The Potential Role of Catheter-Based Renal Sympathetic Denervation in Chronic and End-Stage Kidney Disease

2016 ◽  
Vol 21 (4) ◽  
pp. 344-352 ◽  
Author(s):  
Yusuke Sata ◽  
Markus P. Schlaich
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Kidney Disease ◽  
End Stage Renal Disease ◽  
Renal Denervation ◽  
Potential Role ◽  
Stage Renal Disease ◽  
End Stage ◽  
Renal Sympathetic

Sympathetic activation is a hallmark of chronic and end-stage renal disease and adversely affects cardiovascular prognosis. Hypertension is present in the vast majority of these patients and plays a key role in the progressive deterioration of renal function and the high rate of cardiovascular events in this patient cohort. Augmentation of renin release, tubular sodium reabsorption, and renal vascular resistance are direct consequences of efferent renal sympathetic nerve stimulation and the major components of neural regulation of renal function. Renal afferent nerve activity directly influences sympathetic outflow to the kidneys and other highly innervated organs involved in blood pressure control via hypothalamic integration. Renal denervation of the kidney has been shown to reduce blood pressure in many experimental models of hypertension. Targeting the renal nerves directly may therefore be specifically useful in patients with chronic and end-stage renal disease. In this review, we will discuss the potential role of catheter-based renal denervation in patients with impaired kidney function and also reflect on the potential impact on other cardiovascular conditions commonly associated with chronic kidney disease such as heart failure and arrhythmias.

Medical management of nephropathy in type I diabetes mellitus: current recommendations.

1995 ◽  
Vol 6 (6) ◽  
pp. 1523-1529
Author(s):  
J A Breyer
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Diabetic Nephropathy ◽  
Blood Sugar ◽  
Dietary Protein ◽  
End Stage Renal Disease ◽  
Insulin Dependent ◽  
Rate Of Decline ◽  
Stage Renal Disease ◽  
End Stage

Diabetic nephropathy is the single most common cause of end-stage renal disease in the United States. Recently, several major therapeutic interventions have been developed and demonstrated to slow or halt the progression of renal failure in patients with diabetes and diabetic kidney disease. The Diabetes Control and Complications Trial demonstrated that microalbuminuria developed in fewer patients in the intensive blood sugar control group than in the conventional therapy group. Similarly, the risk of developing proteinuria was reduced by intensive blood sugar control. Multiple studies have demonstrated that in patients with insulin-dependent diabetes and proteinuria, lowering the systemic blood pressure slows the rate of decline in renal function and improves patients' survival. In the recently completed trial of ACE inhibition in diabetic nephropathy, ACE inhibitors were specifically shown to decrease dramatically the risk of doubling of serum creatinine or reaching a combined outcome of end-stage renal disease or death. In studies in small numbers of patients with insulin-dependent diabetes and established diabetic nephropathy, dietary protein restriction has also been demonstrated to slow the rate of decline of renal function. New potential interventions currently undergoing study include the use of aldose reductase inhibitors, the use of drugs that prevent the formation of advanced glycosylation end-products, and the use of angiotensin II receptor antagonists. Thus, several established benefits have recently been demonstrated to help prevent the development of or slow the progression of diabetic nephropathy, including blood pressure control, blood sugar control, and treatment with ACE inhibitors. Dietary protein restriction may also be of benefit. Multiple new interventions are undergoing clinical trials currently.

scholarly journals Blood Pressure Components and End-stage Renal Disease in Persons With Chronic Kidney Disease

2012 ◽  
Vol 172 (1) ◽  
pp. 41 ◽  
Author(s):  
Carmen A. Peralta ◽  
Keith C. Norris ◽  
Suying Li ◽  
Tara I. Chang ◽  
Manjula K. Tamura ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Stage Renal Disease ◽  
End Stage

scholarly journals Contribution of the Renal Nerves to Hypertension in a Rabbit Model of Chronic Kidney Disease

