Selected additional therapy
About 10-15% of cats with CPRD will be hypertensive at the time of diagnosis and another similar number will become hypertensive
during the progression of the disease. If hypertension (MSP = > 160 mmHg) is present, the treatment of choice is amlodipine.
The usual starting dose for amlodipine is 0.625 mg/cat PO q24h. The blood pressure (BP) should be checked after a week of
therapy and the dose may be increased if the desired effect is not observed. Reassessment of BP should be part of the patient
assessment on each subsequent follow up visit to assure that the BP remains under good control and to adjust medications as
Hypokalemia can lead to muscle weakness, gastrointestinal hypomotility, and other problems. Hypokalemic patients should receive
potassium gluconate supplementation, 2-4 mEq PO q12h. There is no clear evidence that hypokalemia contributes to the progression
of renal insufficiency but renal insufficiency definitely can lead to renal potassium wasting and hypokalemia. Many forms
of potassium supplement are available including flavored powders to add to food, tablets (chewable and non-chewable), and
oral gel. Potassium levels should be checked at subsequent follow up visits. If the cat is significantly acidemic, potassium
citrate (15-30 mg/kg or 2.5 mEq q12h) can be used as both a potassium supplement and alkalinizing agent for initial therapy.
Cats with persistent hypokalemia in spite of aggressive K supplementation, particularly if also hypertensive, should be checked
Although most laboratories set the normal value for the feline urine protein/creatinine (UPC) ratio at < 1.0, recent studies
have shown that normal cats should have a ratio of < 0.4. Cats with CPRD and an elevated UPC may benefit from treatment with
an ACE inhibitor such as benazepril (Lotensin) – 0.5 – 1.0 mg/kg PO q24h). There is presently no evidence that ACE inhibitors
improve survival or slow the progression of non-proteinuric renal disease in cats. The ERD test is a reasonable screening
test for proteinuria but high level results should be followed with a UPC because this is more quantitative and sensitive
to smaller changes in urinary protein excretion.
Other adjunctive therapies
There has been a lot of advertising and interest in adjunctive therapies with agents such as epakitin and Azodyl. I agree
with Dr. Larry Nagode's comments about these agents
"Azodyl use is intended to modify the intestinal bacterial population into species of bacteria that will metabolize urea and
creatinine thus lowering their blood levels as certain amounts are circulating through the gut and normally getting reabsorbed
to blood. This is at least part of the supposedly beneficial role they play but of course it would only be so if other "true"
uremic toxins were similarly metabolized by the new population of gut bacteria as again neither urea nor creatinine are toxins
in any way. They are just handy "markers" of extent of deficit of GFR and use of Azodyl in my view ruins their normal utility
as markers of GFR deficit.
Epakitin in some of the company literature one can find is touted as a Pi binder (only the calcium carbonate contained in
Epakitin could do this and I've been told there is so little calcium carbonate that it would not produce hypercalcemia if
used together with calcitriol)—therefore since it takes a LOT of calcium carbonate to be anywhere near as effective as the
much superior binder Al-hydroxide, I have to conclude Epakitin is a VERY POOR gut Pi binder(and the chitin which binds urea
and creatinine does not bind Pi at all by any literature I can find). A poor binder that is in comparison to much lower doses
of Al-hydroxide thats very cheap and very available.
The chitin in Epakitin in some of the literature I have seen is touted to bind urea and creatinine thus improving CRF patients
status. This again is a "false" improvement in my view again as neither of these chemicals is toxic. I feel both Epakitin
and Azodyl are best considered as masterpieces of marketing of possibly questionable real use in therapy of CRF in dogs and
cats—although veterinary users through a profit sharing arrangement with Vetoquinol involving a retail "markup" can turn a
tidy profit by prescribing them for clients. I say this in part because of lack of data I am aware of that Azodyl removes
"real" uremic toxins from patients guts and "word of mouth" I have heard that this perturbation of the normal intestinal bacterial
flora in these patients has often led to significant diarrheal and other intestinal "upset" problems—how often this has been
so I have no idea. Vetoquinol marketed Epakitin first and Azodyl more recently so that the "urea and creatinine lowering"
capacity originally being part of the justification for use of Epakitin is now the rationale for added use of Azodyl. Why
sell clients one product when you can sell them two??. My cynicism with respect to these products may well be misplaced and
they may well be outstanding wonderful products for our dogs and cats—but until I can find data that solidly supports this
view I remain skeptical."-Larry Nagode