eMedicine Specialties > Pediatrics: General Medicine > Nephrology

Oliguria: Treatment & Medication

Author: Prasad Devarajan, MD, Louise M Williams Endowed Chair in Pediatrics, Professor of Pediatrics and Developmental Biology, Director of Nephrology and Hypertension, Director of Clinical Nephrology Laboratories, Chief Executive Officer of Dialysis Unit, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine
Contributor Information and Disclosures

Updated: Dec 3, 2008

Treatment

Medical Care

Treatment of oliguria includes the following:

• 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 acute renal failure, they are capable of converting the oliguric state to a nonoliguric acute renal failure, 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 used to prevent acute renal failure 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.⁴ 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.⁵
  • Once oliguria is established, mannitol may precipitate congestive heart failure; the risk of ototoxicity from furosemide and adverse hemodynamic changes from dopamine is significant.
• Fluid management
  • The major goal of fluid management is to restore and maintain normal intravascular volume. Patients with oliguric acute renal failure 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 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 acute renal failure 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 CNS 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 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 nonsteroidal anti-inflammatory drugs (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 glomerular filtration rate (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 (CNS 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 acute renal failure, predominantly via afferent arteriolar dilatation. In a large study of adults, ANP reduced the need for dialysis and improved survival in some patients with oliguric acute renal failure. 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 insulinlike growth factor, nitric oxide inhibitors, and antagonists of endothelin receptors in human acute renal failure.

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 acute renal failure 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

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

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 acute renal failure, which is more easily managed. These agents may prevent tubule obstruction by increasing intratubular fluid flow via direct renal vasodilatory action.

Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.

Agents for the treatment of hyperkalemia

Hyperkalemia in oliguric acute renal failure 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).

Sodium bicarbonate

Indicated for treatment of hyperkalemia with concomitant acidosis. Sodium bicarbonate increases serum bicarbonate and reacts with hydrogen ions to form water and carbon dioxide. It acts as a buffer against acidosis by raising blood pH.

Calcium gluconate

Indicated if hyperkalemia is accompanied by peaked T waves or if peaked T waves persist after bicarbonate therapy.

Insulin (Novolin, Humulin)

Used as an adjunctive to bicarbonate therapy. Insulin promotes intracellular shift of potassium. Administer with dextrose to maintain serum glucose levels.

Sodium polystyrene sulfonate (Kayexalate)

This is indicated in all cases of hyperkalemia. Exchanges sodium for potassium and binds it in the gut, primarily in the large intestine, and decreases total body potassium. Onset of action after PO administration ranges from 2-12 h, and is longer when administered PR.

Agents for the treatment of hyperphosphatemia

Oliguric acute renal failure is frequently complicated by hyperphosphatemia and hypocalcemia, which respond to calcium-containing oral phosphate binders.

Calcium carbonate (Nephro-Calci, Caltrate)

Successfully normalizes phosphate concentrations in patients on dialysis. Combines with dietary phosphate to form insoluble calcium phosphate, which is excreted in feces. Marketed in various dosage forms and is relatively inexpensive.

Alkalinizing agents

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

Citrate and citric acid (Bicitra, Oracit)

Treats metabolic acidosis and used as an alkalinizing agent when long-term maintenance of alkaline urine is desirable.

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