Renal resistive index in 55 dogs with degenerative mitral valve disease

Background

Azotemia occurs frequently in dogs with degenerative mitral valve disease (DMVD). It could indicate changes in renal hemodynamics.

Hypothesis/Objectives

To assess the renal resistive index (RI) in dogs with DMVD, and the statistical link between heart failure class, azotemia, echo‐Doppler parameters, several plasma variables, and RI.

Animals

Fifty‐five dogs with naturally occurring DVMD were used (ISACHC class 1 [n = 28], 2 [n = 19], and 3 [n = 8]).

Methods

Observational, blinded study, performed under standardized conditions. Physical examination, renal ultrasonography, and echo‐Doppler examinations were performed in awake dogs. The RI of the renal, interlobar, and arcuate arteries were measured. Plasma creatinine, urea, and N‐terminal pro‐B‐type natriuretic peptide concentrations (NT‐proBNP) were determined. Statistical links between variables and RI were tested by means of a general linear model.

Results

Although the RI of renal and arcuate arteries were unaffected by ISACHC class, the left interlobar RI increased (P < .001) from 0.62 ± 0.05 (mean ± SD) in class 1 to 0.76 ± 0.08 in class 3. It was also higher (P < .001) in azotemic (0.74 ± 0.08) than in non‐azotemic (0.62 ± 0.05) dogs. Similar findings were observed for right interlobar RI. Univariate analysis showed a positive statistical link between NT‐proBNP (P = .002), urea (P < .001), creatinine (P = .002), urea‐to‐creatinine ratio (P < .001), left atrium‐to‐aorta ratio (P < .001), regurgitation fraction (P < .001), systolic pulmonary arterial pressure (P < .001), shortening fraction (P = .035), and RI.

Conclusion and Clinical Importance

In dogs with DMVD, interlobar RI increases with heart failure severity and azotemia but a cause and effect relationship remains to be established.     

Clinical assessment of systolic myocardial deformations in dogs with chronic mitral valve insufficiency using two-dimensional speckle-tracking echocardiography

ObjectiveThe objective of this study was to clinically assess myocardial deformations in dogs with chronic mitral valve insufficiency (CMVI) using two-dimensional speckle-tracking echocardiography (2D-STE).Animals87 dogs with CMVI.MethodsDogs were placed into 1 of 3 classes, based on the International Small Animal Cardiac Health Council classification. In addition, 20 weight- and age-matched healthy dogs were enrolled as controls. The dogs were examined for myocardial deformations using 2D-STE, and strain and strain rate in the longitudinal, circumferential, and radial directions were evaluated.ResultsClass II and III dogs had higher circumferential strain than class I dogs (P = 0.002 and P = 0.001, respectively) and controls (P < 0.001 and P < 0.001, respectively). Class III dogs had higher radial strain than class I dogs (P = 0.001) and controls (P < 0.001). Class III dogs had higher radial strain rate than class I dogs (P = 0.006) and controls (P = 0.001). Other deformations, including longitudinal deformations, were not significantly different between classes of CMVI or between CMVI dogs and controls.ConclusionsIn the clinical progression of CMVI in dogs, myocardial deformations, as assessed by 2D-STE, differed according to myocardial contractile direction. Thus, assessments of multidirectional myocardial deformations may be important for better assessment of clinical cardiac function in dogs with CMVI.     

Effect of atorvastatin on oxidative stress and inflammation markers in myxomatous mitral valve disease in dogs: A comparison of subclinical and clinical stages

