Endothelin-1 and F2-isoprostane relate to and predict renal dysfunction in hypertensive patients

Cottone, Santina; Mulè, Giuseppe; Guarneri, Marco; Palermo, Alessandro; Lorito, Maria Carmela; Riccobene, Raffaella; Arsena, Rosalia; Vaccaro, Francesco; Vadalà, Anna; Nardi, Emilio; Cusimano, Paola; Cerasola, Giovanni

doi:10.1093/ndt/gfn489

Cited by 57 publications

(54 citation statements)

References 37 publications

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“…These findings appear to be in contrast to those obtained in human patients with moderate‐to‐severe CKD, in whom plasma F 2 ‐isoprostanes were significantly increased in many studies 1, 7, 10, 11, 12. Urinary and plasma F 2 ‐isoprostanes have been considered to be equivalent markers of chronic (but not acute) oxidative stress,15 but our different findings in cats with CKD could be because of sampling urine rather than plasma.…”

Section: Discussioncontrasting

confidence: 95%

“…Potential sources of renal oxidative stress include tubulointerstitial inflammation, systemic hypertension, and depletion or dysregulation of antioxidant pathways 5, 6, 7, 8. Various plasma biomarkers of oxidative stress, including F 2 ‐isoprostanes, have been shown to correlate with the stages of progressive CKD and declining glomerular filtration rate (GFR) in humans 1, 3, 6, 9, 10, 11, 12.…”

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confidence: 99%

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Urinary F₂‐Isoprostanes in Cats with International Renal Interest Society Stage 1–4 Chronic Kidney Disease

Whitehouse

Quimby

Wan

et al. 2017

Veterinary Internal Medicne

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BackgroundF2‐isoprostanes, a biomarker of oxidant injury, increase with advancing chronic kidney disease (CKD) in humans. In cats, the relationship between CKD and oxidative stress is poorly understood.ObjectivesTo determine whether cats with advancing CKD have increasing urinary F2‐isoprostanes.AnimalsControl cats without evidence of CKD (≥6 years old; n = 11), and cats with IRIS stage 1 (n = 8), 2 (n = 38), 3 (n = 21), and 4 (n = 10) CKD.MethodsThis was a prospective observational study. Urinary F2‐isoprostanes (specifically free 15‐F2t‐isoprostanes) normalized to urine creatinine (IsoPs) were compared among groups and tested for correlations with blood pressure, proteinuria, serum creatinine concentration, and urine specific gravity. The IsoPs also were compared between cats with and without hypertension or proteinuria, and in cats fed predominantly standard versus renal diets.ResultsUrinary IsoPs were increased, but not significantly, in cats with stage 1 CKD (median 263 pg/mg creatinine; range, 211–380) compared to controls (182 pg/mg; range, 80–348) and decreased significantly from stage 1 through advancing CKD (stage 2, 144 pg/mg; range, 49–608; stage 3, 102 pg/mg; range, 25–158; stage 4, 67 pg/mg; range, 26–117; P < .01). Urinary IsoPs were inversely correlated with serum creatinine (r = −0.66, P < .0001).Conclusion and Clinical ImportanceUrinary IsoPs are significantly higher in early CKD (stage 1) compared to cats with more advanced CKD. Additional studies are warranted to characterize oxidative stress in cats with stage 1 CKD and determine whether early antioxidant treatments have a protective effect on CKD progression.

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Section: Discussioncontrasting

confidence: 95%

mentioning

confidence: 99%

Urinary F₂‐Isoprostanes in Cats with International Renal Interest Society Stage 1–4 Chronic Kidney Disease

Whitehouse

Quimby

Wan

et al. 2017

Veterinary Internal Medicne

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“…134,135 OXIDATIVE STRESS AND HUMAN HYPERTENSION Almost all experimental models of hypertension show some form of oxidative excess including genetic forms (spontaneously hypertensive rats, stroke-prone spontaneously hypertensive rats), surgically induced (2K1C, aortic banding), endocrine-induced (Ang II, aldosterone, deoxycorticosterone acetate) and diet-induced hypertension (salt, fat). [21][22][23][136][137][138] Sources of ROS in experimental models include Noxes (Nox1, Nox2 and Nox4), xanthine oxidase, uncoupled nitric oxide synthase and mitochondrial oxidases. Mice deficient in ROSgenerating enzymes have lower blood pressure compared with wild-type counterparts, and Ang II infusion fails to induce hypertension in these mice.…”

Section: Ros and Vascular Biology In Hypertensionmentioning

confidence: 99%

“…[21][22][23] It is still unclear whether oxidative stress causes hypertension in humans and only a few small clinical studies showed a blood pressure-lowering effect of anti-oxidants, [24][25][26] with most large antioxidant clinical trials failing to demonstrate any cardiovascular benefit and blood pressure lowering. [27][28][29] Nevertheless, what is evident is that oxidative stress has a critical role in the molecular mechanisms associated with cardiovascular and renal injury in hypertension and that hypertension itself can contribute to oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

