Pathogenesis. Diseases that prevent urine excretion may cause postrenal azotemia. The kidneys are structurally normal initially and capable
of quantitatively normal function provided the underlying cause is corrected. However, if the underlying cause persists, death
from alterations in water, electrolyte, acid-base and endocrine balance, in addition to metabolic waste product accumulation,
will occur within a few days. If urine outflow is only partially obstructed, allowing the patient to survive for a longer
time, varying degrees of hydronephrosis may subsequently occur.
Causes. Complete urine outflow obstruction (i.e., obstruction in urethra, bladder, or both ureters) for more than 24 hours usually
results in postrenal azotemia. Unilateral ureteral occlusion (an example of renal disease) is not associated with azotemia
unless generalized disease of the nonobstructed kidney is also present. Azotemia resulting from excretory pathway rupture
(usually the bladder) is primarily related to urine absorption from the peritoneal cavity. Unless damaged as a result of hypovolemic
shock or trauma secondary to cause of the excretory pathway rupture, the kidneys are structurally and functionally normal.
Diagnosis. A diagnosis of postrenal azotemia is based on the integration of clinical findings. Lesions causing urine outflow obstruction
are commonly associated with:
> Elevated serum BUN and creatinine concentrations
> Oliguria or anuria, dysuria and tenesmus
> Obstructive lesions detected by physical examination (e.g., urethral plug, herniated bladder), radiography, ultrasonography,
> Variable urine specific gravity values
Rupture of the excretory pathway is commonly associated with:
> Progressively elevated serum BUN or creatinine concentrations
> Progressive depression, painful abdomen, ascites
> A history of trauma and associated physical examination findings
> Inability to palpate the urinary bladder
> Detection of a modified transudate or exudate by abdominocentesis
> Abnormalities detected by ultrasonography or retrograde contrast (positive or negative) cystography or urethrocystography.
Because of variability, the urine specific gravity of patients with postrenal azotemia is not relied on to the same degree
for assessing renal function as it is in patients with primary renal and prerenal azotemia.
Prognosis associated with obstructive lesions. If the patient has total obstruction to urine outflow for three to six days, death from uremia will occur caused by alteration
of fluid, acid-base, electrolyte, nutrient and endocrine balance, as well as accumulation of metabolic waste products. Death
usually occurs before significant hydronephrosis has time to develop. The prognosis is favorable if the obstructive lesion
or lesions are rapidly removed. The long-term prognosis depends on the reversibility of the underlying cause.
Prognosis associated with excretory pathway rupture. If a persistent rent in the excretory pathway results in progressive azotemia, the patient will likely die if the rent is
not repaired. The prognosis for recovery of adequate renal function is favorable if the rent is repaired or heals. The long-term
prognosis depends on the reversibility of the underlying cause.