Should β-Blockers Be Used to Control Hypertension in People With Chronic Kidney Disease?

Hart, Peter D.; Bakris, George L.

doi:10.1016/j.semnephrol.2007.07.003

Cited by 28 publications

(22 citation statements)

References 83 publications

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“…The authors concluded that the beneficial effect of carvedilol may be related to an ability to reduce oxidative stress. It is suggested that nebivolol, like carvedilol, may also have renal-protective effects because of the beneficial effects of this drug to improve bioavailable endothelial derived NO and reduce oxidative stress [51]. Our results within vivonebivolol treatment in transgenic rats are commensurate with this notion.…”

Section: Discussionsupporting

confidence: 81%

Nebivolol Attenuates Maladaptive Proximal Tubule Remodeling in Transgenic Rats

Hayden

Habibi²,

Whaley‐Connell³

et al. 2010

Am J Nephrol

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Background/Aims: The impact of nebivolol therapy on the renal proximal tubular cell (PTC) structure and function was investigated in a transgenic (TG) rodent model of hypertension and the cardiometabolic syndrome. The TG Ren2 rat develops nephropathy with proteinuria, increased renal angiotensin II levels and oxidative stress, and PTC remodeling. Nebivolol, a β₁-antagonist, has recently been shown to reduce albuminuria, in part, through reductions in renal oxidative stress. Accordingly, we hypothesized that nebivolol therapy would attenuate PTC damage and tubulointerstitial fibrosis. Methods: Young Ren2 (R2-N) and SD (SD-N) rats were treated with nebivolol (10 mg/kg/day) or vehicle (R2-C; SD-C) for 3 weeks. PTC structure and function were tested using transmission electron microscopy and functional measurements. Results: Nebivolol treatment decreased urinary N-acetyl-β-D-glucosaminidase, tubulointerstitial ultrastructural remodeling and fibrosis, NADPH oxidase activity, 3-nitrotyrosine levels, and increased megalin and lysosomal-associated membrane protein-2 immunostaining in PTCs. Ultrastructural abnormalities that were improved with therapy included altered canalicular structure, reduced endosomes/lysosomes and PTC vacuoles, basement membrane thickening, and mitochondrial remodeling/fragmentation. Conclusion: These observations support the notion that nebivolol may improve PTC reabsorption of albumin and other glomerular filtered small molecular weight proteins in association with the attenuation of oxidative stress, tubulointerstitial injury and fibrosis in this rat model of metabolic kidney disease.

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Section: Discussionsupporting

confidence: 81%

Nebivolol Attenuates Maladaptive Proximal Tubule Remodeling in Transgenic Rats

Hayden

Habibi²,

Whaley‐Connell³

et al. 2010

Am J Nephrol

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“…49 Although animal models indicate that sympathetic denervation of the kidneys can provide renoprotective effects, 50 there is little evidence that centrally or peripherally acting sympatholytics have unique renoprotective effects in humans. 51 Rather than suggesting a change in clinical practice, we hope our findings will encourage further research to better define the putative role of the autonomic nervous system in precipitating and exacerbating renal disease in humans; this, in turn, may ultimately lead to novel therapeutic approaches once the mechanisms for our findings are better characterized. …”

Section: Discussionmentioning

confidence: 96%

Heart Rate Variability Predicts ESRD and CKD-Related Hospitalization

Brotman¹,

Bash²,

Qayyum³

et al. 2010

Journal of the American Society of Nephrology

142

120

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Autonomic imbalance, a feature of both diabetes and hypertension, may contribute to adverse cardiovascular outcomes. In animal models, sympathetic nerve activity contributes to renal damage but the extent to which autonomic dysfunction precedes the development of CKD and ESRD in humans is unknown. We measured resting heart rate and heart rate variability in 13,241 adults (45-to 64-years old) followed for a median of 16 years in the Atherosclerosis Risk in Communities (ARIC) Study. We examined heart rate parameters by quartiles, defining those in the lowest quartile (by time and frequency domain measures separately) as the risk group of interest. We identified 199 cases of incident ESRD and 541 patients with CKD-related hospitalizations; higher resting heart rate and lower heart rate variability associated with both outcomes. The fully adjusted hazard ratios for ESRD were 1.98 (95% confidence interval [CI] 1.45 to 2.70) among those in the highest heart rate quartile and 1.56 (95% CI 1.14 to 2.14) for high-frequency power. Other time and frequency domain measures were similarly and significantly associated with ESRD and CKD-related hospitalizations. These results suggest that autonomic dysfunction may be an important risk factor for ESRD and CKD-related hospitalizations and call for further studies to define the mechanisms that underlie these associations.

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“…Non-responder group consisted of patients with younger age, lower prevalence of PAD, and higher prevalence of heart failure, although these parameters were not significantly different from responders group, suggesting higher tolerability for β-blocker in nonresponders than responders. Considering that β-blocker decreases renovascular resistance and prevents reduction in renal blood flow in hypertensive patients with renal insufficiency, 36 hypertension in patients with RAS with contraindications to β-blockers may require mechanical intervention.…”

Section: Predictors Of Sufficient Bp Response To Ptramentioning

confidence: 99%