Effects of atorvastatin on oxidative stress in chronic kidney disease

Fassett, Robert G.; Robertson, Iain; Ball, Madeleine J.; Geraghty, Dominic P.; Coombes, Jeff S.

doi:10.1111/nep.12502

Cited by 18 publications

(13 citation statements)

References 39 publications

(88 reference statements)

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“…Measurement of F2-isoprostanes is widely considered the most accurate method to measure oxidant stress in vivo [58,59]. Although it is not clear why F2-IsoP/Cr did not decrease with rosuvastatin in our study, this is consistent with prior studies evaluating the effect of statins on this oxidative stress marker outside of HIV [29,60]. It is possible that HIV-related factors or ART may affect F2-IsoP levels so profoundly that statins are unable to improve these levels in the continued presence of HIV and/or ART effect.…”

Section: Discussionsupporting

confidence: 89%

“…We have previously shown that rosuvastatin decreases monocyte activation [soluble CD14 and the proportion of tissue factor-expressing patrolling monocytes (CD14dimCD16+ cells)], T-cell activation (proportion of CD38+HLA-DR+ T cells), systemic inflammation [cystatin C and interferon γ inducible protein-10 (IP-10)] and vascular inflammation (lipoprotein-associated phospholipase A2) in HIV [20–23]. Statins have antioxidant activity [24,25] and decrease markers of oxidative stress in some [26–28], but not all [29,30] disease states. To our knowledge, the effect of statins on oxLDL or other oxidative stress markers in the setting of chronic HIV infection has not been studied.…”

Section: Introductionmentioning

confidence: 99%

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Changes in oxidized lipids drive the improvement in monocyte activation and vascular disease after statin therapy in HIV

Hileman

Turner

Funderburg

et al. 2016

Aids

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Background Oxidative stress plays a significant role in atherosclerosis development. HIV infection has been linked with heightened cardiovascular disease risk. HMG-CoA reductase inhibitors may reduce oxidative stress and subsequently subclinical vascular disease in HIV. Design/methods This is a randomized, placebo-controlled trial to evaluate the effect of rosuvastatin in HIV-infected adults on stable antiretroviral therapy with low-density lipoprotein less than 130 mg/dl and increased inflammation or T-cell activation on subclinical vascular disease. Changes over 48 weeks in oxidative stress markers, oxidized low-density lipoprotein (oxLDL) and F2-isoprostane/creatinine ratio (F2-Iso-P/Cr), were compared between groups. Spearman correlation and multivariable linear regression were used to evaluate relationships between changes in markers of oxidative stress, inflammation and monocyte activation and carotid intima media thickness (CIMT). Results One hundred and forty-seven adults enrolled (72 to rosuvastatin and 75 to placebo). In the rosuvastatin group, oxLDL decreased significantly over 24 weeks compared to placebo [mean absolute change in log-oxLDL for rosuvastatin −0.2 ± 0.468 log U/l (P < 0.001 within-group) vs. placebo −0.018 ± 0.456 log U/l (P = 0.83 within-group); P = 0.004 between groups] and this change was linked with changes in soluble CD14 and proportion of patrolling monocytes (CD14dimCD16+). Although oxLDL levels increased after initially declining and were not different from placebo at week 48, the early improvement in oxLDL was associated with improved CIMT at week 48. Changes in F2-IsoP/Cr were not significant between groups. Conclusion Rosuvastatin decreases oxLDL levels early after initiation and is associated with decreased monocyte activation. Early improvement in oxLDL is linked with improved CIMT in treated HIV infection.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Changes in oxidized lipids drive the improvement in monocyte activation and vascular disease after statin therapy in HIV

Hileman

Turner

Funderburg

et al. 2016

Aids

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“…Physiological flows induce the disassembly of actin peripheral bands and the formation of long, parallel actin stress fibers aligned to flow direction. 110 , 111 WSS also induces adherens junction stability and promotes glycocalyx formation. 93 , 112 , 113 These phenomena regulate EC permeability of the endothelium and seem to maintain a quiescent EC state.…”

Section: Hemodynamicsmentioning

confidence: 96%

The molecular mechanisms of hemodialysis vascular access failure

Brahmbhatt

Remuzzi

Franzoni

et al. 2016

Kidney International

196

211

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The arteriovenous fistula has been used for more than 50 years to provide vascular access for patients undergoing hemodialysis. More than 1.5 million patients worldwide have end stage renal disease and this population will continue to grow. The arteriovenous fistula is the preferred vascular access for patients, but its patency rate at 1 year is only 60%. The majority of arteriovenous fistulas fail because of intimal hyperplasia. In recent years, there have been many studies investigating the molecular mechanisms responsible for intimal hyperplasia and subsequent thrombosis. These studies have identified common pathways including inflammation, uremia, hypoxia, sheer stress, and increased thrombogenicity. These cellular mechanisms lead to increased proliferation, migration, and eventually stenosis. These pathways work synergistically through shared molecular messengers. In this review, we will examine the literature concerning the molecular basis of hemodialysis vascular access malfunction.

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“…Additional administration of vitamin E did not influence any lipid parameters but significantly reduced in vitro LDL oxizability, likely acting synergistically with the statin treatment [ 162 ]. Data from the LORD study suggest that administration of atorvastatin 10 mg/day for 3 years had no effect on plasma levels of F2-isoprostanes, protein carbonyls, glutathione peroxidase activity, and total antioxidant capacity in CKD patients [ 195 ].…”

Section: Antioxidants and Os In Ckd And Hdmentioning

confidence: 99%

Oxidative Stress in Hemodialysis Patients: A Review of the Literature

Liakopoulos

Roumeliotis

Gorny

et al. 2017

Oxidative Medicine and Cellular Longevity

212

230

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Hemodialysis (HD) patients are at high risk for all-cause mortality and cardiovascular events. In addition to traditional risk factors, excessive oxidative stress (OS) and chronic inflammation emerge as novel and major contributors to accelerated atherosclerosis and elevated mortality. OS is defined as the imbalance between antioxidant defense mechanisms and oxidant products, the latter overwhelming the former. OS appears in early stages of chronic kidney disease (CKD), advances along with worsening of renal failure, and is further exacerbated by the HD process per se. HD patients manifest excessive OS status due to retention of a plethora of toxins, subsidized under uremia, nutrition lacking antioxidants and turn-over of antioxidants, loss of antioxidants during renal replacement therapy, and leukocyte activation that leads to accumulation of oxidative products. Duration of dialysis therapy, iron infusion, anemia, presence of central venous catheter, and bioincompatible dialyzers are several factors triggering the development of OS. Antioxidant supplementation may take an overall protective role, even at early stages of CKD, to halt the deterioration of kidney function and antagonize systemic inflammation. Unfortunately, clinical studies have not yielded unequivocal positive outcomes when antioxidants have been administered to hemodialysis patients, likely due to their heterogeneous clinical conditions and underlying risk profile.

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Effects of atorvastatin on oxidative stress in chronic kidney disease

Abstract: CKD patients had elevated oxidative stress that was not attenuated by atorvastatin 10 mg/day for 3 years.

Cited by 18 publications

References 39 publications

Changes in oxidized lipids drive the improvement in monocyte activation and vascular disease after statin therapy in HIV

Changes in oxidized lipids drive the improvement in monocyte activation and vascular disease after statin therapy in HIV

The molecular mechanisms of hemodialysis vascular access failure

Oxidative Stress in Hemodialysis Patients: A Review of the Literature

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