Objective—To determine whether administration of meloxicam or acetylsalicylic acid alters glomerular filtration rate (GFR) in cats with renal azotemia.
Animals—6 young adult cats.
Procedures—3 sexually intact male cats and 3 sexually intact female cats had surgically reduced renal mass and azotemia comparable to International Renal Interest Society chronic kidney disease stages 2 and 3. Renal function was evaluated by measurement of serum creatinine concentration, urinary clearance of exogenously administered creatinine, and the urine protein-to-creatinine concentration ratio (UP:C). Measurements taken in cats receiving placebo at the beginning and end of the study were compared with results obtained at the end of 7 days of treatment with either meloxicam (0.2 mg/kg, SC, on day 1; 0.1 mg/kg, SC, on days 2 to 7) or acetylsalicylic acid (20 mg/kg, PO, on days 1, 4, and 7).
Results—No significant treatment effects on urinary clearance of exogenously administered creatinine, serum creatinine concentration, or UP:C were detected. Mean ± SEM serum creatinine concentration and urinary clearance of exogenously administered creatinine measurements following 7 days of treatment with meloxicam (serum creatinine concentration, 2.67 ± 0.17 mg/dL; urinary clearance of exogenously administered creatinine, 1.34 ± 0.08 mL/min/kg) and acetylsalicylic acid (serum creatinine concentration, 2.62 ± 0.12 mg/dL; urinary clearance of exogenously administered creatinine, 1.35 ± 0.07 mL/min/kg) were not significantly different from the mean baseline values for these variables (serum creatinine concentration, 2.77 ± 0.14 mg/dL; urinary clearance of exogenously administered creatinine, 1.36 ± 0.07 mL/min/kg).
Conclusions and Clinical Relevance—Neither meloxicam nor acetylsalicylic acid had a measurable effect on urinary clearance of exogenously administered creatinine, serum creatinine concentration, or UP:C. These results are consistent with the hypothesis that GFR of euvolemic cats with normal or reduced renal function is not dependent on cyclooxygenase function.
Objective—To determine whether the angiotensin
converting enzyme inhibitor enalapril would lower
systemic arterial and glomerular capillary pressure
and reduce the magnitude of renal injury in a canine
model of renal insufficiency.
Animals—18 adult dogs that had renal mass reduced
by partial nephrectomy.
Procedure—After surgical reduction of renal mass
and baseline measurements, dogs in 2 equal groups
received either placebo (group 1) or enalapril (0.5
mg/kg, PO, q 12 h; group 2) for 6 months.
Results—Values for systemic mean arterial blood
pressure determined by indirect and direct measurement
after 3 and 6 months of treatment, respectively,
were significantly lower in group 2 than in group 1.
During treatment, monthly urine protein-to-creatinine
ratios were consistently lower in group 2 than in
group 1, although values were significantly different
only at 3 months. At 6 months, significant reduction
in glomerular capillary pressure in group 2 was detected,
compared with group 1, but glomerular filtration
rate in group 2 was not compromised. Glomerular
hypertrophy, assessed by measurement of planar surface
area of glomeruli, was similar in both groups.
Glomerular and tubulointerstitial lesions were significantly
less in group 2, compared with group 1.
Conclusions and Clinical Relevance—Data suggest
that inhibition of angiotensin converting enzyme was
effective in modulating progressive renal injury, which
was associated with reduction of glomerular and systemic
hypertension and proteinuria but not glomerular
hypertrophy. Inhibition of angiotensin converting
enzyme may be effective for modulating progression
of renal disease in dogs. (Am J Vet Res 2003;64:321–327)
Objective—To determine effects of the angiotensin
converting enzyme inhibitor benazepril in cats with
induced renal insufficiency.
Procedure—Renal mass was surgically reduced, and
cats were assigned to 1 of 4 eight-cat groups. Group
1 received placebo, whereas groups 2, 3, and 4
received benazepril hydrochloride orally once daily for
approximately 6.5 months at the following doses:
group 2, 0.25 to 0.50 mg/kg of body weight; group 3,
0.50 to 1.00 mg/kg; and group 4, 1.00 to 2.00 mg/kg.
Arterial blood pressures, glomerular filtration rate
(GFR), and renal plasma flow were determined before
treatment and during the treatment period. Other
determinants of renal hemodynamics were measured
by use of micropuncture techniques. Renal biopsy
specimens were examined microscopically.
Results—Compared with cats that received placebo,
mean systolic arterial blood pressure was significantly
less and GFR significantly greater in cats that
received benazepril. Glomerular capillary pressure
and the ratio of efferent to afferent arteriolar vascular
resistance were also significantly less in treated cats.
However, histologic differences in renal specimens
were not detected.
Conclusions and Clinical Relevance—Treatment
with benazepril sustained single nephron GFR in remnant
nephrons of cats with induced renal insufficiency.
Administration of benazepril was also associated
with a small but significant reduction in degree of systemic
hypertension and an increase in whole kidney
GFR. Benazepril may be an effective treatment to
slow the rate of progression of renal failure in cats
with renal disease. (Am J Vet Res 2001;62:375–383)
Objective—To evaluate the effect of renal autograft ischemia and reperfusion associated with renal transplantation on pulse rate and pressure and arterial blood pressure variables in clinically normal cats.
Procedures—A radiotelemetric implant was placed in each cat to measure hemodynamic variables; baseline data were recorded before surgery. Standard heterotopic renal implantation and contralateral nephrectomy were performed (day 0). Autografts were stored in cold sucrose phosphate solution for 30 minutes (n = 5) or 3 hours (5); cats were anephric during this period. Hemodynamic variables were recorded every 5 minutes for up to 16 days after surgery; mean daily values were calculated.
