Page 1167 - Clinical Small Animal Internal Medicine

121 Glomerular Disease 1105

diets that are reduced in potassium or administering an pressure but also assessing the patient for target organ
VetBooks.ir intestinal potassium binder (e.g., kayexelate). If the target damage, evaluating for conditions that may contribute to
hypertension and determining if any concurrent condi-
reduction in UPC is not achieved and the dog does not
have the before mentioned adverse effects, the dosages
present. Personal preference and experience should dic-
may be increased every 4–6 weeks. tions that may complicate antihypertensive therapy are
tate how the blood pressure is measured; however, the
Modified Dietary Intake substaging by arterial blood pressure system that has
Modification of dietary intake has a central role in the been proposed by the International Renal Interest Society
management of all dogs with kidney disease and has (IRIS) should be used to guide therapy (Table 121.2).
been associated with delaying spontaneous progression Antihypertensive therapy should be initiated when the
of kidney disease and reducing the magnitude of protein- blood pressure exceeds 160 mmHg systolic or 100 mmHg
uria. It is well known that fat content of a diet can affect diastolic (i.e., AP2 or above). The goal of therapy is to
renal outcome. Most commercially available renal diets reduce the blood pressure to less than 150 mmHg sys-
are modified with respect to polyunsaturated fatty acids tolic or 96 mmHg diastolic (i.e., AP0). Lowering the
(PUFA) content with the goal of slowing progression and blood pressure is not an emergency unless there is severe
reducing proteinuria. The consensus recommendation is ocular or central nervous system target organ damage. In
that dogs with glomerular disease should be fed a diet most cases, blood pressure reduction can be achieved
with a reduced n‐6:n‐3 PUFA ratio of approximately 5:1. gradually over a period of several weeks. Effective treat-
It is unknown if there is any additional benefit of supple- ment of hypertension should lead to a concomitant
menting n‐3 PUFA when this ratio is already being pro- reduction in the magnitude of proteinuria in dogs with
vided via the diet. If supplementation is chosen, care glomerular disease. Feeding a salt‐restricted diet alone
should also be taken to provide adequate antioxidants will not lower the blood pressure into the target range
(e.g., vitamin E). Dogs with glomerular disease should be but it may enhance the antihypertensive effects of the
fed modified protein diets because this has been shown inhibitors of RAAS, generally ACEi. However, ACEi are
to reduce proteinuria and slow progression. generally only associated with a 10–15% reduction in
Lastly, the sodium chloride content should be reduced blood pressure. This reduction may be all that is needed
in diets fed to dogs with glomerular disease. Salt restric- for dogs that are only moderately hypertensive (i.e.,
tion may enhance the beneficial effects of agents used to AP2). Dogs that are severely hypertensive (i.e., AP3)
inhibit RAAS and help reduce fluid retention. should have a calcium channel blocker (i.e., amlodipine)
added to their RAAS inhibition therapy. Alternatively,
Antithrombotic Therapy telmisartan can be used as a single agent to manage
Hypercoagulability is a complication of protein‐losing hypertension and proteinuria.
glomerular diseases and thromboembolism can occur in The consensus recommendation is that dogs with IRIS
as many as 25% of dogs with glomerular disease. The chronic kidney disease stages 1 or 2 should have blood
pathogenesis of hypercoagulability in glomerular disease pressure evaluated 3–14 days after any change in antihy-
is complex and incompletely understood. Urinary loss pertensive therapy whereas those in stages 3 or 4 should
of antithrombin has long been given as the explanation
but in reality, the pathogenesis is more complex than Table 121.2 International Renal Interest Society substaging by
this and probably includes vascular stasis as well arterial blood pressure
as increased platelet aggregation, plasma procoagulant
factors, and fibrinogen concentrations. Unfortunately, Systolic blood pressure Substage
serum albumin concentrations, antithrombin activity,
and UPC cannot be used in isolation to predict hyperco- <150 mmHg Normotensive, Minimal Risk
agulability in individual patients. It follows then that it 150–159 mmHg Borderline hypertensive, Mild
remains unclear when to implement thromboprophy- Risk
laxis. Consensus recommendations call for the daily 160–179 mmHg Hypertensive, Moderate Risk
administration of low‐dose aspirin (1–5 mg/kg/day) in >180 mmHg Severely hypertensive, Severe
dogs with protein‐losing glomerular diseases. Clopidogrel Risk
may be an effective alternative.
No evidence of end‐organ nc (no complications)
damage
Antihypertensive Therapy Evidence of end‐organ c (complications)
All dogs with glomerular disease should undergo repeat damage
evaluation for systemic hypertension. This evaluation Blood pressure not measured RND (risks not determined)
should not only include measurement of systemic blood