renal perfusion.

Intrinsic renal failure is associated with structural renal damage. This includes acute tubular necrosis (from prolonged ischemia, drugs, or toxins), primary glomerular diseases, or vascular lesions. Advancements in the care of critically ill neonates, infants with congenital heart disease, and children who undergo bone marrow and solid organ transplantation have lead to a dramatic broadening of the epidemiology of pediatric ARF. While multicenter epidemiological data on pediatric ARF do not exist, single-center data and literature reviews from the 1980s and 1990s reported hemolytic uremic syndrome and other primary renal diseases as the most prevalent causes.

More recent single-center data have detailed the underlying causes of pediatric ARF in large cohorts of children. In a study of 226 children with ARF, Bunchman et al reported that congenital heart disease, acute tubular necrosis, sepsis, and bone marrow transplantation were the most common causes. Another retrospective review of 248 patients with a diagnosis of ARF upon discharge or death revealed acute tubular necrosis and nephrotoxins to be the most common causes of ARF. Thus, the epidemiology of pediatric ARF has evolved in developed countries from primary kidney diseases or prerenal failure to secondary effects of other systemic illnesses or their treatment.

The pathophysiology of ischemic acute tubular necrosis is well studied. Ischemia leads to altered tubule cell metabolism (eg, depletion of adenosine triphosphate [ATP], release of reactive oxygen species) and cell death with resultant cell desquamation, cast formation, intratubular obstruction, backleak of tubular fluid, and oliguria. In most clinical situations, the oliguria is reversible and associated with repair and regeneration of tubular epithelial cells.

Postrenal failure is a consequence of mechanical or functional obstruction to the flow of urine. This form of oliguria and renal insufficiency usually responds to release of the obstruction.

Renal failure is not always associated with oliguria. Renal failure that results from nephrotoxic injury, interstitial nephritis, and neonatal asphyxia is frequently of the nonoliguric type, is related to a less severe renal injury, and has a better prognosis.

Frequency

United States

Frequency varies greatly depending on clinical setting. In adults, incidence is about 1% at admission, 2-5% during hospitalization, and 4-15% after cardiopulmonary bypass. Oliguric ARF occurs in approximately 10% of newborn ICU patients and 2-3% of pediatric ICU patients. Incidence in children undergoing cardiac surgery is as high as 8%.

Mortality/Morbidity

• Mortality rates in oliguric ARF vary widely according to the underlying cause and associated medical condition. It ranges from 5% for patients with community-acquired ARF to 80% among patients with multiorgan failure in the ICU.
• The most common causes of death are sepsis, cardiovascular and pulmonary dysfunction, and withdrawal of life support.

Race

No racial predilection exists.

Sex

Both sexes are equally affected.

Age

• Oliguria affects people of all ages.
• It is more common in the neonatal and older age groups because of comorbid conditions, and it is more common in early childhood because of the high incidence of illnesses leading to dehydration.

CLINICAL

Section 3 of 8  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• References

History

Careful evaluation of the patient's history and physical examination often reveals the cause. This is especially important in prerenal and postrenal processes because early diagnosis and treatment frequently results in complete recovery.

