Hypertension is a well-recognized complication of CRF in both dogs and cats. The most profound clinical effect of hypertension
in cats is hypertensive retinopathy. Jacob et al (2002) reported that systemic hypertension is a risk factor for rapid progression of renal failure, a greater magnitude of proteinuria, and decreased survival time among
dogs with spontaneous CRF. Based on results from this clinical study, the frequency and magnitude of hypertension in dogs
with spontaneous CRF appears to be greater than that in dogs following induced renal failure model. This raises concerns about
clinical applicability of this model. While induced models of CRF have failed to provide evidence for progression of CRF in
cats, clinical studies generally confirm the progressive nature of spontaneous CRF in cats. The effects of systemic hypertension
on progression of renal failure and survival times in cats with CRF have not been reported yet. Nonetheless, it is presumed
that the effects on renal function and survival times in cats will be similar.
The general consensus of the definition of hypertension in dogs is a systolic blood pressures (bp) >160 mm Hg. The Hypertension
Consensus Group report in 2002 classified risks associated with systolic blood pressure in cats. The consensus was a systolic
bp < 150 mm Hg was associated with minimal risk; systolic bp of 150-159 mm Hg was associated with low risk; a systolic bp
of 160-179 mm Hg was associated with moderate risk; and a systolic bp of>180 mm Hg was associated with severe risk.
Such as enalopril and benazopril, currently appear to be the drugs of choice for managing hypertension in dogs. ACE inhibitors were found be superior to calcium channel blockers for renoprotective effects in dogs with induced diabetes mellitus, and they reduce proteinuria and slow development of lesions in dogs with reduced renal mass.
Amlodipine, a calcium channel antagonist, currently appears to be the drug of choice for managing hypertension in cats. It has been shown to be effective for lowering blood pressure in at least one clinical trial (Snyder, 1998). In contrast,
ACE inhibitors and-blocking drugs do not appear as effective in lowering blood pressure in cats.
Uremic gastritis is characterized by glandular atrophy, edema of the lamina propria, mast cell infiltration, fibroplasia,
mineralization, and submucosal arteritis. Clinically, as the severity of azotemia worsens, uremic signs of vomiting, nausea,
and anorexia develop. Although some of these clinical signs may be the result of uremic toxins on the medullary emetic chemoreceptor
trigger zone (CRT), uremic gastritis may also contribute to these problems.
Cats with CRF have been shown to have increased serum gastrin concentrations, which contribute to the pathogenesis of uremic
gastritis. Although vomiting is a frequent, but inconsistent finding in uremic dogs, many cats with uremic gastritis show
only partial to complete anorexia as the clinical signs rather than vomiting. Besides anorexia and vomiting, uremic gastritis
may also result in gastrointestinal bleeding. Unfortunately, uremic gastritis is often not addressed by veterinarians until
a dog is vomiting or a cat is anorexic. It is recommended to be more proactive in treatment of this problem in dogs and cats
to lesson the likelihood that clinical signs will develop. A general recommendation is to administer an H
receptor antagonist, such as ranitidine or famotidine to patients with CRF once serum creatinine levels are above 3.0 mg/dl and prior to the
onset of any clinical signs. In the United States, ranitidine and famotidine can be purchased by a client without a prescription.
Recommended dosages are: