Excerpt from Oliguria

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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.

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