Myxomatous mitral valve disease (MMVD) is the most common acquired cardiac disorder found in dogs. The disease process can lead to heart failure (HF) and has been found to be associated with oxidative stress and inflammation. Statins exert antioxidant and anti‐inflammatory effects in human HF patients. However, the beneficial effects of statins in MMVD dogs are still unclear. Thirty MMVD dogs were enrolled in the study and were divided into two groups: MMVD without HF dogs (n = 15) and MMVD with HF dogs (n = 15). Atorvastatin (8 mg kg^?1 day^?1) was administered orally to all dogs for 4 weeks. All dogs underwent physical examination and cardiac examination at the beginning and end of the experiment, including baseline values for hematology, blood chemistry profile, lipid profile, N‐terminal pro B‐type natriuretic peptide, oxidative stress marker (8‐isoprostane), and inflammatory marker (tumor necrosis factor alpha). The results showed that atorvastatin reduced plasma cholesterol levels in both groups. In addition, plasma concentrations of 8‐isoprostane, tumor necrosis factor alpha, and N‐terminal pro B‐type natriuretic peptide were significantly lower after atorvastatin administration, but only in MMVD dogs in the HF group. Atorvastatin found to be associated with possible antioxidant and inflammatory effects in dogs with HF secondary to MMVD. The potential benefits of statins in dogs with HF merits further investigation in larger, placebo‐controlled studies.     

Association of hyponatremia and hyperglycemia with outcome in dogs with congestive heart failure

Objective: To evaluate plasma sodium and glucose concentrations in dogs with congestive heart failure (CHF) prior to treatment and evaluate the differences between survivors and non‐survivors. Design: Retrospective study. Animals: Fifty‐nine dogs with CHF prior to receiving cardiac medication. Interventions: None. Measurements and main results: The mean plasma sodium concentration in dogs with CHF was below the reference range (144–156 mmol/L) and significantly lower (P=0.009) in non‐survivors (141±6 mmol/L) compared with survivors (147±4 mmol/L). The mean plasma glucose concentration was above the reference range (76–117 mg/dL) and significantly higher (P=0.004) in non‐survivors (128±52 mg/dL) compared with survivors (100±13 mg/dL). Forty‐four percent of non‐survivors had concurrent low plasma sodium and high plasma glucose concentrations, whereas no survivors had both abnormalities (P<0.0001). Conclusions: Lower plasma sodium and higher plasma glucose are associated with a worse outcome in dogs with CHF.     

Association of Iatrogenic Hypothyroidism with Azotemia and Reduced Survival Time in Cats Treated for Hyperthyroidism

Background: Iatrogenic hypothyroidism can occur after treatment of hyperthyroidism, and is correlated with a reduced glomerular filtration rate in humans and dogs. Hypothesis: Cats with iatrogenic hypothyroidism after treatment for hyperthyroidism will have a greater incidence of azotemia than euthyroid cats. Animals: Eighty client owned cats with hyperthyroidism. Methods: Two retrospective studies. (1) Longitudinal study of 12 hyperthyroid cats treated with radioiodine (documented as euthyroid after treatment), to assess changes in plasma thyroid stimulating hormone (TSH) concentration over a 6‐month follow‐up period, (2) Cross‐sectional study of 75 hyperthyroid cats (documented as euthyroid) 6 months after commencement of treatment for hyperthyroidism to identify the relationship between thyroid status and the development of azotemia. Kaplan‐Meier survival analysis was performed to identify relationships between thyroid and renal status and survival. Results: Plasma TSH concentrations were not suppressed in 7 of 8 cats with hypothyroidism 3 months after radioiodine treatment. The proportion of cats with azotemia was significantly (P= .028) greater in the hypothyroid (16 of 28) than the euthyroid group (14 of 47). Twenty‐eight of 41 cats (68%) with plasma TT4 concentration below the laboratory reference range had an increased plasma TSH concentration. Hypothyroid cats that developed azotemia within the follow‐up period had significantly (P= .018) shorter survival times (median survival time 456 days, range 231–1589 days) than those that remained nonazotemic (median survival time 905 days, range 316–1869 days). Conclusions and Clinical Importance: Iatrogenic hypothyroidism appears to contribute to the development of azotemia after treatment of hyperthyroidism, and reduced survival time in azotemic cats.     

