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Re: [CRF] crf-heart medication and effects on the kidneys

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  • Maud Essen
    Please note that this is information regarding human patients, not feline patients, and that not all information is known to transfer between species.
    Message 1 of 2 , Jan 24, 2001
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      Please note that this is information regarding human patients, not
      feline patients, and that not all information is known to transfer
      between species. According to a veterinary document called Clinical
      Cardiology Concepts for Dogs and Cats at
      for example, ACE inhibitors are not proven to provide feline heart
      patients with any benefit. So be sure to take this human page with a
      grain of salt. Maud and Tripod (and Motley)

      At 8:25 PM -0500 1/24/01, Anyes Moscrip wrote:
      >Here is a good web page explaining crf, and the effect of blood pressure
      >and medications on crf. It has lots more info on various aspects of crf
      >beside the cardiac medications.
      >Anyes, angel Lucie, Georgina and Angelica
      >Here are some highlights:
      >Whereas BP control with any agent appears to slow the progression of
      >renal disease, there is mounting evidence that ACE inhibitors are more
      >renoprotective than other antihypertensive agents. Some calcium channel
      >blockers (CCBs) may also have renoprotective properties. Other
      >antihypertensive drugs should
      > be added if monotherapy with ACE inhibitors does not lower BP
      >adequately. Also, other agents should be used if ACE inhibitor-related
      >adverse effects cannot be overcome. Adequate BP control, no matter how
      >it is accomplished, is better than uncontrolled hypertension.[10]
      >Use of ACE inhibitors. The renoprotective effect of ACE inhibitors
      >appears to be independent of their antihypertensive action. These drugs
      >decrease proteinuria and delay the progression of renal disease.
      >Although initial data were acquired in patients with diabetic
      >nephropathy (DN), encouraging results have
      > also been obtained in nondiabetics with renal disease. The salutary
      >effects of ACE inhibitors may be related to their ability to dilate
      >efferent arterioles, thereby reducing intraglomerular pressure. The
      >beneficial effects may also be the result of the restoration of
      >glomerular permselectivity in proteinuric
      > nephropathies.[11,12] This may explain why ACE inhibitors delay the
      >progression of renal disease in normotensive diabetics with
      >The largest study conducted in patients with IDDM and microalbuminuria
      >showed that captopril, relative to placebo, reduced the progression to
      >overt proteinuria by 75%.[14] In a landmark study of patients with IDDM,
      >overt nephropathy, and serum creatinine values <2.5 mg/dL, captopril,
      >relative to other
      > antihypertensives, significantly reduced the doubling of serum
      >creatinine values and the progression to ESRD.[15] Based on these
      >findings, most authorities recommend the use of ACE inhibitors in both
      >hypertensive and normotensive patients with IDDM and any degree of DN.
      >Primary care physicians often hesitate to prescribe ACE inhibitors in
      >patients with renal failure, mainly because they fear provoking adverse
      >reactions such as the acute worsening of renal function and
      >hyperkalemia. However, acute renal failure occurs primarily in a
      >subgroup of patients with bilateral renovascular disease or in those who
      >have decreased effective circulating volume. Provided that renal
      >function is monitored in such patients after initiation of ACE inhibitor
      >therapy, there is no contraindication to starting therapy since the
      >renal dysfunction is reversible. The same considerations apply to the
      >risk of hyperkalemia. In the AIPRI study, of 300 patients given
      >benazepril, three had a rapid increase in serum creatinine requiring
      >drug withdrawal and five developed clinically significant
      >hyperkalemia.[16] Neither adverse event occurred significantly more
      >often in the benazepril group than in the placebo group.
      >Use of calcium channel blockers. Although not as well studied as the ACE
      >inhibitors, CCBs may also have renoprotective properties. The mechanism
      >of this protective effect may differ between the dihydropyr-idines (eg,
      >amlodipine, nifedipine, felodipine) and other CCBs such as verapamil or
      >diltiazem. The latter two drugs may reduce intraglo-merular pressure in
      >a manner similar to that of ACE inhibitors; studies in patients with
      >renal disease have shown that these drugs, as compared with the ß
      >blocker atenolol, led to a greater reduction in proteinuria and a slower
      >progression of renal disease. One study has demonstrated an additive
      >reduction in proteinuria when a low-dose ACE inhibitor and verapamil
      >were combined.
      >There is a web page that explains all this. Check the following link
      >for more info:
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      >All messages sent to feline-crf-support@egroups.com are Copyright
      >2001 by the original author. Do not forward or excerpt to another
      >group or nonmember without the author's permission.
      >Any medical advice given on this list is an opinion of the author. Please
      >verify all treatment plans with a qualified veterinarian.
      >Shortcut URL to this page:
      > http://www.egroups.com/community/Feline-CRF-Support

      Maud Essen
      Essential Services
      4163 West Pine Boulevard
      Saint Louis, MO 63108-2801

      314.531.8098 (voice)
      314.535.5119 (fax)
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