• Fluid losses
• • Recent history of diarrhea or vomiting should be sought because this is the most common cause in children.
  • Less commonly, fluid loss may result from traumatic hemorrhage, burns, or following polyuric states such as diabetes insipidus and diabetes mellitus.
  • Loss of intravascular fluid volume into the interstitial space accompanies surgery, shock syndromes, and nephrotic syndrome. Children with fluid losses may report thirst, dizziness, palpitations, and fatigue, and a history of weight loss may be present.
• Drugs
• A detailed history of recent medications should be obtained. In the presence of mild prerenal insufficiency, administration of medications that impair renal autoregulation can precipitate oliguric ARF.
• Cyclosporine, tacrolimus, and contrast agents are direct afferent arteriolar constrictors that interfere with the myogenic response.
• NSAIDs inhibit the renal synthesis of vasodilatory prostaglandins. They are an important cause when administered to febrile children with intercurrent dehydration.
• Drugs that induce direct tubular necrosis include aminoglycosides, amphotericin B, cyclosporine, tacrolimus, antineoplastic agents (eg, methotrexate, cisplatin), and contrast agents.
• Acyclovir and sulfonamides can precipitate within the tubular lumen and result in obstruction.
• In addition, a large number of medications, especially penicillins, cephalosporins, sulfonamides, ciprofloxacin, NSAIDs, and diuretics, can cause interstitial nephritis.
• History of ingesting undercooked meat may suggest hemolytic-uremic syndrome.
• Endogenous tubular toxins
• • Myoglobin (released following crush injuries, myositis, and prolonged grand mal seizures)
  • Hemoglobin (hemolysis)
  • Uric acid (tumor lysis syndrome)
• Symptoms of glomerular disease
• • Many children have a history of gross hematuria and edema. An antecedent streptococcal infection may suggest a postinfectious glomerulonephritis, and a history of bloody diarrhea often precedes the hemolytic-uremic syndrome.
  • Suspect systemic lupus erythematosus or allergic interstitial nephritis in children with fever, joint symptoms, and skin rashes who present with oliguria.
  • A history of recurrent sinusitis or lower respiratory tract infections may suggest Wegener granulomatosis, and hemoptysis may suggest Goodpasture disease.
• Symptoms of urinary tract obstruction
• • Complete absence of urine output
  • Alternating periods of polyuria and oligo-anuria
  • Poor urinary stream or dribbling
• Symptoms of chronic renal failure
• • Although oliguria is usually acute at initial presentation, it may also be a presenting symptom of chronic renal failure.
  • Children may have additional symptoms suggestive of previous renal disease such as frequent urinary tract infections, hematuria, proteinuria, hypertension, edema, fatigue, pallor, anorexia, and bone pain.

Physical

• Signs of intravascular volume depletion
  • Tachycardia
  • Orthostatic hypotension
  • Decreased skin turgor
  • Dry mucous membranes
• Signs of acute renal failure
• • Children may present with edema, anemia, and signs of congestive heart failure such as hepatomegaly, gallop rhythm, and pulmonary edema.
  • Hypertension is common, especially in acute glomerulonephritis, and may be secondary to volume overload and alterations in vascular tone.
  • Although many children with hypertension are asymptomatic, encountering patients with signs of congestive heart failure, visual disturbances, or encephalopathy is common.
• Signs specific to the underlying renal disease
• • A butterfly rash on the face and joint swelling are highly suggestive of systemic lupus erythematosus.
  • Patients with Henoch-Schönlein disease present with a characteristic purpuric rash over the buttocks and extensor surface of the lower extremity.
  • Acute interstitial nephritis may be accompanied by fever, arthralgias, and fleeting maculopapular or urticarial rashes.
  • A variety of skin rashes may be detected in vasculitides.
  • Oliguria with palpable kidneys during infancy suggests renal vein thrombosis, polycystic kidneys, multicystic dysplasia, or hydronephrosis. In older children, enlarged kidneys should also raise the suspicion of tumors. A transplanted kidney that is tender to palpation is indicative of rejection.
• Signs of postrenal failure
• • Poor urinary stream, urinary dribbling, and a palpably enlarged urinary bladder are indicative of obstruction. Diagnosis may be strengthened by reestablishment of urine output after gentle passage of a catheter.
  • The external genitalia may reveal meatal stenosis or urethral trauma. Patients with indwelling urinary catheters who develop oliguria should undergo flushing of the catheter to rule out blockage.
• Signs of chronic renal failure
• • Poor growth
  • Hypertension
  • Edema
  • Anemia
  • Renal osteodystrophy