Serum α‐1‐acid glycoprotein concentration in clinically healthy puppies and adult dogs and in dogs with various diseases

Background: α‐1‐acid glycoprotein (AGP) is an acute‐phase protein and a serum marker of inflammation and neoplasia in humans. AGP concentrations in diseased dogs and the potential effects of age, breed, and sex have not been elucidated. Objective: The purpose of this study was to examine differences in AGP concentration based on age, sex, and breed in a large population of clinically healthy dogs and to compare AGP concentrations in dogs with various diseases. Methods: Serum was obtained from clinically healthy puppies (n=74) and adults (n=172) of both sexes, and included mongrels (n=205) and Beagles (n=41). Serum also was obtained from 192 dogs with various diseases, including 8 with pyometra that were sampled before, and 1, 2, 3, and 10 days after surgery. AGP concentration was measured by single radial immunodiffusion. Statistical comparisons were made among age, sex, breed, and disease groups. Results: Serum AGP in healthy adult mongrels was 364±106 mg/L (reference interval, 152–576 mg/L). AGP was lowest in newborns (n=11, 122±54 mg/L) and gradually increased to adult levels by 3 months of age. Median AGP concentration was highest in dogs with parvovirus (n=17, 2100 mg/L), distemper (n=7, 1250 mg/L), and pyometra (n=18, 2480 mg/L) and was also significantly higher in dogs with acute filariasis, renal failure, urolithiasis, pancreatitis, hepatitis, trauma, hyperadrenocorticism, and immune‐mediated hemolytic anemia. Dogs with acute filariasis and acute hepatopathy had significantly higher AGP concentrations than dogs with chronic filariasis and chronic hepatopathy. Serum AGP concentration decreased gradually following surgery for pyometra but remained increased after 10 days (896±175 mg/L). Conclusions: Because of significantly lower AGP in puppies, the age of dogs should be considered when using AGP as a marker of disease. Serum AGP may be a useful marker of inflammatory disease in dogs and may help differentiate acute and chronic stages of disease.     

Tolerability of metronomic administration of lomustine in dogs with cancer

Background: Metronomic chemotherapy with alkylating agents has been shown to suppress tumor angiogenesis and prevent tumor recurrence in some settings. The use of adjuvant lomustine (1‐(2‐chloroethyl)‐3‐cyclohexyl‐1‐nitrosourea) administered in a metronomic fashion has not been evaluated in dogs. Hypothesis: Oral metronomic administration of lomustine will be well tolerated in dogs with spontaneously occurring malignant neoplasms. Animals: Eighty‐one dogs with naturally occurring primary or metastatic tumors received metronomic administration of lomustine. Methods: Dogs were enrolled prospectively after cytological or histological diagnosis of a tumor that was unresectable, incompletely resected, refractory to chemotherapy, or metastatic. Dogs received once daily lomustine (2.84 mg/m² PO). End points of the trial were clinical, hematologic, or biochemical evidence of toxicosis, tumor progression, or death. Results: Starting dosage (median) was 2.84 mg/m² PO daily and treatment duration was 98 days (median, range, 1–770 days). The drug was discontinued in 22 dogs because of toxicoses. Toxicoses occurred in 13 dogs with gastrointestinal toxicosis, 4 dogs with thrombocytopenia, 3 dogs with increased alanine transaminase, 1 dog with neutropenia, and 1 dog with progressive azotemia. Eight dogs developed some degree of azotemia during treatment. Hepatotoxicosis was observed at a median of 265 days in 11 dogs. Thrombocytopenia was identified at a median of 432 days of administration. Conclusions and Clinical Importance: In dogs with metastatic or terminal neoplasms without renal compromise, metronomic administration of lomustine was well tolerated. This can provide a treatment strategy for dogs that do not have other standard‐care treatment options, and warrants evaluation in primary therapy.     

