Urine Output, Decreased
Katherine MacRae Dell
INTRODUCTION
Decreased urine output can be caused by either a decrease in urine production (oliguria) or an obstruction to urinary flow. Oliguria is defined as a urine output <0.5 mL/kg per hour in a child or adolescent or <1.0 mL/kg per hour in a neonate. Decreased urine output may result from prerenal, intrarenal, or postrenal factors. Oliguria may occur as the result of an acute process or an acute exacerbation of an unrecognized chronic kidney disease.
DIFFERENTIAL DIAGNOSIS LIST
HINT: The term acute renal failure has generally been replaced by a newer designation, acute kidney injury (AKI).Prerenal
Decreased Intravascular Volume
Dehydration (typically caused by gastrointestinal losses)
Hemorrhage
Inadequate fluid intake
Sepsis (with capillary leak)
Ineffective Intravascular Blood Volume (“Edematous States”)
Hypoalbuminemia/decreased oncotic pressure
Nephrotic syndrome
Hepatic dysfunction
Impaired Cardiovascular Status
Congestive heart failure
Sepsis (with peripheral vasodilation and/or cardiac depression)
Intrarenal
Glomerular Causes
Primary glomerulonephritis (e.g., acute postinfectious, membranoproliferative)
Secondary GN associated with systemic disease (e.g., lupus nephritis)
Tubulointerstitial
Acute tubular necrosis (ATN)
Prolonged prerenal azotemia or ischemia
Medications
Toxins
Pigment deposition—myoglobin or hemoglobin
Acute interstitial nephritis (drugs, infections)
Vascular
Hemolytic uremic syndrome (HUS)
Renal venous or arterial thrombosis
Postrenal
Congenital or Anatomic
Congenital obstructive uropathies (e.g., posterior urethral valves)
Urinary stone
Trauma
Abdominal mass
Functional
Acute urinary retention
Neurogenic bladder
Others
Syndrome of inappropriate antidiuretic hormone (meningitis, pneumonia)
DIFFERENTIAL DIAGNOSIS DISCUSSION
Prerenal Etiologies
Dehydration
Dehydration is the most common cause of oliguria in the pediatric population. The causes, clinical features, and evaluation are discussed in detail in Chapter 25, “Dehydration.” Treatment is directed toward restoring intravascular volume. If dehydration is mild, oral rehydration may be attempted. If the patient cannot tolerate oral fluids, or if the dehydration is more severe, initial fluid resuscitation with normal saline should be performed, followed by oral or intravenous rehydration. In most patients, urine output improves within a few hours when these simple measures are used.
Edematous States
A variety of disorders can result in hypoalbuminemia, with resultant decreased oncotic pressure (e.g., nephrotic syndrome, see Chapter 62, “Proteinuria”). In these instances, there is adequate (and actually increased) total body volume, but it is not perceived so by the kidney because of the decreased oncotic pressure. This results in homeostatic responses that are identical to those of patients with dehydration, including avid salt and water retention. This is reflected in laboratory studies showing elevated blood urea nitrogen (BUN) to creatinine ratio, high urine specific gravity, and low urine sodium. Unlike dehydration, however, the treatment does not involve fluid administration (which will worsen the edema). Instead, the treatment of edematous states typically includes use of diuretics, fluid restriction, and/or albumin infusions based on the clinical situation.
HINT: Because kidney function is preserved, prerenal azotemia is rapidly reversible if the underlying cause is corrected (e.g., restoring intravascular volume in a dehydrated patient). Intrarenal causes are not usually readily reversible.Intrarenal Etiologies
Acute Tubular Necrosis
Etiology
Acute tubular necrosis is the final common pathway of a number of renal insults, including prolonged prerenal ischemia, sepsis, toxicity, and pigment deposition. ATN is a relatively common occurrence in severely ill patients in intensive care units; these patients often have multiple causes for the ATN (e.g., sepsis with hypotension plus aminoglycoside therapy).
Clinical Features
ATN traditionally has three phases:
Oliguric phase. The oliguric phase may last for days or several weeks. The hallmarks of this phase are decreased urine output and loss of renal concentrating ability, resulting in an elevated urine sodium level and a decreased urine specific gravity. As with other forms of AKI, hypertension may be present.
Diuretic phase. In the diuretic phase, urine output increases dramatically; urine sodium and water losses may be significant.
Recovery phase. In the recovery phase, urine output returns to a normal rate and concentrating ability returns.