Hypertension ◽  
2020 ◽  
Vol 76 (5) ◽  
pp. 1470-1479
Author(s):  
Yusuke Sata ◽  
Sandra L. Burke ◽  
Cindy Gueguen ◽  
Kyungjoon Lim ◽  
Anna M.D. Watson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Renal Function ◽  
Kidney Disease ◽  
Rabbit Model ◽  
Renal Nerves ◽  
Monocyte Chemoattractant Protein 1 ◽  
Stage Renal Disease ◽  
Normalized Units ◽  
Renal Sympathetic

Overactivity of the sympathetic nervous system and high blood pressure are implicated in the development and progression of chronic kidney disease (CKD) and independently predict cardiovascular events in end-stage renal disease. To assess the role of renal nerves, we determined whether renal denervation (RDN) altered the hypertension and sympathoexcitation associated with a rabbit model of CKD. The model involves glomerular layer lesioning and uninephrectomy, resulting in renal function reduced by one-third and diuresis. After 3-week CKD, blood pressure was 13±2 mm Hg higher than at baseline ( P <0.001), and compared with sham control rabbits, renal sympathetic nerve activity was 1.2±0.5 normalized units greater ( P =0.01). The depressor response to ganglion blockade was also +8.0±3 mm Hg greater, but total norepinephrine spillover was 8.7±3.7 ng/min lower (both P <0.05). RDN CKD rabbits only increased blood pressure by 8.0±1.5 mm Hg. Renal sympathetic activity, the response to ganglion blockade and diuresis were similar to sham denervated rabbits (non-CKD). CKD rabbits had intact renal sympathetic baroreflex gain and range, as well as normal sympathetic responses to airjet stress. However, hypoxia-induced sympathoexcitation was reduced by −9±0.4 normalized units. RDN did not alter the sympathetic response to hypoxia or airjet stress. CKD increased oxidative stress markers Nox5 and MCP-1 (monocyte chemoattractant protein-1) in the kidney, but RDN had no effect on these measures. Thus, RDN is an effective treatment for hypertension in this model of CKD without further impairing renal function or altering the normal sympathetic reflex responses to various environmental stimuli.

scholarly journals Impact of Left Ventricular End-Diastolic Wall Stress on Plasma B-Type Natriuretic Peptide in Heart Failure with Chronic Kidney Disease and End-Stage Renal Disease

2009 ◽  
Vol 55 (7) ◽  
pp. 1347-1353 ◽  
Author(s):  
Shinichiro Niizuma ◽  
Yoshitaka Iwanaga ◽  
Takaharu Yahata ◽  
Yodo Tamaki ◽  
Yoichi Goto ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Kidney Disease ◽  
Renal Function ◽  
Kidney Disease ◽  
Renal Disease ◽  
Natriuretic Peptide ◽  
End Stage Renal Disease ◽  
Wall Stress ◽  
Stage Renal Disease ◽  
End Stage

Abstract Background: Plasma B-type natriuretic peptide (BNP) is a diagnostic and prognostic marker in heart failure (HF). Although renal function is reported as an important clinical determinant, precise evaluations of the relationships of renal function with hemodynamic factors in determining BNP have not been performed. Therefore, we evaluated the association of plasma BNP concentrations with LV end-diastolic wall stress (EDWS) in a broad range of HF patients including those with chronic kidney disease (CKD) and end-stage renal disease (ESRD). Methods: In 156 consecutive HF patients including those with CKD and ESRD, we measured plasma BNP and performed echocardiography and cardiac catheterization. LV EDWS was calculated as a crucial hemodynamic determinant of BNP. Results: Plasma BNP concentrations increased progressively with decreasing renal function across the groups (P &lt; 0.01) and were correlated with LV EDWS (r = 0.47) in the HF patients overall. This relationship was also present when patients were subdivided into systolic and diastolic HF (P &lt; 0.01). In multivariable analysis, higher EDWS was associated with increased BNP concentration independently of renal dysfunction (P &lt; 0.01). Anemia, systolic HF, and decreased BMI also contributed to increased BNP concentrations. Conclusions: These results suggest that LV EDWS is a strong determinant of BNP even in patients with CKD and ESRD. Anemia, obesity, and HF type (systolic or diastolic) should also be considered in interpreting plasma BNP concentrations in HF patients. These findings may contribute to the clinical management of HF patients, especially those complicated with CKD and ESRD.

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