Lithium dilution cardiac output and oxygen delivery in conscious dogs with systemic inflammatory response syndrome

Objective: Compare cardiac index (CI) and oxygen delivery index (DO₂I) in conscious, critically ill dogs to control dogs; evaluate the association of CI and DO₂I with outcome. Design: Prospective non‐randomized clinical study. Setting: Veterinary teaching hospital. Animals: Eighteen client‐owned dogs with systemic inflammatory response syndrome (SIRS) and 8 healthy control dogs. Measurements and Main Results: CI of dogs with SIRS was measured using lithium dilution at times 0, 4, 8, 16, and 24 hours. Data collected included physical exam, arterial blood gas (ABG) and hemoximetry. CI of control dogs was measured 3 times with 1 measurement of ABG. Mean CI ± SE in SIRS patients was 3.32 ± 0.95 L/min/m²; lower than controls at 4.18 ± 0.22 L/min/m² (P<0.001). Mean DO₂I ± SE in SIRS patients was 412.91 ± 156.67 mL O₂/min/m²; lower than controls at 785.24 ± 45.99 mL O₂/min/m² (P<0.001). There was no difference in CI (P=0.49) or DO₂I (P=0.51) for dogs that survived to discharge versus those that did not. There was no difference in mean CI (P=0.97) or DO₂I (P=0.50) of survivors versus non‐survivors for 28‐day survival. Survivors had lower blood glucose (P=0.03) and serum lactate concentrations (P=0.04) than non‐survivors. Conclusions: CI and DO₂I in conscious dogs with SIRS were lower than control dogs, which differs from theories that dogs with SIRS are in a high cardiac output state. CI and DO₂I were not significantly different between survivors and non‐survivors. Similar to previous studies, lactate and glucose concentrations of survivors were lower than non‐survivors.     

Evaluation of platelet function in dogs with cardiac disease using the PFA‐100 platelet function analyzer

Background: Cardiac disease has the potential to alter platelet function in dogs. Evaluation of platelet function using the PFA‐100 analyzer in dogs of multiple breeds and with a broad range of cardiac conditions would help clarify the effect of cardiac disease on platelets. Objectives: The objective of this study was to assess differences in closure time (CT) in dogs with cardiac disease associated with murmurs, when compared with that of healthy dogs. Methods: Thirty‐nine dogs with cardiac murmurs and turbulent blood flow as determined echocardiographically were included in the study. The dogs represented 23 different breeds. Dogs with murmurs were further divided into those with atrioventricular valvular insufficiency (n=23) and subaortic stenosis (n=9). Fifty‐eight clinically healthy dogs were used as controls. CTs were determined in duplicate on a PFA‐100 analyzer using collagen/ADP cartridges. Results: Compared with CTs in the control group (mean±SD, 57.6±5.9 seconds; median, 56.5 seconds; reference interval, 48.0–77.0 seconds), dogs with valvular insufficiency (mean±SD, 81.9±26.3 seconds; median, 78.0 seconds; range, 52.5–187 seconds), subaortic stenosis (71.4±16.5 seconds; median, 66.0 seconds; range, 51.5–95.0 seconds), and all dogs with murmurs combined (79.6±24.1 seconds; median, 74.0 seconds; range, 48.0–187 seconds) had significantly prolonged CTs (P<.01). Conclusions: The PFA‐100 analyzer is useful in detecting platelet function defects in dogs with cardiac murmurs, most notably those caused by mitral and/or tricuspid valvular insufficiency or subaortic stenosis. The form of turbulent blood flow does not appear to be an important factor in platelet hypofunction in these forms of cardiac disease.     

Peritoneal dialysis in the management of acute renal failure in 5 dogs with leptospirosis

