Efficacy and Safety of Benazepril for Advanced Chronic Renal Insufficiency

Hou, Fan Fan; Zhang, Xun; Zhang, Guo Hua; Xie, Di; Chen, Ping Yan; Zhang, Wei Ru; Jiang, Jian; Liang, Min; Wang, Guo Bao; Liu, Zheng Rong; Geng, Ren Wen

doi:10.1056/nejmoa053107

Cited by 599 publications

(464 citation statements)

References 19 publications

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“…21 The subsequent study, however, has shown that benazepril effectively prevents the progression of CKD with baseline serum creatinine levels between 3.0 and 5.0 mg dl À1 . 27 In the current analysis, we actually observe a more favorable effect of candesartan on renal survival than that of amlodipine in stage 4 ( Figure 4). A similar observation was documented in the IDNT Study, showing that irbesartan improved renal survival, whereas amlodipine failed to prevent the progression of CKD.…”

Section: Arb Vs Ca Antagonist In Ckdsupporting

confidence: 47%

Effects of candesartan and amlodipine on cardiovascular events in hypertensive patients with chronic kidney disease: subanalysis of the CASE-J Study

et al. 2009

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We examined the effects of candesartan and amlodipine on cardiovascular events in hypertensive patients with chronic kidney disease (CKD) using the data from the Candesartan Antihypertensive Survival Evaluation in Japan (CASE-J) trial. CKD was defined as proteinuria and/or decreased GFR (o60 ml per min per 1.73 m 2 ) at enrollment. Among 2720 subjects with CKD, there were 1376 and 1344 patients in the candesartan and the amlodipine group, respectively. During a 3.2-year follow-up, cardiovascular event rate did not differ in the two groups (7.2% for candesartan and 7.6% for amlodipine). In the subgroup analysis based on the CKD stage, there were no significant differences in the incidence rates of cardiovascular events between the two groups in stages 1+2 and 3 CKD. In stage 4 CKD, however, candesartan reduced the incidence of cardiovascular events (55% risk reduction), particularly of renal events (81% risk reduction), compared with amlodipine. Furthermore, composite cardiovascular events were increased as the CKD stage progressed, and this effect was exaggerated in the presence of proteinuria. Finally, the new onset of diabetes was less in the candesartan-based regimen in stage 3 CKD. In conclusion, candesartan protected hypertensive patients with CKD more potently against renal events, particularly in moderately-to-severely impaired CKD. Furthermore, candesartan prevented a new onset of diabetes in CKD, which would be favorable for the long-term management of CKD.

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Section: Arb Vs Ca Antagonist In Ckdsupporting

confidence: 47%

Effects of candesartan and amlodipine on cardiovascular events in hypertensive patients with chronic kidney disease: subanalysis of the CASE-J Study

et al. 2009

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“…Antagonism of the RAA system using ACE inhibitors or ANG receptor blockers corrects hypertension and suppresses the progression of chronic renal failure [5,8]. Since the advent of ACE inhibitors, various types of ACE inhibitor have been developed and, along with ANG receptor blockers, have become mainstay conservative treatments for chronic renal failure in humans [8,18,35,42]. Effects of such ACE inhibitors as enalapril and benazepril on renal failure are also being recognized in dogs and cats [9,10,15].…”

Section: Discussionmentioning

confidence: 99%

Development of Hypertension and Effects of Benazepril Hydrochloride in a Canine Remnant Kidney Model of Chronic Renal Failure

