Sympathetic Nerve Traffic and Asymmetric Dimethylarginine in Chronic Kidney Disease

Grassı, Guıdo; Seravalle, Gino; Ghiadoni, Lorenzo; Tripepi, Giovanni; Bruno, Rosa Maria; Mancia, Giuseppe; Zoccali, Carmine

doi:10.2215/cjn.06970711

Cited by 50 publications

(39 citation statements)

References 37 publications

(46 reference statements)

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“…Indeed, in stage 2-4 CKD patients, Grassi et al [55] demonstrated a strong negative association between increased muscle SNA and decreased GFR, as well as a significant positive correlation between high muscle SNA and proteinuria. Interstitial fibrosis, glomerulosclerosis [56], accelerated atherosclerosis, vasoconstriction, and proliferation of smooth muscle cells and adventitial fibroblasts in the vessel wall are other deleterious consequences of sympathetic overactivity related to progression of renal damage [57,58].…”

Section: Altered Autonomic Control Of Cardiovascular Function In Ckdmentioning

confidence: 98%

Cardiovascular Autonomic Dysfunction in Chronic Kidney Disease: a Comprehensive Review

Salman

2015

Curr Hypertens Rep

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Cardiovascular autonomic dysfunction is a major complication of chronic kidney disease (CKD), likely contributing to the high incidence of cardiovascular mortality in this patient population. In addition to adrenergic overdrive in affected individuals, clinical and experimental evidence now strongly indicates the presence of impaired reflex control of both sympathetic and parasympathetic outflow to the heart and vasculature. Although the principal underlying mechanisms are not completely understood, potential involvements of altered baroreceptor, cardiopulmonary, and chemoreceptor reflex function, along with factors including but not limited to increased renin-angiotensin-aldosterone system activity, activation of the renal afferents and cardiovascular structural remodeling have been suggested. This review therefore analyzes potential mechanisms underpinning autonomic imbalance in CKD, covers results accumulated thus far on cardiovascular autonomic function studies in clinical and experimental renal failure, discusses the role of current interventional and therapeutic strategies in ameliorating autonomic deficits associated with chronic renal dysfunction, and identifies gaps in our knowledge of neural mechanisms driving cardiovascular disease in CKD.

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Section: Altered Autonomic Control Of Cardiovascular Function In Ckdmentioning

confidence: 98%

Cardiovascular Autonomic Dysfunction in Chronic Kidney Disease: a Comprehensive Review

Salman

2015

Curr Hypertens Rep

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“…Besides extrarenal effects, sympathetic overactivity influences renal sodium excretion and reabsorption, renal perfusion, glomerular filtration rate, and renin release [9,10]. Moreover, increased activity of the sympathetic nervous system is associated with estimated glomerular filtration rate (eGFR) and proteinuria suggesting that the activation of this system is a progression factor in CKD patients [11]. …”

Section: Introductionmentioning

confidence: 99%

Impact of Baroreflex Activation Therapy on Renal Function - A Pilot Study

Wallbach¹,

Lehnig²,

Schroer

et al. 2014

Am J Nephrol

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Background/Aims: Resistant hypertension and chronic kidney disease (CKD) are interlinked via sympathetic overdrive. Baroreflex activation therapy (BAT) has been shown to chronically reduce blood pressure (BP) in patients with resistant hypertension. The effect of BAT on renal function in CKD patients with resistant hypertension has not been reported. The aim of this study was to investigate the effect of sympathetic inhibition on renal function in CKD patients. Methods: 23 CKD patients with resistant hypertension were prospectively treated with BAT. Analyses were performed before and 6 months after the start of BAT. The renal function was analyzed by creatinine, cystatin C, glomerular filtration rate (GFR), renin, aldosterone, fractioned and 24-hour sodium excretion and analyses of urine marker proteins. The purpose of the control group was to investigate the influence of treating patients in a center for hypertension and regression to the mean on investigated variables. Results: The office mean BP decreased from 116.9 ± 20.9 mm Hg to 104.2 ± 22.2 mm Hg (p < 0.01), while the number of prescribed antihypertensive classes decreased from 6.6 ± 1.6 to 6.1 ± 1.7 (p = 0.02). Proteinuria and albuminuria decreased from a median of 283.9 and 47.7 to 136.5 (p = 0.01) and 45.0 mg/g creatinine (p = 0.01) with pronounced effects in higher CKD stage III + IV compared to I + II (p < 0.01). CKD-EPI cystatin C equation improved from 53.6 ± 22.7 to 60.4 ± 26.1 ml/min (p = 0.02). While creatinine and GFR were impaired after a period of 6 months, no changes of proteinuria, albuminuria, or BP were obtained in control patients. Conclusion: The data of this prospective trial demonstrate potential nephroprotective effects of BAT in therapy-resistant hypertension in CKD patients by a reduction of BP, proteinuria and moreover, a stabilization of estimated GFR.