Objective: To describe the use of peritoneal dialysis (PD) in the management of 5 dogs with acute renal failure (ARF) caused by leptospirosis. Case Series Summary: All dogs were treated for leptospirosis with intravenous (IV) fluids and ampicillin prior to PD. Median age of dogs was 5 years (range 2–6 years). All dogs had positive titers for Leptospira bratislava. Median duration of PD was 4 days (range 3–16 days). PD resulted in a decrease in azotemia in all dogs. Median serum blood urea nitrogen at the start of PD was 192 mg/dL (range 140–235 mg/dL) and at the end of PD was 63 mg/dL (range 48–139 mg/dL). Median serum creatinine at the start of PD and the end was 12.8 mg/dL (range 7.7–16.9 mg/dL) and 3.4 mg/dL (range 1.4–11.1 mg/dL), respectively. Complications identified during PD included hypokalemia (n=3, 60%), hypoalbuminemia (n=2, 40%), hypomagnesemia (n=1, 20%), pelvic limb edema (n=2, 40%), central nervous system signs (n=2, 40%), dialysate retention (n=1, 20%), and leakage from the catheter site (n=1, 20%). Peritonitis was not identified in any of the dogs. Four dogs (80%) survived to discharge from the hospital. PD was effective for management of uremia in dogs with ARF caused by leptospirosis.     

EFFECTS OF INTRAVENOUS DEXMEDETOMIDINE ON CARDIAC CHARACTERISTICS MEASURED USING RADIOGRAPHY AND ECHOCARDIOGRAPHY IN SIX HEALTHY DOGS

Dexmedetomidine is a highly specific and selective α2‐adrenergic receptor agonist widely used in dogs for sedation or analgesia. We hypothesized that dexmedetomidine may cause significant changes in radiographic and echocardiographic measurements. The objective of this prospective cross‐sectional study was to test this hypothesis in a sample of six healthy dogs. Staff‐owned dogs were recruited and received a single dose of dexmedetomidine 250 μg/m² intravenously. Thoracic radiography and echocardiography were performed 1 h before treatment, and repeated 10 and 30 min after treatment, respectively. One observer recorded cardiac measurements from radiographs and another observer recorded echocardiographic measurements. Vertebral heart score and cardiac size to thorax ratio on the ventrodorsal projection increased from 9.8 ± 0.6 v to 10.3 ± 0.7 v (P = 0.0007) and 0.61 ± 0.04 to 0.68 ± 0.03 (P = 0.0109), respectively. E point‐to‐septal separation and left ventricle internal diameter in diastole and systole increased from 2.4 ± 1.1 to 6.6 ± 1.9 mm, 32.3 ± 8.1 to 35.5 ± 8.8 mm, and 19.4 ± 6 to 27.0 ± 7.2 mm, respectively (P < 0.05). Fractional shortening and sphericity index decreased from 40.7 ± 5.8 to 24.4 ± 2.9%, and 1.81 ± 0.07 to 1.58 ± 0.04, respectively (P < 0.05). Moderate‐to‐severe mitral regurgitation and mild pulmonic regurgitation occurred in all dogs after dexmedetomidine administration. Findings indicated that dexmedetomidine could cause false‐positive diagnoses of valvular regurgitation and cardiomegaly in dogs undergoing thoracic radiography and echocardiography.     

Use of capillary electrophoresis to quantitate carbamylated hemoglobin concentrations in dogs with renal failure

OBJECTIVE: To evaluate quantification of the amount of carbamylated hemoglobin (CarbHb), using capillary electrophoresis (CE) and a new dynamic capillary coating system to separate hemoglobin derivatives, and to assess the use of CarbHb amounts to evaluate long-term urea exposure and differential diagnoses of azotemia in dogs. ANIMALS: 8 dogs with renal failure, 2 dogs with diabetes mellitus, and 7 control dogs. PROCEDURE: Optimal analytic conditions for separation of CarbHb and other hemoglobin derivatives in blood samples obtained from dogs were determined, using a commercial analysis system developed for the detection of glycohemoglobin Hb A1c (GlycHb) in human blood samples. Relative content of hemoglobin derivatives in blood from 10 dogs with renal failure or endocrine diseases were compared with values for 7 dogs without renal or endocrine diseases. RESULTS: Satisfactory resolution of hemoglobin derivatives was obtained, which permitted identification and quantitation of the amount of CarbHb as a percentage of the total amount of hemoglobin. Normal or increased amounts of GlycHb did not interfere with CarbHb analysis. Dogs with chronic renal failure had considerably higher peak amounts of CarbHb than dogs with acute renal failure, a dog with chronic renal failure that was treated by use of hemodialysis, or dogs without renal disease. CONCLUSIONS AND CLINICAL RELEVANCE: Amounts of CarbHb in blood samples obtained from dogs can be readily quantified by use of capillary electrophoresis. Assessment of the amount of CarbHb can be used to facilitate evaluation of the cause of azotemia in dogs.     

