The Medical Assessment and Management of

Oliguria

Luis Daniel Lugo, MDMedical Resident

Roger Williams Medical Center Boston University School of Medicine

Providence, Rhode Island

Definitions

• Oliguria: urine output < 400 mL / day in adults

• Common hallmark of acute kidney injury

• In most clinical situations, acute oliguria is reversible and does not result in intrinsic renal failure.

Etiology

• Oliguria may result from prerenal, intrinsic renal, or postrenal processes.

• 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 and as many as 60% of hospital-acquired cases.

• Baroreceptor-mediated activation of the sympathetic nervous system and renin-angiotensin axis results in renal vasoconstriction and the resultant reduction in the GFR.

Prerenal Acute Kidney Injury

• The early phase also includes enhanced tubular reabsorption of salt and water (stimulated by the renin-angiotensin-aldosterone system and sympathetic nervous system), resulting in a decrease in fractional excretion of sodium (FENa) and decreased urine output.

• The early phase of renal compensation for reduced perfusion includes autoregulatory maintenance of the GFR via afferent arteriolar dilatation (induced by myogenic responses, tubuloglomerular feedback, and prostaglandins) and via efferent arteriolar constriction (mediated by angiotensin II).

Prerenal – Causes

• Perinatal asphyxia and Respiratory distress syndrome

• Hemorrhage (maternal antepartum, twin-twin transfusion, and intraventricular)

• Hemolysis and Polycythemia

• Sepsis or shock

• Congenital heart disease

• Dehydration

• Drugs (indomethacin, maternal nonsteroidal anti-inflammatory drugs (NSAIDs), and maternal ACE inhibitors)

Beware!

• 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 acute renal failure in individuals with reduced renal perfusion.

Intrinsic Acute Kidney Injury

• 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.

• 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.

Intrinsic – Causes

• Acute tubular necrosis

• Exogenous toxins (aminoglycosides, amphotericin B, and contrast agents)

• Endogenous toxins (hemoglobin, myoglobin, and uric acid)

• Congenital kidney disease (agenesis, polycystic kidney, hypoplasia, and dysplasia)

• Vascular (renal vein thrombosis and renal artery thrombosis)

• Transient renal dysfunction of the newborn

Postrenal Acute Kidney Injury

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

valves)• Neurogenic bladder• Ureteral obstruction, bilateral • Blocked catheters

The Assessment of Oliguria

• The following studies are indicated in oliguria:• Urinalysis• Urinary indexes• Blood urea nitrogen (BUN) and serum

creatinine• Serum sodium• Serum potassium• Serum phosphate and calcium• Acid-base balance• Complete blood count (CBC)

The Assessment of Oliguria

• Decreased complement levels (C3, C4) are characteristic of acute poststreptococcal glomerulonephritis but can also be observed in lupus nephritis and membranoproliferative glomerulonephritis. • 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.

The Assessment of Oliguria

• Imaging studies in oliguria include the following:• Renal ultrasonography• Voiding cystourethrography• Indicated for suspected bladder outlet obstruction

• Radionuclide renal scanning• In the assessment of transplant rejection and

obstruction

• Chest radiography • Indicated if pulmonary edema is suspected

• Echocardiography • In the presence of congestive heart failure

Urine Analysis

• 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.

• The %FENa is typically less than 1% in prerenal azotemia and greater than 2% in intrinsic renal failure.

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) & 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.

BUN and 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).

The Management of Oliguria

Prevention

• In clinical situations in which renal hypoperfusion or toxic injury is anticipated, therapy with fluids, mannitol, diuretics, and renal-dose dopamine is used to prevent or reverse renal injury.

• Vigorous fluid administration has been successfully used to prevent acute kidney injury following cardiac surgery, cadaveric renal transplantation, hemoglobinuria, myoglobinuria, hyperuricosuria, radiocontrast infusion, and therapy with amphotericin B or cisplatinum.

Trial of Diuresis*

• A trial of intravenous (IV) mannitol or furosemide should be attempted in a patient with oliguria for less than 48 hours who has not responded to adequate hydration.

• 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).

Volume Overload & Oliguria

• 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. In practice, the definitive therapy for significant hyperkalemia accompanying oliguric acute kidney injury frequently includes dialysis.

Indications for Hemodialysis (AEIOU)

• A cidosis, especially if severe (pH < 7.2 and refractory to HCO3 or unable to give HCO3 due to volume overload) or symptomatic (arrhythmias).

• E lectrolytes, especially potassium with EKG changes. Temporize with Ca, D50, insulin, bicarb, kayexalate.

• I ngestions, especially those that cause renal failure such as salicylates or ethylene glycol.

• O verload, i.e. volume overload causing pulmonary edema. Temporize with nitrates and mega doses of Lasix (160–200 mg IV) – push slowly to avoid ototoxicity.

• U remia, i.e. confusion, pericarditis, seizures, platelet dysfunction with severe bleeding, intractable N/V.

Hyperkalemia

• 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.

Medical Management

• Oliguria caused by hypovolaemia can be reversed if a fluid challenge is immediately administered. This is a key treatment intervention aimed at preventing acute renal failure in the general ward setting.

• The aim of a fluid challenge is to produce a significant and rapid increase in plasma volume which will stabilise the patient’s condition. Contaminant use of furosemide may be used.

Medical Therapy

• Oliguria with volume overload requires fluid restriction and IV furosemide. If the patient fails to respond to furosemide, acute tubular necrosis, rather than renal hypoperfusion, may be present, and fluid may have to be removed by dialysis or hemofiltration, especially if signs of pulmonary edema are evident.

• In patients with hyperkalemia, a cation exchange resin, such as sodium polystyrene sulfonate (Kayexalate), is administered when serum potassium levels rise to 5.5 mEq/L or above. When potassium exceeds 6.5 mEq/L or if peaked T waves are present on electrocardiography, calcium gluconate should be administered along with it.

• Sodium bicarbonate is also used in cases of hyperkalemia but is recommended only when severe acidosis is present concomitantly. This agent can precipitate hypocalcemia and sodium overload and should therefore be used with caution.

Complications

• Cardiovascular complications are a result of fluid and sodium retention. They include hypertension, congestive heart failure, and pulmonary edema.• Hyperkalemia results in electrocardiographic

abnormalities and arrhythmias.

Prognosis

• Mortality rates in oliguric acute kidney injury widely vary according to the underlying cause and associated medical condition. It ranges from 5% for patients with community-acquired kidney injury failure to 80% among patients with multiorgan failure in the ICU.

• Infections develop in 30-70% of patients and affect the respiratory system, urinary tract, and indwelling catheters. Impaired defenses due to uremia and the inappropriate use of broad-spectrum antibiotics may contribute to the high rate of infectious complications.

Prognosis

• 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.

• The outcome depends upon the etiology, age of the child, and comorbidities. • Treat the underlying cause!

References

• Medscape. (2014). Oliguria. Retrieved from http://emedicine.medscape.com/article/983156-overview/.

• Uptodate. (2014). Nonoliguric versus Oliguric Acute Tubular Necrosis. Retrieved from http://www.uptodate.com/contents/nonoliguric-versus-oliguric-acute-tubular-necrosis/.