What is oliguria?
The term oliguria has been used to describe decreased urine formation by kidneys or decreased elimination of urine from the body. Oliguria
associated with formation of a reduced quantity of urine is related to renal function and may be physiologic or pathologic
in nature. Here we look at the characteristics of both.
> Physiologic oliguria. Physiologic, compensatory oliguria occurs when normal kidneys conserve water in excess of solute in order to maintain or restore
the body's normal fluid balance. Physiologic oliguria is characterized by formation of a small volume of urine of high specific
gravity and high osmolality.
The production of a decreased volume of highly concentrated urine in patients with prerenal azotemia is a notable example
of physiologic compensatory oliguria. Prerenal azotemia is often caused by abnormalities that reduce renal function by reducing
renal perfusion (i.e. dehydration, shock, cardiac disease, hypoadrenocorticism). Since blood pressure provides the force necessary for glomerular
filtration, marked decrease in blood pressure will result in reduction of glomerular filtrate and, thus, a variable degree
of retention of substances normally filtered by glomeruli (i.e. urea, creatinine, phosphorus) results.
To combat low perfusion pressure and reduced blood volume, the body secretes ADH to promote conservation of water filtered
through glomeruli. Production of urine of high specific gravity, high osmolality and low volume is the normal response (see
Table 1). Prerenal azotemia provides evidence that the kidneys are structurally adequate to maintain homeostasis and are initially
capable of quantitatively adequate function—provided the prerenal cause is rapidly removed. However, if the prerenal cause
is allowed to persist, primary ischemic renal disease leading to renal failure may develop.
> Pathologic oliguria. Pathologic oliguria refers to a volume of urine that is inadequate for excretion of the body's normal metabolic wastes. Prompt
recognition of pathologic oliguria is important because it dictates the volume of fluid that can safely be administered.
Formation of inappropriately concentrated urine in quantities of less than 0.5 ml/kg/hour is evidence of pathologic oliguria
in dogs and cats. Urine production of approximately 0.5 to 1.5 ml/kg/hour should be considered inappropriate (i.e. relative oliguria) if it persists in rehydrated patients with acute renal failure. If a patient has adequate renal function,
diuresis (> 2 ml/kg/hour) should occur in association with intravenous administration of fluids to correct dehydration and
expand extracellular fluid volume. Rapid onset of diuresis in an oliguric patient associated with intravenous infusion of
fluids suggests that the oliguria had a prerenal component.
Pathologic oliguria may occur during the early phase of acute primary renal failure due to generalized ischemic or nephrotoxic
tubular disease (see Table 1). The exact pathophysiology involved in the production of oliguria in patients with acute renal
failure involves several mechanisms.
Depending on the inciting cause, any one or combination of the following four pathophysiologic mechanisms may be involved:
> Marked vasoconstriction of preglomerular arterioles
> Decreased glomerular permeability
> Obstruction of tubular lumens with casts
> Extraluminal compression associated with edema or inflammation or abnormal reabsorption of filtrate through damaged tubular
Pathologic oliguria associated with acute renal failure may persist for hours, days or even weeks. However, in some instances,
its duration is so transient that it is not detected. In this situation, polyuria may be observed.
In some patients, particularly those with drug-induced nephrotoxicity, the term nonoliguric is used to reflect a relatively constant, but still inappropriate, volume of urine that is intermediate between oliguria
Generally, patients with acute nonoliguric renal failure have a more favorable prognosis for recovery than patients with acute
oliguric renal failure. However, prognosis is dependent on many factors, including the specific initiating cause, the magnitude
and severity of intrinsic damage to renal tissues and the experience of those providing specific, supportive and symptomatic
The specific gravity and osmolality of urine (regardless of volume) formed by patients with acute renal failure will reflect
impaired concentrating capacity if a sufficient quantity of nephrons have been damaged (see Table 1). The damage may be reversible
or irreversible. Irreversible damage may be nonprogressive or progressive.
A state of pathologic oliguria may develop in patients with primary polyuric renal failure if some prerenal abnormality (i.e. vomiting, decreased water consumption, cardiac decompensation) develops (see Table 1). The oliguria is related to reduced
renal perfusion resulting in reduction in the amount of glomerular filtrate that is formed. If this prerenal cause is reversible
or if adequate renal perfusion is restored, polyuria will resume. Oliguria or a nonpolyuric state may develop as a terminal
event in patients with chronic progressive generalized renal disease (see Table 1).
Oliguria in the context of reduction of the volume of urine expelled from the urinary bladder during the voiding phase of
micturition is associated with diseases of the lower urinary system (i.e. ureters, urinary bladder, urethra) that impair flow of urine through the excretory pathway. Examples of such diseases include
neoplasms, strictures or uroliths that partially occlude the urethral lumen; herniation of the urinary bladder that partially
obstructs urine outflow through the urethra or urine inflow through the ureters; and rupture of the urinary bladder. In healthy
dogs, very little urine should be retained in the urinary bladder following micturition (approximately 0.1 to 0.2 ml/kg).
What is anuria?
The term anuria has been used to indicate the absence of urine formation by the kidneys and absence of elimination of urine from the body.
It is possible that anuria could occur as a result of complete shutdown of renal function due to lack of renal perfusion caused
by thromboembolic disease or severe bilateral renal medullary papillary necrosis. However, anuria is usually associated with
total obstruction to urine outflow or rents in the lower urinary tract.
Dr. Carl A. Osborne is the director of the Minnesota Urolith Center and a professor at the College of Veterinary Medicine
at the University of Minnesota. Dr. Eugene Nwaokorie is pursuing a PhD at the University of Minnesota.