ACE Inhibitors and CRF Cats
From the Diplomates
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I emailed 52 Diplomates of the American Board of Veterinary Practice certified in Feline Practice on 1/1/03, asking for their thoughts on the use of ACE inhibitors and calcitriol to treat feline CRF. Following are their responses. |
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Dear David, I'd like to address the Q of benazepril use in renal insufficiency. Because ACE inhibitors work by increasing the blood flow within the kidney, it would seem like they would play a beneficial role in improving the health of remaining nephrons. However, by detouring the blood through the renal tissue, it is diverted from the glomeruli, where blood is filtered and becomes urine. Thus, while increasing RENAL blood flow, ACEI decrease GLOMERULAR FILTRATION. So, it might not be a good thing. What we have to try to remember, is that there are different causes for kidney insufficiency in cats despite the fact that they look identical clinically (PU/PD, dehydration, muscle wasting, lethargy). The place where ACEI may be beneficial is in the group of conditions that cause protein to be lost from the body, through the glomeruli, into the urine. By diverting blood, less flows through the glomeruli and therefore, less protein is lost into the urine. The vast majority of cases of renal insufficiency in cats are caused by chronic interstitial nephritis, however. A very large, long-term study is currently underway by the BENRIC group, funded by Novartis, to look at the effects of using benazepril in cats with chronic renal insufficiency (CRI). A midpoint, interim report was given at the World Small Animal Veterinary Association Congress in September of 2002 in Spain. The conclusion is very important i.e. a) that using benazepril or not didn't make any significant difference and also b) that it may be helpful in cats with protein losing glomerulonephropathies, which are extremely rare. I don't know about other ABVP feline practitioners, but I haven't diagnosed more than 2 cats with this condition in over 20 years of practice, 16 of which have been 100% feline. The paper referred to (Scott Brown) is using the surgical remnant kidney model in which cats with normal renal function undergo surgical removal of one kidney and 3/4 of the remaining kidney leaving them with 1/4 (or it might even only be 5/6th) of a kidney left. Needless to say, this does not mirror the natural development of declining kidney function that our cats experience as they become older. Effect of Benazepril in Chronic Renal Insufficiency in Cats: Interim Results from the Benric Clinical Trial *J.N.King, A. Font, for the BENRIC Study Group, Novartis Animal Health Inc OBJECTIVES
MATERIALS
RESULTS
I hope this raises a few points to ponder. Happy New Year! Margie
Scherk DVM, DABVP (feline) http://www.vin.com/promo/Consultants/consultant1.htm]
Cindy Cynthia
L. Bowlin DVM http://www.ncvei.org/BiographyDetail.asp?ID=26]
Sisson also presented some data on aldo levels in dogs and cats with cardiomyopathy at the WSAVA as well as the effects of ACE inhibitors on aldo levels in those species. Perhaps there is an opportunity to look at both cardiac disease and renal disease together and the effects that hemodynamics and neuroendocrine pathways play in multiple disease processes . Finally, with respect to Scott Brown's renal model. I think is early to be too harsh with respect to what his model does or doesn't demonstrate. The model seems to be excellent for inducing robust hypertension in cats and assessing the ability of various pharmaceuticals to control that hypertension. In my opinion, how well the model exemplifies chronic renal disease in cats or how effective the model will be in predicting the effects of pharmaceuticals on the management of renal disease is still to be assessed. I know Scott would consider this to be a work in progress. I give him tremendous credit for being a leader in attempting to understand the underlying physiologic mechanisms responsible for inducing renal disease in cats. DKR
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