Examination of hemostatic parameters to detect hypercoagulability in dogs with severe protein‐losing nephropathy

Objective – To identify hemostatic abnormalities in dogs with protein‐losing nephropathies (PLN) that represent risk factors for pathologic thrombosis. Design – Cross‐sectional observational study of client‐owned dogs with PLN, nonprotein losing renal failure (RF), and systemic illness (SI) exclusive of primary renal disease. Setting – Urban University Referral Center. Animals – A total of 29 dogs (n=11 PLN, n=7 RF, n=11 SI) were enrolled between January 2001 and July 2002. Samples were also collected from 20 clinically normal dogs to serve as hemostasis assay controls. Interventions – None. Hemostasis Testing – Citrate anticoagulated blood was collected for point‐of‐care testing with a viscoelastic monitor (thromboelastograph [TEG]) and citrate plasma was prepared for coagulation screening tests and specific assay of the following hemostatic proteins: antiplasmin, antithrombin, D‐dimer, Factor VIII, fibrinogen, plasminogen, protein C, and von Willebrand factor. Results – Dogs with PLN and RF demonstrated TEG abnormalities consistent with hypercoagulability (eg, short clotting time, high clot amplitude) and both groups had significantly lower antithrombin than the SI group. The PLN dogs had significantly higher protein C than either the RF or SI group. Hyperfibrinogenemia was a consistent finding among all 3 disease groups, and the coagulation index a measure of hypercoagulability derived from TEG parameters, directly correlated with fibrinogen values of all study dogs. Conclusions – Hemostatic abnormalities consistent with systemic hypercoagulability are common in dogs with RF and PLN, however, no prothrombotic factors unique to PLN were identified in our study. The thrombotic tendency of PLN may therefore involve parameters we did not directly assess such as platelet reactivity, fibrinolysis, perturbations in blood flow, and/or endothelial dysfunction. High protein C is a novel finding in PLN dogs of unknown clinical relevance.     

Echocardiographic and tissue Doppler imaging alterations associated with spontaneous canine systemic hypertension

Background: Feline systemic arterial hypertension (SHT) is associated with a wide spectrum of left ventricular (LV) geometric patterns as well as diastolic, and to a lesser extent, systolic myocardial dysfunction. However, little is known about SHT‐related cardiac changes in dogs. Hypothesis: SHT in dogs is responsible for morphological and functional cardiac alterations. Animals: Thirty dogs with spontaneous untreated SHT and 28 age‐ and body weight‐matched healthy dogs as controls. Methods: Prospective observational study. Conventional echocardiography and 2‐dimensional color tissue Doppler imaging were performed in SHT dogs by trained observers and compared with controls. Results: Forty‐seven percent of SHT dogs (14/30) had diffuse concentric hypertrophy. None had left atrial dilatation and 10/30 (33%) had aortic insufficiency (AoI) associated with proximal aortic dilatation. Longitudinal diastolic left ventricular free wall (LVFW) motion was altered in all SHT dogs at the base (early to late diastolic wave ratio, E/A = 0.5 ± 0.1 versus 1.3 ± 0.3 for controls, P < .0001) and the apex (E/A = 1.6 ± 1.7 versus 3.9 ± 3.1, P < .05). Longitudinal motion of the interventricular septum at the base (E/A = 0.7 ± 0.4 versus 1.1 ± 0.1, P < .01) and radial LVFW motion in the subendocardium (E/A = 0.9 ± 0.5 versus 1.6 ± 0.3, P < .01) were also altered in dogs with SHT. Longitudinal LVFW systolic velocities and gradients were also significantly decreased (P < .05) in SHT dogs. Conclusion and Clinical Importance: As in SHT in cats, SHT in dogs is associated with myocardial dysfunction independently of the presence of myocardial hypertrophy. However, unlike feline SHT, it results in a homogeneous LV geometric pattern with a relatively high prevalence of AoI.     

