Objective—To evaluate excretion of urinary albumin (UAlb) and urinary retinol-binding protein (URBP) in dogs with naturally occurring renal disease.
Animals—64 client-owned dogs.
Procedures—Dogs were assigned to groups according to plasma creatinine concentration, urinary protein-to-urinary creatinine ratio (UP:UC), and exogenous plasma creatinine clearance (P-ClCr) rates: group A (n = 8), nonazotemic (plasma creatinine < 125 μmol/L) and nonproteinuric (UP:UC < 0.2) with P-ClCr rate > 90 mL/min/m2; group B (26), nonazotemic and nonproteinuric with P-ClCr rate 50 to 89 mL/min/m2; group C (7), nonazotemic but proteinuric with P-ClCr rate 53 to 98 mL/min/m2; group D (8), azotemic and borderline proteinuric with P-ClCr rate 22 to 45 mL/min/m2); and group E (15), azotemic and proteinuric (P-ClCr not evaluated). The UAlb and URBP concentrations were measured via ELISA; UAlb-to-urinary creatinine (UAlb:UC) and URBP-to-urinary creatinine (URBP:UC) ratios were determined.
Results—UAlb:UC and URBP:UC did not differ between groups A and B. Increased UAlb: UCs and URBP:UCs were paralleled by increased UP:UCs in groups C, D, and E relative to values from groups A and B, independent of azotemia. There were significant positive correlations of UP:UC with UAlb:UC and of UAlb:UC with URBP:UC (r = 0.82 and 0.46, respectively). However, UP:UC, UAlb:UC, and URBP:UC were not significantly correlated with P-ClCr rate.
Conclusions and Clinical Relevance—UAlb and URBP concentrations were paralleled by urinary protein concentrations and may be useful in assessing renal management of plasma proteins. Determination of urinary protein, UAlb, or URBP concentration was not sufficiently sensitive to detect reduced P-ClCr in nonazotemic dogs. (Am J Vet Res 2010;71:1387—1394)
OBJECTIVE To use proteomic analysis to determine the protein constituents of synovial fluid samples from the stifle joints of dogs with and without osteoarthritis secondary to cranial cruciate ligament rupture (CCLR).
ANIMALS 12 dogs with clinically normal stifle joints (controls) and 16 dogs with osteoarthritis secondary to CCLR.
PROCEDURES A synovial fluid sample was obtained from all dogs. Synovial fluid total protein concentration was determined by the Bradford assay. Proteins were separated by use of a 1-D SDS-PAGE to detect protein bands that differed between dogs with and without osteoarthritis. Those protein bands then underwent trypsin digestion and were analyzed by matrix-assisted laser desorption-ionization time-of-flight mass spectrometry, the results of which were compared with a curated protein sequence database for protein identification. One of the most frequently identified proteins, apoprotein (apo) A-I, was then quantified in all synovial fluid samples by use of a competitive-inhibition ELISA. Results were compared between dogs with and without osteoarthritis.
RESULTS Median synovial fluid total protein and apo A-I concentrations for dogs with osteoarthritis were significantly greater than those for control dogs. The most abundant proteins identified in the synovial fluid were albumin and apo A-I.
CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that quantification of synovial fluid total protein and apo A-I concentrations might facilitate diagnosis of osteoarthritis secondary to CCLR in dogs. Further research and validation of synovial fluid apo A-I concentration as a biomarker for osteoarthritis in dogs are necessary before it can be recommended for clinical use.
Objective—To evaluate cartilage thickness of the talus (especially at sites predisposed to osteochondrosis dissecans [OCD]) in growing and adult dogs not affected with OCD.
Sample—Tarsocrural joints from cadavers of 34 juvenile (approx 3 months old) and 10 adult dogs.
Procedures—Tarsal cartilage thickness was examined via a stereophotography microscopic system. Articular cartilage thickness was determined at 11 locations on longitudinal slices of the trochlear ridges and the sulcus between the ridges and at 2 locations in the cochlea tibiae. Cartilage thickness was measured at the proximal, proximodorsal, dorsal, and distal aspects of the trochlear ridges; proximodorsal, dorsal, and distal aspects of the trochlear sulcus; and craniolateral and caudomedial aspects of the cochlea tibiae. Differences within a joint and between sexes were evaluated.
