HMG-CoA Reductase Inhibitors and Renal Function

Campese, Vito M.; Park, Jeanie

doi:10.2215/cjn.04060907

Cited by 12 publications

(9 citation statements)

References 42 publications

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“…26 This limits LDL oxidation, which has beneficial cardiac effects and inhibits the proliferative effects of oxidized LDL on renal mesangial cells. 27 Statins also improve endothelial dysfunction by blocking the mevalonate pathway and decreasing Ras and Rho production, which in turn prevent cell proliferation and hypertrophy and increase nitric oxide production. 28 Increased nitric oxide availability has been shown to prevent end-organ damage including decreased proteinuria in a rat hypertension model.…”

Section: Discussionmentioning

confidence: 99%

Relation of Improvement in Estimated Glomerular Filtration Rate With Atorvastatin to Reductions in Hospitalizations for Heart Failure (from the Treating to New Targets [TNT] Study)

Waters

Kean

et al. 2012

The American Journal of Cardiology

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Impaired kidney function often accompanies heart failure (HF) and is associated with a worse prognosis. This post hoc analysis of the Treating to New Targets (TNT) trial examined whether the observed decrease in HF hospitalizations with high- compared to low-dose atorvastatin could be related to improvements in kidney function. Of 10,001 TNT participants, 9,376 had estimated glomerular filtration rate (eGFR) measurements at baseline and 1 year and were included in this analysis. The association of change in year-1 eGFR and subsequent HF hospitalization was examined using Cox regression models. In total 218 participants developed subsequent HF hospitalization. Little change in eGFR occurred over 1 year in the atorvastatin 10-mg group, whereas eGFR improved in the 80-mg group by 1.48 ml/min/1.73 m2 (95% confidence interval 1.29 to 1.67, p <0.0001). Subsequent HF was preceded by a decrease in eGFR over 1 year compared to modest improvement in those without subsequent HF (−0.09 ± 7.89 vs 0.81 ± 6.90 ml/min/1.73 m2, p = 0.0015). After adjusting for baseline eGFR, each 5-ml/min/1.73 m2 increase in eGFR at 1 year was associated with a lower risk of subsequent HF hospitalization (hazard ratio 0.85, 95% confidence interval 0.77 to 0.94, p = 0.002). This relation was independent of treatment effect or change in low-density lipoprotein cholesterol level at 1 year. In conclusion, treatment with high- compared to low-dose atorvastatin was associated with improvement in eGFR at 1 year, which was related to a decrease in subsequent HF hospitalization. This suggests that improvement in kidney function may be related to the beneficial effect of high-dose atorvastatin on HF hospitalization.

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Section: Discussionmentioning

confidence: 99%

Relation of Improvement in Estimated Glomerular Filtration Rate With Atorvastatin to Reductions in Hospitalizations for Heart Failure (from the Treating to New Targets [TNT] Study)

Waters

Kean

et al. 2012

The American Journal of Cardiology

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“…These drugs have great potential in the blockade of RAAS-mediated kidney injury through reduction of oxidative stress via inhibition of Rac1 translocation to the membrane, possible reduction in inflammation via NF-κB, IL-6, C-reactive peptide (hsCRP) and TNF-α 97,100. Again, the benefits are BP-independent, through decrease in inflammation and fibrosis, increase in plaque stability and, finally, decrease in glomerular filtration barrier injury.…”

Section: Therapy For Excess Raas-mediated Kidney Injurymentioning

confidence: 99%

“…In addition, it has also been postulated to bind to (P)RR, decrease the gene expression of (P)RR and alter the 3D configuration of renin 101. However, it may not alter the binding of renin to (P)RR 100. We and others have shown that independent of BP reduction, direct renin inhibition leads to reduction in 3- NT staining, decrease in perivascular fibrosis, albuminuria, improved insulin sensitivity in ex vivo samples (unpublished observations) 101…”

Section: Therapy For Excess Raas-mediated Kidney Injurymentioning

confidence: 99%

Renin-angiotensin-aldosterone system-mediated redox effects in chronic kidney disease

Nistala¹,

Wei²,

Sowers³

et al. 2009

Translational Research

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The renin-angiotensin-aldosterone-system (RAAS) is central to the pathogenesis of hypertension, cardiovascular and kidney disease. Emerging evidence support various pathways through which a local renal RAAS can affect kidney function, hypertension, and cardiovascular disease. A prominent mechanism appears to be loss of redox homeostasis and formation of excessive free radicals. Free radicals such as reactive oxygen species (ROS) are necessary in normal physiologic processes including development of nephrons, erythropoeisis and tubular sodium transport. However, loss of redox homeostasis contributes to pro-inflammatory and pro-fibrotic pathways in the kidney that in turn lead to reduced vascular compliance, podocyte pathology and proteinuria. Both blockade of the RAAS and oxidative stress produces salutary effects on hypertension and glomerular filtration barrier injury. Thus, the focus of current research is on understanding the pathophysiology of chronic kidney disease in the context of an elevated RAAS and unbalanced redox mechanisms.

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“…At discharge, statins were administered in 79.7% versus 64.7% in the French patient population, reninangiotensin system inhibitors in 74.2% versus 54.0%, and beta-blockers in 62.4% versus 26.4%, respectively. 15 It has been shown previously that statin use improves renal function, contributes to prevention of renal decline, [28][29][30][31] and results in significantly lower rates of CV events [32][33][34] and death, 34 so the finding of better survival rates in our patients may be due to the higher prescription rates of statins in all CKD groups.…”

Section: Discussionmentioning

confidence: 72%

Long-Term Mortality After Invasive Angiography and Endovascular Revascularization in Patients With PAD Having Chronic Kidney Disease

et al. 2015

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Peripheral arterial disease (PAD) and chronic kidney disease (CKD) are associated with increased mortality rates. We assessed long-term outcomes of patients with PAD and CKD. Patients with PAD undergoing invasive angiography and/or endovascular revascularization between 2005 and 2010 were retrospectively classified into 5 CKD stages. A follow-up was performed and 572 patients were included, 116 patients (20%) had normal renal function, 245 were in CKD stage 2 (43%), 156 in CKD stage 3 (27%), and 55 in CKD stages 4 + 5 (10%). Diabetes mellitus, hypertension, and anemia were more frequent in higher CKD stages (P < .03). During follow-up (mean 1135 days; 95% confidence interval 1159-1259), cumulative mortality was 21% and increased with advanced CKD stages (9%, 16%, 29%, and 47%, respectively, P < .001). In multivariate Cox regression models, higher CKD stages were significantly associated with poor survival. Medication adherence for secondary prevention was significantly lower than recommended but irrespective of CKD stages. Kidney function is an independent predictor of worse long-term survival in patients with PAD. While standard medications were used less often than recommended, no differences between CKD stages were noted.

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HMG-CoA Reductase Inhibitors and Renal Function

Cited by 12 publications

References 42 publications

Relation of Improvement in Estimated Glomerular Filtration Rate With Atorvastatin to Reductions in Hospitalizations for Heart Failure (from the Treating to New Targets [TNT] Study)

Relation of Improvement in Estimated Glomerular Filtration Rate With Atorvastatin to Reductions in Hospitalizations for Heart Failure (from the Treating to New Targets [TNT] Study)

Renin-angiotensin-aldosterone system-mediated redox effects in chronic kidney disease

Long-Term Mortality After Invasive Angiography and Endovascular Revascularization in Patients With PAD Having Chronic Kidney Disease

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