Proteomic analysis of urine from male dogs during early stages of tubulointerstitial injury in a canine model of progressive glomerular disease

Background: Sensitive and specific noninvasive biomarkers for tubulointerstitial injury are lacking, and proteomic techniques provide a powerful tool for biomarker discovery. Objective: The aim of this study was to identify novel urinary biomarkers of early tubulointerstitial injury in canine progressive renal disease using both 2‐dimensional differential in‐gel electrophoresis (2‐D DIGE), which identifies individual proteins, and surface‐enhanced laser desorption ionization time‐of‐flight mass spectrometry (SELDI‐TOF), which generates protein peak profiles. Methods: Urine was collected from 6 male dogs with X‐linked hereditary nephropathy (XLHN) at 2 time points (TP): 1) the onset of overt proteinuria (urine protein:creatinine ratio>2) and 2) the onset of azotemia (creatinine ≥1.2 mg/dL); corresponding renal biopsies were analyzed from 3 of the dogs. Urine samples from the 6 dogs were subjected to analysis by 2‐D DIGE and SELDI‐TOF. Urinary retinol‐binding protein (RBP) was evaluated in 25 male dogs with XLHN and normal control dogs by Western blot analysis. Results: Clinical data and histologic evaluation revealed reduced renal function and increased tubulointerstitial fibrosis at TP 2. A number of urine proteins and protein peaks were differentially present at the 2 time points, with several known biomarkers of renal disease identified in addition to several promising new biomarkers. RBP was first detected in urine approximately 2 months before onset of azotemia (TP 2), but after onset of overt proteinuria, and amounts increased with progression of disease. Conclusions: Proteomic techniques were successfully used to identify urinary biomarkers of renal disease in dogs with XLHN. Urinary RBP is a promising biomarker for early detection of tubulointerstitial damage and progression to end‐stage renal disease.     

Microalbuminuria is not associated with cisplatin-induced azotemia in dogs

BACKGROUND: Cisplatin is an effective antineoplastic agent but its use is limited by renal toxicity. Microalbuminuria is a marker of renal damage and might be an indicator of cisplatin-induced azotemia. NULL HYPOTHESIS: Microalbuminuria is not associated with azotemia in dogs treated with cisplatin. ANIMALS: This study used 32 client-owned dogs. METHODS: This was a prospective observational study in which cancer-bearing dogs were treated with cisplatin chemotherapy. Cisplatin-induced azotemia was defined as an increase of serum creatinine concentration above the reference range. Serum creatinine concentration, other routine tests of renal function, and microalbuminuria were measured after each cisplatin treatment. Variables potentially associated with azotemia were compared by use of Fisher's exact test and Wilcoxon's rank-sum test. RESULTS: Cisplatin-induced azotemia occurred in 10 (31%) dogs after 1-5 treatments. At each of the first 3 treatments, the proportions of dogs with microalbuminuria were similar between dogs with and without azotemia. CONCLUSIONS AND CLINICAL IMPORTANCE: Microalbuminuria measured after each treatment was not associated with azotemia through the first 3 treatments. Testing for microalbuminuria as a marker for cisplatin-induced renal damage is insensitive and not recommended.     