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“…Pulmonary hypertension in CKD-5 or ESRD on HD may be induced or aggravated by left ventricular dysfunction, volume overload [16][17][18], an arterial-venous istula [7,11,[19][20][21][22][23], sleep disorders [24][25][26][27][28][29][30], exposure to dialysis membranes [31], endothelial dysfunction [32], vascular calci ication and stiffness, and severe anemia. Controlling volume overload and left ventricular disorders are important for relieving PH.…”

Section: Hepatopulmonary Syndrome (Hps)mentioning

confidence: 99%

Untitled

2017

Arch Vas Med

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How to cite this article: Magbri A, El-Magbri M, El-Magbri E. Hepato-Pulmonary syndrome and Porto-Pulmonary Hypertension: Rare combination cause of Hypoxemia in patient with end-stage renal failure on Hemodialysis and hepatitis C Induced Decompensated Cirrhosis. Arch Vas Med. 2017; 1: 008-012. Case ReportThe case is that of 83 year-old African American man with hypertension, hepatitis C induced decompensated cirrhosis with ascites, end-stage renal disease (ESRD) on hemodialysis, luid overload with peripheral edema and chronic hypotension. The patient was referred to the dialysis access center of Pittsburgh, PA for evaluation of his prolonged bleeding from the left upper arm brachial-basilic arterial-venous istula (BBAVF).On examination, he was found to be severely hypoxic with oxygen saturation of 80-92 mm Hg. Chest was clear on auscultation. Abdominal examination showed hepatosplenomegaly with ascites. Extremities showed 3+ peripheral edema bilaterally. His chest x-ray showed cardiomegaly with clear lung ields. His laboratory workup showed, WBC of 3.4, RBC 3.69, MCH 31.2, MCHC 32, and platelets 104 K/L. Chemistry showed Na 134, Cl 99, CO2 24, Total protein 7.2 with albumin of 2.9. SGOT was high at 44, vitamin D 42. Laboratory data were also indicative of chronic liver disease with bilirubin of 2.8, INR of 1.2, and albumin of 2.9, and platelet count of 104. Immunology for Hepatitis B Ag was negative, Hepatitis B Ab was 22 H, Hepatitis C Ab was positive. Arterial blood gas analysis showed PaO2 of 54 mmHg while breathing room air.Abdominal ultra-sound revealed features suggestive of portal hypertension (hepatosplenomegaly with ascites). Transthoracic echocardiogram showed elevated right ventricular systolic pressure of 52 mmHg with mild-moderate dilatation of the right atrium and right ventricle with normal left ventricular function. A contrast echocardiogram was suggestive of hepatopulmonary syndrome (appearance of the bubbles in the left ventricle after 5 beats of their appearance in the right ventricle). Right heart catheterization was not done but his angiogram revealed re lux of dye into the right innominate vein up to the subclavian vein and right IJ. Other causes of pulmonary hypertension were excluded on history and clinical examination. DiscussionHepatic diseases are associated with 3 main pulmonary syndromes associated with portal hypertension:1. Porto-pulmonary hypertension (POPH), pulmonary arterial hypertension in the absence of other causes.

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Sympathetic Nerve Traffic and Asymmetric Dimethylarginine in Chronic Kidney Disease

Cited by 50 publications

References 37 publications

Cardiovascular Autonomic Dysfunction in Chronic Kidney Disease: a Comprehensive Review

Cardiovascular Autonomic Dysfunction in Chronic Kidney Disease: a Comprehensive Review

Impact of Baroreflex Activation Therapy on Renal Function - A Pilot Study

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