Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

III. Tests of Kidney Function
493
TABLE 16-1 Main Causes of Variations of P-Creatinine in the Dog
P-Creatinine
Primary renal disease
amyloidosis
glomerulosclerosis
polycystic disease
uremic crisis
kidney graft rejection
congenital renal diseases
Secondary renal disease
babesiosis
leptospirosis
trypanosomiasis
histiocytosis
Extrarenal disease
ureteral obstruction
P-Creatinine
portosystemic shunts
early babesiosis
hyperthyroidism
Intoxication by arsenate
fluoride
citrinin
ochratoxin
vitamin D
leishmaniasis
borreliosis
encephalitozoonosis
heartworm disease
uroperitoneum
cachexia
kidney graft
For references, see Braun et al. (2003 ).
which can lead to increased P-Urea in dehydrated patients
or in patients with hemorrhage or to decreased P-Urea in
overhydrated patients. Some urea also filters into the intestine,
where it is degraded by bacteria into ammonium,
which is absorbed and provides a notable proportion of the
ammonium supply to the liver. Another important source
of ammonium is the catabolism of amino acids. Proteins
are thus a major source of ammonium for urea synthesis.
Intense recycling of urea occurs in ruminants by transfer
to the gastrointestinal tract and to saliva. Urea can also be
added to ruminant food ( Cirio et al. , 2000 ; Marini and Van
Amburgh, 2003 ), whence it is incorporated into bacterial
proteins. The dietary supply of urea is low in other species.
b . Preanalytical Factors of Variation
● Specimen: No difference between canine serum and
heparin plasma was observed and only minor changes were
noted when specimens were stored frozen for up to 8 months
(Thoresen et al. , 1995 ). P-Urea is little affected by hemolysis
(up to 25 g hemoglobin/l) and icterus in cattle, horses, cats, or
dogs; it is decreased by lipemia in dogs ( Jacobs et al. , 1992 ;
O’Neill and Feldman, 1989 ). P-Urea is stable in plasma
and whole blood stored for up to 3 days at 20°C ( Thoresen
et al. , 1992 ) and in serum or plasma stored frozen at 20°C
and at 70°C up to 8 months ( Thoresen et al. , 1995 ).
● Diet and meals: P-Urea is increased in dogs after
meals. Peak postprandial increase can be as high as
7 mmol/l about 6 h after the meal and last for more than
18 h; it is greater with high-protein diets or in animals
fed large amounts ( Anderson and Edney, 1969 ; Epstein
et al. , 1984 ; Evans, 1987 ; Vogin et al. , 1967 ). In most species,
basal P-Urea reflects the balance between nitrogen
utilization and excretion and can be greatly influenced by
nutrition ( Kohn et al. , 2005 ). The fasting concentration of
P-Urea was lower in dogs on low-protein diets with normal
or reduced renal function ( Polzin et al. , 1983, 1991 ;
Reynolds et al. , 1999 ), in horses ( Doreau and Martin-
Rosset, 1985 ), in sheep ( Rabinowitz et al. , 1973 ), in goats
( Valtonen et al. , 1982 ), and in cats ( Hesta et al. , 2005 ).
P-Urea was also increased by prolonged fasting, because
of catabolism of body proteins ( Rabinowitz et al. , 1973 ).
● Hydration status: Dehydration had little effect on
P-Urea in dogs ( 12.5 mmol/l in 4 days, with weight loss up
to 16%) ( Hardy and Osborne, 1979 ), but it produced a twofold
increase in calves within 4 days ( Bianca et al. , 1965 ).
● Drugs: P-Urea was unchanged by halothane anesthesia
in dogs ( Lobetti and Lambrechts, 2000 ) and was
increased at high doses of trimethoprim-sulfadiazine
( Lording and Bellamy, 1978 ).
● Physical exercise: P-Urea in sled dogs was higher
after 12 weeks of training, probably as a result of increased
protein intake ( Reynolds et al. , 1999 ). In greyhounds,
P-Urea was unchanged by a 235 m sprint and moderately
increased 30 min after a 420 m run ( Snow et al. , 1988 ).
c . Analytical Factors of Variation
Most techniques are based on the specific action of a bacterial
urease. The accuracy of P-Urea measurements is not
usually reported.