Causes

• Etiology varies with age, and the common causes in neonates and children are listed separately.
• Principal causes of oliguric ARF in neonates
• • Prerenal
    • Perinatal asphyxia
    • Respiratory distress syndrome
    • Hemorrhage (eg, maternal antepartum, twin-twin transfusion, intraventricular)
    • Hemolysis
    • Polycythemia
    • Sepsis or shock
    • Congenital heart disease
    • Dehydration
    • Drugs (eg, indomethacin, maternal NSAIDs, maternal ACE inhibitors)
  • Intrinsic renal
    • Acute tubular necrosis
    • Exogenous toxins (eg, aminoglycosides, amphotericin B, contrast agents)
    • Endogenous toxins (eg, hemoglobin, myoglobin, uric acid)
    • Congenital kidney disease (eg, agenesis, polycystic kidney, hypoplasia, dysplasia)
    • Vascular (eg, renal vein thrombosis, renal artery thrombosis)
    • Transient renal dysfunction of the newborn
  • Postrenal
    • Bladder outlet obstruction (eg, posterior urethral valves, meatal stenosis)
    • Neurogenic bladder
    • Ureteral obstruction, bilateral
• Principal causes of oliguric ARF in children
• • Prerenal
    • Gastrointestinal losses (eg, vomiting, diarrhea)
    • Blood losses (eg, hemorrhage)
    • Renal losses (eg, diabetes insipidus, diabetes mellitus, diuretics, salt-wasting nephropathy)
    • Cutaneous losses (eg, burns)
    • Third space losses (eg, surgery, trauma, nephrotic syndrome, capillary leak)
    • Shock (eg, septic, toxic, anaphylactic)
    • Impaired autoregulation (eg, cyclosporine, tacrolimus, ACE inhibitors, NSAIDs)
    • Impaired cardiac output (eg, congenital and acquired heart disease)
  • Intrinsic renal
    • Acute tubular necrosis (eg, prolonged prerenal failure)
    • Glomerulonephritis
    • Interstitial nephritis, vascular (eg, hemolytic-uremic syndrome, vasculitis)
    • Exogenous toxins (eg, aminoglycosides, amphotericin B, cyclosporine, chemotherapy, heavy metals, contrast agents)
    • Endogenous toxins (eg, hemoglobin, myoglobin, uric acid)
    • Transplant rejection
  • Postrenal
    • Bladder outlet obstruction (eg, posterior urethral valves, blocked catheter, urethral trauma)
    • Neurogenic bladder
    • Ureteral obstruction, bilateral

WORKUP

Section 4 of 8  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• References

Lab Studies

• 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.
• Urinary indexes
• • Simultaneous measurement of urinary and serum sodium, creatinine, and osmolality can help differentiate between prerenal azotemia, in which the reabsorptive capacity of tubular cells and concentrating ability of the kidney are preserved or even enhanced, and intrinsic renal failure, in which these functions are impaired because of structural damage.
  • In prerenal failure, urine specific gravity is high (>1020), the ratio of urinary to plasma creatinine is high (>40), the ratio of urinary to plasma osmolality is high (>1.5), and the urinary sodium concentration is low (<20 mEq/L).
  • In intrinsic renal failure, the opposite findings are encountered, which are a urine–to–plasma creatinine ratio less than 20, a urine–to–plasma osmolality ratio less than 1.1, and urine sodium concentration greater than 40 mEq/L.
  • The fractional excretion of sodium (FENa) is the percentage of filtered sodium that is excreted. It is easily calculated by the formula: %FENa = [(U/P)Na]/[(U/P)Cr] X 100, where Na and Cr represent the concentrations of sodium and creatinine in the urine (U) and plasma (P) respectively. The %FENa is typically less than 1% in prerenal azotemia and greater than 2% in intrinsic renal failure.
  • Interpretation of urinary indexes requires caution. Blood and urine specimens should be collected before the administration of fluids, mannitol, or diuretics. The urine should be free of glucose, contrast material, or myoglobin. Urinary indexes suggestive of prerenal failure (eg, %FENa <1, urinary sodium <20 mEq/L) can also be encountered in early glomerulonephritis, vasculitis and vascular occlusion, early postrenal failure, contrast nephropathy, and rhabdomyolysis. Also, the FENa may be falsely elevated in patients with prerenal failure and with increased urinary excretion of ketoacids or glucose.
• BUN and serum creatinine
• In prerenal failure, elevation of BUN is marked and the BUN-to-Cr ratio is greater than 20. This reflects increased proximal tubular reabsorption of urea. The hallmark of established ARF is a daily increase in serum creatinine (0.5-1.5 mg/dL/d) and in BUN (10-20 mg/dL/d).
• Elevations in BUN can also result from steroid therapy, parenteral nutrition, gastrointestinal 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.
• 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 ARF 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 treated promptly and aggressively primarily because of its depolarizing effect on cardiac conduction pathways.
  • Symptoms may include malaise, nausea, and muscle weakness.
• Serum phosphate and calcium
• • Hyperphosphatemia and hypocalcemia frequently complicate oliguric ARF. 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 gastrointestinal 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 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 cell 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 ARF can result in functional platelet disorders.
• Serologic tests
• • 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