The Influence of High‐Intensity Moderate Duration Exercise on Cardiac Troponin I and C‐Reactive Protein in Sled Dogs

Background: C‐reactive protein (CRP) and cardiac troponin I (cTnI) are biomarkers of systemic inflammation and cardiac damage, respectively. Objective: To investigate the effects of short‐duration high‐intensity exercise on plasma cTnI and serum CRP concentrations in sprint racing sled dogs. Animals: Twenty‐two Alaskan sled dogs of 2 different teams participating in a 2‐day racing event. Methods: In this prospective field study, cephalic venipuncture was performed on all dogs before racing and immediately after racing on 2 consecutive days. Plasma cTnI and serum CRP concentrations were evaluated at each time point. Results: There was a mild, significant rise (P < .01) in median cTnI concentrations from resting (0.02 ng/mL; 0.0–0.12 ng/mL) on both days after racing (day 1 = 0.06, 0.02–0.2 ng/mL; day 2 = 0.07, 0.02–0.21 ng/mL). Serum CRP concentrations showed a mild significant increase (P < .01) on day 2 after racing mean (9.2 ± 4.6 μg/mL) as compared with resting (6.5 + 4.3 μg/mL) and day 1 after racing (5.0 + 2.9 μg/mL). Neither cTnI or CRP concentrations exceeded the upper reference range for healthy dogs. Conclusions and Clinical Relevance: Strenuous exercise of short duration did not result in cTnI concentrations above the reference range for healthy dogs. Although increased after 2 days of short‐duration strenuous exercise, CRP did not reach concentrations suggestive of inflammation, as reported previously in the endurance sled dogs. Therefore, we surmise that moderate exercise does not present a confounding variable in the interpretation of cTnI and CRP concentrations in normal dogs.     

The echocardiographic effects of romifidine in dogs with and without prior or concurrent administration of glycopyrrolate

Objective To determine the cardiopulmonary response to romifidine (RO) in the dog with or without prior or concurrent administration of glycopyrrolate. Study Design Randomized, cross‐over experimental study. Animals Six (three male, three female) cross‐bred dogs weighing 23 ± 2.4 kg. Methods Two‐dimensional guided M‐mode echocardiography was performed in conscious dogs simultaneously with measurement of systolic arterial blood pressure (SBP) and heart rate (HR). Dimensions of the left ventricle (LVID), interventricular septum (IVS), and left ventricular free wall (LVFW) were obtained in systole (S) and diastole (D). Amplitude of motion (Amp) of the IVS and LVFW were also measured. From these, measures of wall stress (WS) and fractional shortening (FS) of the left ventricle were derived. Baseline echocardiographic measurements were recorded, following which one of the five treatments was administered. Glycopyrrolate (G) 0.01 mg kg^?1, or saline (S) 0.5 mL, was administered IM as pre‐medication (Gp or Sp), or G was administered concurrently (Gc) with romifidine (RO). Treatments were: T₁, Sp + RO (40 μg kg^?1); T₂, Gp + RO (40 μg kg^?1); T₃, Sp + RO (120 μg kg^?1); T₄, Gp + RO (120 μg kg^?1); and T₅, Sp + Gc +RO (120 μg kg^?1). Romifidine or RO + Gc was administered SC 20 minutes after pre‐medication (time 0), and further measurements were taken 10, 20, 30, 60, and 90 minutes after RO. Results Echocardiographic indices of cardiac systolic function (LVID‐S, FS, Amp‐LVFW) and HR were decreased in RO‐sedated dogs (p < 0.0001) . The magnitude of change in cardiac indices was least with low‐dose RO. At most sampling times, high‐dose RO produced significantly more alteration in cardiac indices. Systolic blood pressure increased in all treatment groups, with the greatest increases in those groups receiving G. Glycopyrrolate significantly increased HR; however, cardiac indices were further reduced. Wall stress significantly increased, with a more dramatic increase in groups receiving G. Conclusions Indices of LV systolic function were reduced in RO‐sedated dogs in a dose‐related manner. Glycopyrrolate further reduced these indices and dramatically increased measurements of wall stress in dogs sedated with RO. Clinical relevance Use of low‐dose RO minimizes cardiac dysfunction; however, it should still be used cautiously in dogs with cardiomyopathy or heart failure. The routine use of G is not recommended to alleviate the bradycardia associated with RO in conscious dogs.