Results—Mean cartilage thickness decreased from proximal to distal in juvenile (lateral trochlear ridge, 1.52 to 0.41 mm; medial trochlear ridge, 1.10 to 0.40 mm) and from proximal to dorsal in adult (lateral trochlear ridge, 0.41 to 0.34 mm; medial trochlear ridge, 0.33 to 0.23 mm) dogs. Cartilage was thickest at the proximal aspect of the lateral trochlear ridge in both groups. Differences in proximodorsal, dorsal, and distal aspects of the ridges were not evident.
Conclusions and Clinical Relevance—Healthy tarsocrural joints did not have thicker cartilage in sites predisposed to development of OCD. Evaluation of affected tarsocrural joints is necessary to exclude influences of cartilage thickness. These data are useful as a reference for distribution of cartilage thickness of the trochlea of the talus in dogs.
Objective—To determine plasma and urine concentrations
of retinol, retinyl esters, retinol-binding protein
(RBP), and Tamm-Horsfall protein (THP) in dogs
with chronic renal disease (CRD).
Animals—17 dogs with naturally developing CRD and
21 healthy control dogs.
Procedure—A diagnosis of CRD was established on
the basis of clinical signs, plasma concentrations of
creatinine and urea, and results of urinalysis.
Concentrations of retinol and retinyl esters were measured
by use of reverse-phase high-performance liquid
chromatography. Concentrations of RBP and THP
were measured by use of sensitive ELISA systems.
Results—Dogs with CRD had higher plasma concentrations
of retinol, which were not paralleled by differences
in plasma concentrations of RBP. Calculated
ratio of urinary total vitamin A (sum of concentrations
of retinol and retinyl esters to creatinine concentration)
and ratio of the concentration of urinary retinyl esters
to creatinine concentration did not differ between
groups. However, we detected a significantly higher
retinol-to-creatinine ratio in the urine of dogs with
CRD, which was paralleled by a higher urinary RBP-to-creatinine
ratio. Thus, in dogs with CRD, the estimated
fractional clearance of total vitamin A, retinol, and RBP
was increased. Furthermore, dogs with CRD had a
reduced urinary THP-to-creatinine ratio.
Conclusions and Clinical Relevance—Results of
this study documented that CRD affects the concentrations
of retinol in plasma and urine of dogs.
Analysis of the data indicates that measurement of
urinary RBP and urinary THP concentrations provides
valuable information that can be helpful in follow-up
monitoring of dogs with CRD. (Am J Vet Res 2003:64:874–879)
Case Description—An 8-month-old sexually intact male rabbit was examined because of a 2-day history of anorexia, epiphora of the left eye, bruxism, hypersalivation, and ataxia.
Clinical Findings—Physical examination of the rabbit revealed bilateral conjunctivitis, hypersalivation, and severe signs of CNS dysfunction such as incoordination, intermittent myoclonic seizures, and opisthotonus. Results of hematologic and serum biochemical analyses revealed only lymphopenia, a relative monocytosis, and an increase in serum activity of creatine phosphokinase and serum concentration of total protein. Serum antibodies against Encephalitozoon cuniculi and Toxoplasma gondii were not detected.
Treatment and Outcome—Despite IV administration of crystalloid fluids and treatment with antimicrobials, vitamin B complex, nutritional support, and prednisolone, the condition of the rabbit deteriorated; it was euthanized 7 days after admission. Histologic evaluation of brain tissue revealed lesions characteristic of severe, diffuse, nonsuppurative meningoencephalitis and a few large, eosinophilic, intranuclear inclusion bodies in neurons and glial cells. The DNA of human herpesvirus-1 was detected in the nuclei of glial cells, lymphocytes, and neurons by means of in situ hybridization. The rabbit's owner, who reported having had a severe labial and facial herpesvirus infection 5 days before the onset of clinical signs in the rabbit, was suspected to be the origin of infection for the rabbit.
Clinical Relevance—Human herpesvirus-1 may be transmissible from humans to rabbits, and infection with this virus should be considered as a differential diagnosis in rabbits with CNS signs of disease.