• 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, 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 obstruction of the bladder outlet or below.
• Other imaging studies
• • Voiding cystourethrography is indicated with 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.

Other Tests

• Electrocardiography
• • This test is indicated if hyperkalemia is suspected or 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

Procedures

• 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.

Histologic Findings

Histology depends on the underlying cause. Only ischemic and nephrotoxic acute tubular necroses are discussed. In human ischemic acute tubular necrosis, frank tubule cell necrosis is rarely encountered. Instead, the prominent morphologic features include effacement and loss of proximal tubule brush border, patchy loss of tubule cells, focal areas of proximal tubular dilatation and distal tubular casts, and areas of cellular regeneration. Necrosis is inconspicuous and restricted to the highly susceptible outer medullary regions of the kidney. The glomeruli are usually unimpressive, unless a primary glomerular disease had caused the oliguria. This apparent disparity between the severe impairment of renal function and the relatively subtle histologic changes has traditionally been puzzling.

More recently, however, reconciliation has been forthcoming from a consistent finding of apoptotic cell death in both distal and proximal tubules in both ischemic and nephrotoxic forms of intrinsic renal failure In addition, a great deal of attention has been directed toward the peritubular capillaries, which display striking vascular congestion, endothelial damage, and leukocyte accumulation.

In contrast, in nephrotoxic acute tubular necrosis, the findings on light microscopy are generally characterized by more extensive and uniform tubular necrosis. Most of the proximal tubules display necrotic cell death, desquamation, and dilatation. A moderately severe interstitial edema may be observed. The glomeruli appear normal. Morphologically, several leukocyte subtypes have been shown to aggregate in peritubular capillaries, interstitial space, and even within tubules following ischemic ARF, and their relative roles remain under investigation. Neutrophils are the earliest leukocytes to accumulate in the postischemic kidney.

TREATMENT

Section 5 of 8  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• References