Reactive oxygen species and vascular biology: implications in human hypertension

2010

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Increased vascular production of reactive oxygen species (ROS; termed oxidative stress) has been implicated in various chronic diseases, including hypertension. Oxidative stress is both a cause and a consequence of hypertension. Although oxidative injury may not be the sole etiology, it amplifies blood pressure elevation in the presence of other pro-hypertensive factors. Oxidative stress is a multisystem phenomenon in hypertension and involves the heart, kidneys, nervous system, vessels and possibly the immune system. Compelling experimental and clinical evidence indicates the importance of the vasculature in the pathophysiology of hypertension and as such much emphasis has been placed on the (patho)biology of ROS in the vascular system. A major source for cardiovascular, renal and neural ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), including the prototypic Nox2 homolog-based NADPH oxidase, as well as other Noxes, such as Nox1 and Nox4. Nox-derived ROS is important in regulating endothelial function and vascular tone. Oxidative stress is implicated in endothelial dysfunction, inflammation, hypertrophy, apoptosis, migration, fibrosis, angiogenesis and rarefaction, important processes involved in vascular remodeling in hypertension. Despite a plethora of data implicating oxidative stress as a causative factor in experimental hypertension, findings in human hypertension are less conclusive. This review highlights the importance of ROS in vascular biology and focuses on the potential role of oxidative stress in human hypertension.

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“…acid-reactive substances (TBARS) and 8-epi-isoprostanes, are elevated in patients with hypertension (45,116). Antioxidant capacity and levels of antioxidant vitamins and enzymes have been shown to be reduced in patients with hypertension (66,107).…”

Section: Introductionmentioning

confidence: 99%

Reactive Oxygen Species, Vascular Noxs, and Hypertension: Focus on Translational and Clinical Research

Montezano

Touyz²

2014

Antioxidants & Redox Signaling

229

177

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Significance: Reactive oxygen species (ROS) are signaling molecules that are important in physiological processes, including host defense, aging, and cellular homeostasis. Increased ROS bioavailability and altered redox signaling (oxidative stress) have been implicated in the onset and/or progression of chronic diseases, including hypertension. Recent Advances: Although oxidative stress may not be the only cause of hypertension, it amplifies blood pressure elevation in the presence of other pro-hypertensive factors, such as salt loading, activation of the renin-angiotensin-aldosterone system, and sympathetic hyperactivity, at least in experimental models. A major source for ROS in the cardiovascular-renal system is a family of nicotinamide adenine dinucleotide phosphate oxidases (Noxs), including the prototypic Nox2-based Nox, and Nox family members: Nox1, Nox4, and Nox5. Critical Issues: Although extensive experimental data support a role for increased ROS levels and altered redox signaling in the pathogenesis of hypertension, the role in clinical hypertension is unclear, as a direct causative role of ROS in blood pressure elevation has yet to be demonstrated in humans. Nevertheless, what is becoming increasingly evident is that abnormal ROS regulation and aberrant signaling through redoxsensitive pathways are important in the pathophysiological processes which is associated with vascular injury and target-organ damage in hypertension. Future Directions: There is a paucity of clinical information related to the mechanisms of oxidative stress and blood pressure elevation, and a few assays accurately measure ROS directly in patients. Such further ROS research is needed in humans and in the development of adequately validated analytical methods to accurately assess oxidative stress in the clinic. Antioxid. Redox Signal. 20,[164][165][166][167][168][169][170][171][172][173][174][175][176][177][178][179][180][181][182]

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Endothelin-1 and F2-isoprostane relate to and predict renal dysfunction in hypertensive patients

Abstract: Our findings are a clear-cut demonstration of a strong and negative correlation of both oxidative stress and ET-1 with renal function stages in HT. ET-1 and 8-isoprostane are predictive of eGFR.

Cited by 57 publications

References 37 publications

Urinary F₂‐Isoprostanes in Cats with International Renal Interest Society Stage 1–4 Chronic Kidney Disease

Urinary F₂‐Isoprostanes in Cats with International Renal Interest Society Stage 1–4 Chronic Kidney Disease

Reactive oxygen species and vascular biology: implications in human hypertension

Reactive Oxygen Species, Vascular Noxs, and Hypertension: Focus on Translational and Clinical Research

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Endothelin-1 and F2-isoprostane relate to and predict renal dysfunction in hypertensive patients

Abstract: Our findings are a clear-cut demonstration of a strong and negative correlation of both oxidative stress and ET-1 with renal function stages in HT. ET-1 and 8-isoprostane are predictive of eGFR.

Cited by 57 publications

References 37 publications

Urinary F2‐Isoprostanes in Cats with International Renal Interest Society Stage 1–4 Chronic Kidney Disease

Urinary F2‐Isoprostanes in Cats with International Renal Interest Society Stage 1–4 Chronic Kidney Disease

Reactive oxygen species and vascular biology: implications in human hypertension

Reactive Oxygen Species, Vascular Noxs, and Hypertension: Focus on Translational and Clinical Research

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Product

Resources

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Urinary F₂‐Isoprostanes in Cats with International Renal Interest Society Stage 1–4 Chronic Kidney Disease

Urinary F₂‐Isoprostanes in Cats with International Renal Interest Society Stage 1–4 Chronic Kidney Disease