Cause of urinary output

Prerenal failure
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. A decrease
in circulatory volume evokes a systemic response aimed at normalizing intravascular volume at
the expense of the glomerular filtration rate (GFR). Baroreceptor-mediated activation of the
sympathetic nervous system and renin-angiotensin axis results in renal vasoconstriction and the
resultant reduction in the GFR. 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. See the image below.

Pathogenesis of prerenal failure

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). These changes are shown in the image below.

Compensatory mechanisms for preventing a fall in glomerular filtration rate (GFR) in the presence of
prerenal failure

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.
 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 often secondary to dehydration and 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.

Intrinsic renal failure

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 led to a dramatic
broadening of the etiology of pediatric acute kidney injury. Although multicenter etiologic data
on pediatric acute renal failure are not available, 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.[3, 4]
Subsequent single-center data have detailed the underlying causes of pediatric acute renal
failure in large cohorts of children. In a study of 226 children with acute renal failure, Bunchman
et al reported that congenital heart disease, acute tubular necrosis, sepsis, and bone marrow
transplantation were the most common causes.[5]
A retrospective review of 248 patients with a diagnosis of acute renal failure upon
discharge or death revealed acute tubular necrosis and nephrotoxins to be the most common
causes of acute kidney injury.[6] Thus, the etiology of pediatric acute renal failure has evolved in
industrialized 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. (See the image below.)

Mechanisms of intrinsic acute renal failure.

 In most clinical situations, the oliguria is reversible and associated with repair and
regeneration of tubular epithelial cells.

Postrenal failure
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.

Principal causes of oliguric acute kidney injury in neonates

The etiology of oliguria varies with age, and the common causes in neonates and children
are listed separately. Patients with acute kidney injury secondary to nephrotoxins, interstitial
nephritis, and perinatal asphyxia frequently do not have oliguria.
Prerenal causes include the following:
 Perinatal asphyxia
 Respiratory distress syndrome
 Hemorrhage - Eg, maternal antepartum, twin-twin transfusion, and intraventricular
 Hemolysis
 Polycythemia
 Sepsis or shock
 Congenital heart disease
 Dehydration
 Drugs - Eg, indomethacin, maternal nonsteroidal anti-inflammatory drugs (NSAIDs), and
maternal ACE inhibitors

Intrinsic renal causes include the following:

 Acute tubular necrosis
 Exogenous toxins - Eg, aminoglycosides, amphotericin B, and contrast agents
 Endogenous toxins - Eg, hemoglobin, myoglobin, and uric acid
 Congenital kidney disease - Eg, agenesis, polycystic kidney, hypoplasia, and dysplasia
 Vascular - Eg, renal vein thrombosis and renal artery thrombosis
 Transient renal dysfunction of the newborn

Postrenal causes include the following:

 Bladder outlet obstruction - Eg, posterior urethral valves and meatal stenosis
 Neurogenic bladder
 Ureteral obstruction, bilateral
Principal causes of oliguric acute kidney injury in children
Prerenal causes include the following:
 Gastrointestinal (GI) losses - Eg, vomiting and diarrhea
 Blood losses - Eg, hemorrhage
 Renal losses - Eg, diabetes insipidus, diabetes mellitus, diuretics, and salt-wasting
nephropathy
 Cutaneous losses - Eg, burns
 Third space losses - Eg, surgery, trauma, nephrotic syndrome, and capillary leak
 Shock - Eg, septic, toxic, and anaphylactic
 Impaired autoregulation - Eg, cyclosporine, tacrolimus, ACE inhibitors, and NSAIDs
 Impaired cardiac output - Eg, congenital and acquired heart disease

Intrinsic renal causes include the following:

 Acute tubular necrosis - Eg, prolonged prerenal failure
 Glomerulonephritis
 Interstitial nephritis, vascular - Eg, hemolytic-uremic syndrome and vasculitis
 Exogenous toxins - Eg, aminoglycosides, amphotericin B, cyclosporine, chemotherapy,
heavy metals, and contrast agents
 Endogenous toxins - Eg, hemoglobin, myoglobin, and uric acid
 Transplant rejection

Postrenal causes include the following:

 Bladder outlet obstruction - Eg, posterior urethral valves, blocked catheter, and urethral
trauma
 Neurogenic bladder
 Ureteral obstruction, bilateral

Referens : http://emedicine.medscape.com/article/983156-overview#aw2aab6b2b2. 03/23/205.

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