Results—Data from 6 cats were available for analysis. Two cats developed ureteral obstructions and became azotemic at 111 and 197 hours after kidney reperfusion. Mean serum creatinine and BUN concentrations were greater than baseline values on days 1 and 2. Although changes from baseline hemodynamic values were detected in some cats, arterial blood pressure measurements did not change significantly from baseline at any time point. Compared with baseline data, mean pulse rate was increased on days 1 and 2 and days 6 through 12; mean pulse pressure was increased on days 1 and 2.
Conclusions and Clinical Relevance—In clinically normal cats, hypertension was not induced by clinically relevant periods of ischemia-reperfusion injury of renal autografts and was not an inherent consequence of the transplantation process. Causes of marked posttransplantation hypertension in cats with chronic kidney disease require further investigation.
Objective—To compare 2 techniques of inducing
combined renal insufficiency and systemic hypertension
Animals—22 cats 6 to 12 months of age.
Procedure—Cats were randomly assigned to 1 of 3
groups. Control (C) group cats had 2 intact kidneys,
remnant kidney (RK) group cats underwent unilateral
partial renal infarction and contralateral nephrectomy,
and remnant-wrap (W) group cats underwent unilateral
partial renal infarction and partial abtation and wrapping
of the contralateral kidney. Systemic arterial blood
pressure (BP) was measured continuously by use of
implanted radiotelemetric devices. Renal function was
assessed via determination of glomerular filtration
rate, measurement of serum creatinine and BUN concentrations,
and determination of urine protein-to-creatinine
ratio (UP/C). Serum aldosterone concentration
and plasma renin activity were measured on day 75.
Results—Systolic BP was significantly higher in
groups RK and W than in group C, and systolic BP
was significantly higher in group W than in group RK.
Serum aldosterone concentration and plasma renin
activity were significantly higher in group W, compared
with groups C and RK. Glomerular filtration rate
was significantly lower in groups RK and W, compared
with group C. Histologic indices of renal injury
and UP/C were significantly higher in group W, compared
with groups C and RK.
Conclusions and Clinical Relevance—Hypertensive
renal insufficiency in group W was characterized by
marked sustained systemic hypertension, decreased
renal function, proteinuria, activation of the reninangiotensin-aldosterone axis, and renal structural
injury. Results support the hypothesis that marked
systemic hypertension, activation of the reninangiotensin-
aldosterone axis, and proteinuria may
damage the kidney of cats with preexisting renal
insufficiency. ( Am J Vet Res 2004;65:1006–1013)
Objective—To determine whether amlodipine besylate
decreases systemic arterial blood pressure (BP)
and reduces the prevalence of complications in cats
with induced hypertensive renal insufficiency.
Animals—20 cats with partial nephrectomy.
Procedure—Following reduction in renal mass, 10
cats were administered 0.25 mg of amlodipine/kg,
PO, q 24 h (group A). Ten cats served as a control
group (group C). Systolic BP (SBP), diastolic BP (DBP),
and mean BP (MBP), physical activity, and pulse rate
were measured continuously for 36 days by use of
Results—Compared with values for clinically normal
cats, SBP, DBP, and MBP were significantly increased
in cats of group C. Cats in group A had significant
reductions in SBP, DBP, and MBP, compared with values
for cats in group C. Albuminuria but not urine protein-
to-creatinine ratio was significantly correlated
( R2 = 0.317) with SBP in hypertensive cats.
Prevalence of ocular lesions attributable to systemic
hypertension in group C (7 cats) was greater than that
observed in group A (2). Two cats in group C were
euthanatized on day 16 because of nuerologic complications
attributed to systemic hypertension. One normotensive
cat in group A was euthanatized because
of purulent enteritis of unknown cause on day 27.
Conclusion and Clinical Relevance—Amlodipine
had an antihypertensive effect in cats with coexistent
systemic hypertension and renal insufficiency. Its use
may improve the prognosis for cats with systemic
hypertension by decreasing the risk of ocular injury or
neurologic complications induced by high BP. (Am J
Vet Res 2002;63:833–839)
Objective—To determine whether administration of
Crandell-Rees feline kidney (CRFK) cell lysates or vaccines
against feline viral rhinotracheitis, calicivirus,
and panleukopenia (FVRCP vaccines) that likely contain
CRFK cell proteins induces antibodies against
CRFK cell or feline renal cell (FRC) lysates in cats.
Animals—14 eight-week-old cats.
Procedure—Before and after the study, renal biopsy
specimens were obtained from each cat for histologic
evaluation. Each of 4 FVRCP vaccines was administered
to 2 cats at weeks 0, 3, 6, and 50. Between
weeks 0 and 50, another 3 pairs of cats received 11
CRFK cell lysate inoculations SC (10, 50, or 50 µg
mixed with alum). Clinicopathologic evaluations and
ELISAs to detect serum antibodies against CRFK cell
or FRC lysates were performed at intervals.
Results—Cats had no antibodies against CRFK cell
or FRC lysates initially. All cats administered CRFK
cell lysate had detectable antibodies against CRFK
cell or FRC lysates on multiple occasions. Of 6 cats
vaccinated parenterally, 5 had detectable antibodies
against CRFK cell lysate at least once, but all 6 had
detectable antibodies against FRC lysate on multiple
occasions. Cats administered an intranasal-intraocular
vaccine did not develop detectable antibodies
against either lysate. Important clinicopathologic or
histologic abnormalities were not detected during
Conclusions and Clinical Relevance—Parenteral
administration of vaccines containing viruses likely
grown on CRFK cells induced antibodies against
CRFK cell and FRC lysates in cats. Hypersensitization
with CRFK cell proteins did not result in renal disease
in cats during the 56-week study. (Am J Vet Res 2005;66:506–511)