Angiotensin converting enzyme (ACE) inhibitors (e.g., enalapril, benazepril) reduce glomerular capillary hydraulic pressure by decreasing postglomerular arteriolar resistance and, thus, reduce proteinuria. This beneficial effect must be balanced against their potential to worsen azotemia. In one study, enalapril (0.5 mg/kg PO every 12-24 hours) reduced proteinuria (as assessed by urine protein-to-creatinine ratio), reduced blood pressure, and slowed progression of renal disease in dogs with GN.
CAFNAU
Minimal risk of toxicity with benazepril because of non-renal elimination.
Lefebvre, H.P., et al. (1999). Effects of renal impairment on the disposition of orally administered enalapril, benazepril, and their active metabolites.
A number of studies have been performed in human patients with chronic kidney disease that indicate treatment with angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARB) may be superior to treatment with other anti-hypertensive agents, and that this is due to greater reduction in urinary protein excretion that occurswith these drugs (Maschio et al. 1996; Agodoa et al. 2001). The ACE-inhibitor benazepril has been shown to reduce glomerular capillary pressure in cats with experimentally reduced renal mass (Brown et al. 2001). The anti-proteinuric effect of benazepril has been demonstrated in clinical cases of naturally occurring chronic kidney disease (King et al. 2006; Mizutani et al. 2006). Asmight be expected, reduction in proteinuria is greatest in those patients that aremost proteinuric before treatment (King et al. 2006;Mizutani et al. 2006). Unfortunately, despite the demonstrated efficacy of ACE-inhibitors in reducing proteinuria, demonstrable benefit in terms of increased survival times (King et al. 2006), or reduction in the number of cats with an increase in the severity of azotaemia over a follow-up period of 6 months (Mizutani et al. 2006), could not be demonstrated, although favorable trends were evident in both studies. These results are disappointing. It is possible that clear benefit to ACE-inhibitor therapy could be demonstrated by carefully selecting the population that was studied to include only cats thatwere grossly proteinuric, had mild azotaemia at the study outset and allowing for a prolonged period of follow-up.However, if this were the case, it would not be representative of many cats with chronic kidney disease.
NAUSEA
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