Water deprivation testing
If a nondehydrated, nonazotemic patient suspected of having pathologic polyuria does not have a urine specific gravity that
indicates that the kidneys can definitely concentrate urine, further "provocative" tests are required before you can conclude
anything about the kidneys' capacity to concentrate urine. By depriving a nonazotemic, nondehydrated patient of water consumption
for an appropriate period of time, antidiuretic hormone will normally be released from the posterior pituitary gland as a
compensatory response to hydropenia. Antidiuretic hormone enhances fluid reabsorption from the distal tubules and collecting
ducts by increasing tubular epithelial cell permeability to water.
Clinical experience has revealed that the results of water deprivation tests are often difficult to reproduce. Boundary values
have been established, above which renal function is assumed to be adequate and below which it is assumed to be impaired.
A zone of doubt exists in between.
Uncontrolled clinical observations indicate that dogs with "adequate" renal function will excrete urine with a high specific
gravity (1.030), high osmolality and relatively small volume (physiologic oliguria). Studies of dogs with completely normal
renal function were interpreted to indicate that 95 percent of normal dogs subjected to water deprivation sufficient to produce
a slight degree of dehydration should have a urine specific gravity of at least 1.048, a urine osmolality of at least 1,787
mOsm/kg and a U/Posm ratio of at least 5.7 to 1.1 If such values are not obtained, nephron dysfunction may exist. The degree of dysfunction, however, may not be severe enough
to be associated with clinical signs. Evaluate patients unable to concentrate urine after appropriately conducted water deprivation
tests for diseases that cause medullary solute depletion, central diabetes insipidus or renal diabetes insipidus.
Mechanisms of polyuria in primary renal failure
When urine specific gravity reflects an impaired ability to concentrate (or dilute) urine, it is more an index of nephron
function than of distal tubular and collecting duct function. Why? In addition to generalized tubular lesions that impair
the function of the countercurrent system, this abnormality may be intensified as a result of factors not specifically related
to tubular damage. These factors include:
> Compensatory increase in glomerular filtration (so-called hyperfiltration) that occurs as a result of a decrease in the quantity of functional nephrons. Increased production of glomerular filtrate
floods the distal tubules and collecting ducts with solute and water. It is associated with decreased fractional tubular reabsorption
of sodium and phosphorus by viable nephrons.
> Decrease in the number of functioning nephrons. The latter is associated with an impaired ability of the countercurrent mechanism
to maintain the high osmotic gradient normally present in renal medulla.
> Osmotic diuresis in the remaining functional nephrons as a result of increased filtration of solutes (azotemia, hyperphosphatemia,
etc.) in them secondary to reduced glomerular filtration (Tables 1, 2, 3). This accentuates the degree of obligatory polyuria.
The next article in this series will discuss urine specific gravity values and localization of azotemia.
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.
1. Hardy RM, Osborne CA. Water deprivation test in the dog: maximal normal values. J Am Vet Med Assoc 1979;174(5):479-483.