Medical Care

• Prevention
  • In clinical situations where renal hypoperfusion or toxic injury is anticipated, therapy with fluids, mannitol, diuretics, and renal-dose dopamine are used to prevent or reverse renal injury. Although these maneuvers do not alter the natural history of ARF, they are capable of converting the oliguric state to a nonoliguric ARF, which is more easily managed because it obviates the need for fluid restriction and allows for maximal nutritional support.
  • Vigorous fluid administration has been successfully employed to prevent ARF following cardiac surgery, cadaveric renal transplantation, hemoglobinuria, myoglobinuria, hyperuricosuria, radiocontrast infusion, and therapy with amphotericin B or cisplatinum.
  • A trial of intravenous mannitol or furosemide should be attempted in a patient with oliguria for less than 48 hours who has not responded to adequate hydration. The benefit of renal-dose dopamine therapy is controversial. Current recommendations are for considering the use in patients who are adequately hydrated and resistant to furosemide, although meta-analysis studies have failed to document a clear benefit of either furosemide or mannitol therapy.
  • Once oliguria is established, mannitol may precipitate congestive heart failure; the risk of ototoxicity from furosemide and adverse hemodynamic changes from dopamine are significant.
• Fluid management
  • The major goal of fluid management is to restore and maintain normal intravascular volume. Patients with oliguric ARF 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 FENa.
  • Children with intravascular volume depletion require prompt and vigorous fluid resuscitation. Initial therapy includes isotonic sodium chloride or lactated Ringer solution at 20 mL/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.
  • 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.
• Hyperkalemia
  • Serum potassium levels of 5.5-6.5 mEq/L should be treated by eliminating all sources of potassium from the diet or intravenous 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 6.5 mEq/L or if peaked T waves are present. In addition to Kayexalate, patients should receive calcium gluconate (with continuous ECG 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.
  • In practice, the definitive therapy for significant hyperkalemia accompanying oliguric ARF frequently includes dialysis. The forms of therapy outlined above serve primarily to tide over the crisis.
• Other electrolytes and acid-base balance
  • The primary treatment of hyponatremia is free water restriction; however, serum sodium less than 120 mEq/L or accompanied central nervous system dysfunction may require 3% sodium chloride infusion.
  • 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 it 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 intravenous bicarbonate therapy. Recognize that bicarbonate therapy requires adequate ventilation (to excrete 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 intravenous tromethamine (THAM), with provision of adequate ventilatory support pending institution of dialysis.
• 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 intravenous 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 is controlled, oral long-acting agents can be initiated.
• Medication and dialysis
  • Nephrotoxic agents should be avoided because they may worsen the renal injury and delay recovery of function. Such agents include contrast media, aminoglycosides, and NSAIDs.
  • Prescribing medication requires knowledge of the route of elimination and adjustments in dose or frequency based on residual renal function.
  • Patients in the early phase with a rising creatinine should be assumed to have a GFR of less than 10 mL/min, irrespective of the absolute value for serum creatinine.
  • 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 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; and symptomatic uremia (central nervous system symptoms, pericarditis, pleuritis).
  • The choice between hemodialysis, peritoneal dialysis, and continuous venovenous hemodialysis (CVVH) depends on the overall clinical condition, availability of technique, etiology of the renal failure, institutional preferences, and specific indications or contraindications.
  • In general, peritoneal dialysis is a gentler and was a more preferred continuous method in children in the past. It is not the treatment of choice for acute, severe fluid overload or hyperkalemia because the onset of action is slower. Specific contraindications include abdominal wall defects, bowel distention, perforation or adhesions, and communications between chest and abdominal cavities.
  • Hemodialysis requires vascular access, heparinization, 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
  • A potentially important advance is the use of synthetic dialysis membranes to improve recovery of renal function. Over the past decade, CVVH has emerged as 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 inefficient. The patient requires the presence of trained personnel and specialized equipment that are available only at select tertiary care centers.
  • During the past decade, experimental studies in animals and humans have focused on restoration of renal hemodynamics and tubule cell integrity. Atrial natriuretic peptide (ANP) has been shown to improve renal function in animal models of ischemic ARF, predominantly via afferent arteriolar dilatation. In a recent large study of adults, ANP reduced the need for dialysis and improved survival in some patients with oliguric ARF. Further clinical trials with ANP are required to better define its therapeutic profile and optimal target population.
  • Other ongoing clinical trials include the role of growth factors such as insulin-like growth factor, nitric oxide inhibitors, and antagonists of endothelin receptors in human ARF.

Surgical Care

• 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 urine flow rate, urine electrolytes, and serum electrolytes.

Consultations

• Consult a pediatric nephrologist for management of all cases of oliguria, except in children with prerenal insufficiency from dehydration who promptly respond to fluid therapy or those with mild nephrotoxic injury who respond to discontinuing the medication.
• Consult a pediatric urologist for management of obstruction.

Diet

• Children with oliguric ARF 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.
• 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 enteral feedings are not possible, central intravenous 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.

Activity

Children are usually hospitalized; therefore, activity is restricted.

MEDICATION

Section 6 of 8  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• References

In this section, the use of medications for prevention of ARF and treatment of hyperkalemia, metabolic acidosis, and hyperphosphatemia is described. For the treatment of hypertension, see Hypertension.

Drug Category: Agents for the prevention of ARF

In patients with recent-onset oliguria from prerenal or toxic injury who do not respond to hydration, agents such as mannitol, or furosemide can convert the oliguric state to a nonoliguric ARF, which is more easily managed. These agents may prevent tubule obstruction by increasing intratubular fluid flow via direct renal vasodilatory action.