Mishina

Watanabe

2008

The Journal of Veterinary Medical Science

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ABSTRACT. In order to determine whether hypertension would develop in dogs with chronic renal failure, we performed 7/8 renal ablation in 6 healthy dogs and compared pre-and post-ablation blood pressures determined by telemetry. One month after the renal ablation, blood urea nitrogen and creatinine were significantly increased (p<0.05), creatinine clearance was decreased (p<0.05), and blood pressure was increased significantly (p<0.05). Simultaneously, plasma renin activity, angiotensin I and II, and aldosterone were elevated significantly (p<0.05) compared with the values obtained from 11 healthy dogs with intact renal function. The dogs with induced renal failure and hypertension were administered an angiotensin-converting enzyme inhibitor, benazepril hydrochloride, once daily for 2 weeks at 2 mg/kg body weight, and changes in blood pressure and the renin-angiotensin-aldosterone (RAA) system were determined. During the administration of benazepril hydrochloride, blood pressure, angiotensin II and aldosterone decreased significantly (p<0.05) and, upon discontinuation of administration, increased to the pre-administration levels (p<0.05). Plasma renin activity and angiotensin I showed no significant changes throughout the administration study. These results provide experimental evidence that hypertension develops in dogs with chronic renal failure through mechanisms involving the RAA system and demonstrate that benazepril hydrochloride improves renal hypertension in dogs. KEY WORDS: angiotensin-converting enzyme inhibitor, benazepril, canine, renal ablation, renal hypertension.J. Vet. Med. Sci. 70 (5): [455][456][457][458][459][460] 2008 Hypertension is classified into essential and secondary hypertension and, in humans, essential hypertension accounts for 80 to 90% of hypertension patients [24]. In contrast, essential hypertension is relatively rare in veterinary practice [7,33]. Underlying reasons are that hypertension per se has no characteristic symptoms and blood pressure is not routinely determined in veterinary practice. Therefore, it is important to diagnose diseases that would lead to secondary hypertension and to identify the risk of developing secondary hypertension. Causes of secondary hypertension include renoparenchymal diseases, renovascular diseases, diabetes, Cushing syndrome, primary hyperaldosteronism, pheochromocytoma and hypothyroidism and, of those, renoparenchymal disease-associated hypertension is most common in humans [24]. The mechanism of renal hypertension is thought to involve renal insufficiency-associated body fluid retention, increases in cardiac output and peripheral vessel resistance, activation of the renin-angiotensin-aldosterone (RAA) system and suppression of the kallikrein-kinin-prostaglandin system [2,3,17].A link between chronic renal failure and hypertension has been suggested in dogs and cats [1,6,12,13,22,26,27,29,30,34,[36][37][38]. Activation of the RAA system and development of hypertension in association with renal failure have been reported in cats [20,30,41]. ...

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“…Smadconnective tissue growth factor (CTGF) pathways transmit TGF-b1 receptor signalling to regulate the expression of profibrotic genes and the epithelial-to-mesenchymal transition in tubular cells (Liu, 2010). Currently, pharmacological intervention with angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists provide only partial renoprotection in diabetes and non-diabetes CKD by reducing glomerular and tubulointerstitial damage (mesangial activation, podocyte injury, tubulointerstitial injury and inflammatory cell infiltration) (Brenner et al, 2001;Izuhara et al, 2005;Hou et al, 2006). Efforts to explore other potential agents to achieve more comprehensive renoprotection are essential.…”

Section: Introductionmentioning

confidence: 99%

Honokiol ameliorates renal fibrosis by inhibiting extracellular matrix and pro‐inflammatory factors in vivo and in vitro

Chiang

Sheu

Lin

et al. 2011

British J Pharmacology

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BACKGROUND AND PURPOSE Renal fibrosis acts as the common pathway leading to the development of end-stage renal disease. The present study investigated, in vivo and in vitro, the anti-fibrotic and anti-inflammatory effects, particularly on the epithelial to mesenchymal transition of renal tubular cells, exerted by honokiol, a phytochemical used in traditional medicine, and mechanisms underlying these effects. EXPERIMENTAL APPROACH Anti-fibrotic effects in vivo were assayed in a rat model of renal fibrosis [the unilateral ureteral obstruction (UUO) model]. A rat tubular epithelial cell line (NRK-52E) was stimulated by transforming growth factor-beta 1 (TGF-beta 1) and treated with honokiol to explore possible mechanisms of these anti-fibrotic effects. Gene or protein expression was analysed by Northern or Western blotting. Transcriptional regulation was investigated using luciferase activity driven by a connective tissue growth factor (CTGF) promoter. KEY RESULTS Honokiol slowed development of renal fibrosis both in vivo and in vitro. Honokiol treatment attenuated tubulointerstitial fibrosis and expression of pro-fibrotic factors in the UUO model. Honokiol also decreased expression of the mRNA for the chemokine CCL2 and for the intracellular adhesion molecule-1, as well as accumulation of type I (alpha 1) collagen and fibronectin in UUO kidneys. Phosphorylation of Smad-2/3 induced by TGF-beta 1 and CTGF luciferase activity in renal tubular cells were also inhibited by honokiol. CONCLUSIONS AND IMPLICATIONS Honokiol suppressed expression of pro-fibrotic and pro-inflammatory factors and of extracellular matrix proteins. Honokiol may become a therapeutic agent to prevent renal fibrosis

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Efficacy and Safety of Benazepril for Advanced Chronic Renal Insufficiency

Abstract: Benazepril conferred substantial renal benefits in patients without diabetes who had advanced renal insufficiency. (ClinicalTrials.gov number, NCT00270426.)

Cited by 599 publications

References 19 publications

Effects of candesartan and amlodipine on cardiovascular events in hypertensive patients with chronic kidney disease: subanalysis of the CASE-J Study

Effects of candesartan and amlodipine on cardiovascular events in hypertensive patients with chronic kidney disease: subanalysis of the CASE-J Study

Development of Hypertension and Effects of Benazepril Hydrochloride in a Canine Remnant Kidney Model of Chronic Renal Failure

Honokiol ameliorates renal fibrosis by inhibiting extracellular matrix and pro‐inflammatory factors in vivo and in vitro

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