Drug Category: Agents for the treatment of hyperkalemia

Hyperkalemia in oliguric ARF is a medical emergency, which may be managed by shifting potassium into cells (sodium bicarbonate, glucose/insulin infusion, beta-agonists), increasing removal of potassium (exchange resins, dialysis), and by protecting the myocardium (calcium).

Drug Category: Agents for the treatment of hyperphosphatemia

Oliguric ARF is frequently complicated by hyperphosphatemia and hypocalcemia, which respond to calcium-containing PO phosphate binders.

Drug Category: Alkalinizing agents

Mild metabolic acidosis is treated with PO sodium citrate. Severe acidosis requires IV bicarbonate, as detailed under hyperkalemia.

FOLLOW-UP

Section 7 of 8  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• References

Transfer

• If the patient requires close monitoring of hemodynamic status or if indications for acute dialysis are present, transfer the patient to a center with ICU facilities.

Complications

• Infections develop in 30-70% of patients and affect the respiratory system, urinary tract, and indwelling catheters. Impaired defenses due to uremia and inappropriate use of antibiotics may contribute to the high rate of infectious complications.
• Cardiovascular complications are a result of fluid and sodium retention. They include hypertension, congestive heart failure, and pulmonary edema.
• Hyperkalemia results in ECG abnormalities and arrhythmias.
• Other complications include the following:
• • Gastrointestinal - Anorexia, nausea, vomiting, ileus, and bleeding
  • Hematologic - Anemia and platelet dysfunction
  • Neurologic - Confusion, asterixis, somnolence, and seizures
  • Other electrolyte/acid-base disorders - Metabolic acidosis, hyponatremia, hypocalcemia, and hyperphosphatemia

Prognosis

• Despite significant advances in supportive care and renal replacement therapy, high mortality rates in the setting of multiorgan failure have not significantly improved in the past few decades.
• Patients die with renal failure; however, they do not die not because of renal failure. The patient succumbs because of involvement of other systems during the period of renal insufficiency. Oliguric ARF is an independent risk factor for mortality, as well as for nonrenal complications.
• On the other hand, prognosis from prerenal causes or from acute tubular necrosis in the absence of significant comorbid conditions is usually quite good if appropriate therapy is instituted in a timely fashion.

Patient Education

• For excellent patient education resources, see eMedicine's Diabetes Center. Also, visit eMedicine's patient education articles Acute Kidney Failure and Chronic Kidney Failure.

REFERENCES

Section 8 of 8

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• References

• American Society of Nephrology. American Society of Nephrology Renal Research Report. J Am Soc Nephrol. Jul 2005;16(7):1886-903. [Medline]. [Full Text].
• Andreoli SP. Acute renal failure. Curr Opin Pediatr. Apr 2002;14(2):183-8. [Medline].
• Bellomo R, Ronco C, Kellum JA, et al. Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. Aug 2004;8(4):R204-12. [Medline]. [Full Text].
• Bonventre JV, Zuk A. Ischemic acute renal failure: an inflammatory disease?. Kidney Int. Aug 2004;66(2):480-5. [Medline].
• Bunchman TE, McBryde KD, Mottes TE, et al. Pediatric acute renal failure: outcome by modality and disease. Pediatr Nephrol. Dec 2001;16(12):1067-71. [Medline].
• Cantarovich F, Rangoonwala B, Lorenz H, et al. High-dose furosemide for established ARF: a prospective, randomized, double-blind, placebo-controlled, multicenter trial. Am J Kidney Dis. Sep 2004;44(3):402-9. [Medline].
• Chertow GM, Burdick E, Honour M, et al. Acute kidney injury, mortality, length of stay, and costs in hospitalized patients. J Am Soc Nephrol. Nov 2005;16(11):3365-70. [Medline].
• Devarajan P. Cellular and molecular derangements in acute tubular necrosis. Curr Opin Pediatr. Apr 2005;17(2):193-9. [Medline].
• Friedewald JJ, Rabb H. Inflammatory cells in ischemic acute renal failure. Kidney Int. Aug 2004;66(2):486-91. [Medline].
• Gambaro G, Bertaglia G, Puma G, D'Angelo A. Diuretics and dopamine for the prevention and treatment of acute renal failure: a critical reappraisal. J Nephrol. May-Jun 2002;15(3):213-9. [Medline].
• Goldstein SL. Pediatric acute renal failure: demographics and treatment. Contrib Nephrol. 2004;144:284-90. [Medline].
• Gouyon JB, Guignard JP. Management of acute renal failure in newborns. Pediatr Nephrol. Sep 2000;14(10-11):1037-44. [Medline].
• Hui-Stickle S, Brewer ED, Goldstein SL. Pediatric ARF epidemiology at a tertiary care center from 1999 to 2001. Am J Kidney Dis. Jan 2005;45(1):96-101. [Medline].
• Klahr S, Miller SB. Acute oliguria. N Engl J Med. Mar 5 1998;338(10):671-5. [Medline].
• Lameire N, Van Biesen W, Vanholder R. Acute renal failure. Lancet. Jan 29-Feb 4 2005;365(9457):417-30. [Medline].
• Lameire NH, De Vriese AS, Vanholder R. Prevention and nondialytic treatment of acute renal failure. Curr Opin Crit Care. Dec 2003;9(6):481-90. [Medline].
• Mehta RL, Chertow GM. Acute renal failure definitions and classification: time for change?. J Am Soc Nephrol. Aug 2003;14(8):2178-87. [Medline]. [Full Text].
• Mehta RL, Pascual MT, Soroko S, et al. Spectrum of acute renal failure in the intensive care unit: the PICARD experience. Kidney Int. Oct 2004;66(4):1613-21. [Medline].
• Molitoris BA, Sutton TA. Endothelial injury and dysfunction: role in the extension phase of acute renal failure. Kidney Int. Aug 2004;66(2):496-9. [Medline].
• Perico N, Cattaneo D, Sayegh MH, Remuzzi G. Delayed graft function in kidney transplantation. Lancet. Nov 13-19 2004;364(9447):1814-27. [Medline].
• Racusen LC. The morphologic basis of acute renal failure. In: Molitoris BA, Finn WF, eds: Acute Renal Failure. WB Saunders, Philadelphia, Penn; 2004: 1-12.
• Safirstein RL. Acute renal failure: from renal physiology to the renal transcriptome. Kidney Int Suppl. Oct 2004;S62-6. [Medline].
• Schrier RW, Wang W, Poole B, Mitra A. Acute renal failure: definitions, diagnosis, pathogenesis, and therapy. J Clin Invest. Jul 2004;114(1):5-14. [Medline]. [Full Text].
• Schrier RW, Wang W. Acute renal failure and sepsis. N Engl J Med. Jul 8 2004;351(2):159-69. [Medline].
• Schrier RW. Need to intervene in established acute renal failure. J Am Soc Nephrol. Oct 2004;15(10):2756-8. [Medline]. [Full Text].
• Siegel NJ, Van Why SK, Devarajan P. Pathogenesis of acute renal failure. In: Avner ED, Harmon WE, Niaudet P, eds. Pediatric Nephrology. Philadelphia, Penn; Lippincott Williams & Wilkins, 2004: 1223.
• Star RA. Treatment of acute renal failure. Kidney Int. Dec 1998;54(6):1817-31. [Medline].
• Thadhani R, Pascual M, Bonventre JV. Acute renal failure [see comments]. N Engl J Med. May 30 1996;334(22):1448-60. [Medline].
• Uchino S, Kellum JA, Bellomo R, et al. Acute renal failure in critically ill patients: a multinational, multicenter study. JAMA. Aug 17 2005;294(7):813-8. [Medline].
• Warnock DG. Towards a definition and classification of acute kidney injury. J Am Soc Nephrol. Nov 2005;16(11):3149-50. [Medline].
• Williams DM, Sreedhar SS, Mickell JJ, Chan JC. Acute kidney failure: a pediatric experience over 20 years. Arch Pediatr Adolesc Med. Sep 2002;156(9):893-900. [Medline].

Article Last Updated: Aug 17, 2006