The Chronic Kidney Disease Epidemic

Kiberd, Bryce A.

doi:10.1681/asn.2006020123

Cited by 56 publications

(35 citation statements)

References 63 publications

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“…Given the epidemic of obesity and type 2 diabetes (5) and the increasing burden of CKD in the American population (1,37), understanding the cause of obesity-related CKD is of critical importance. Previous literature suggested that VAT and SAT convey differential risk (31).…”

Section: Implications For Further Researchmentioning

confidence: 99%

Association of Visceral and Subcutaneous Adiposity with Kidney Function

Young¹,

Hwang²,

Sarnak³

et al. 2008

Clinical Journal of the American Society of Nephrology

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Background and objectives: Obesity is a risk factor for incident chronic kidney disease (CKD). Visceral (VAT) and subcutaneous adipose tissue (SAT) may confer differential metabolic risk profiles. The relations of VAT and SAT were analyzed with CKD as estimated by creatinine-and cystatin-based estimating equations.Design, setting, participants, & measurements: Participants from the Framingham Offspring Study who underwent abdominal computed tomography for VAT and SAT quantification were included (n ‫؍‬ 1299; 53% women; mean age 60 yr). CKD was defined as estimated GFR <60 ml/min per 1.73 m 2 , as estimated using creatinine (n ‫؍‬ 89) in the Modification of Diet in Renal Disease (MDRD) formula or by cystatin C (n ‫؍‬ 136). Regression models evaluated the cross-sectional relations between VAT and SAT with CKD and cystatin C, with age and gender adjustment and cardiovascular risk factor adjustment.Results: Neither VAT nor SAT was associated with CKD as estimated by the MDRD equation. In contrast, both VAT and SAT were associated with CKD when defined using cystatin-based equations. The estimated decrease in estimated GFR by cystatin C per 1-SD increase of VAT was 1.9 ml/min per 1.73 m 2 and for SAT was 2.6 ml/min per 1.73 m 2 in a multivariableadjusted model.Conclusions: VAT and SAT were associated with CKD when defined using cystatin C estimating equations but not when using a creatinine-based estimating equation. Mechanisms linking adipose tissue to cystatin C warrant further research.

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Section: Implications For Further Researchmentioning

confidence: 99%

Association of Visceral and Subcutaneous Adiposity with Kidney Function

Young¹,

Hwang²,

Sarnak³

et al. 2008

Clinical Journal of the American Society of Nephrology

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“…2,3 However, the use of these inhibitors has not yet resulted in reduced incidence of CKD. 4 Therefore, it is important to consider another strategy to halt the development of CVD associated with CKD, in addition to the use of RAAS inhibitors.…”

Section: Introductionmentioning

confidence: 99%

Oral adsorbent AST-120 ameliorates endothelial dysfunction independent of renal function in rats with subtotal nephrectomy

et al. 2009

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It is important to consider a strategy to halt the development of cardiovascular disease (CVD) in patients with chronic kidney disease (CKD). Oral adsorbent AST-120 retards deterioration in renal function, reducing indoxyl sulfate (IS) accumulation. The aim of this study was to determine whether AST-120 improves endothelial dysfunction by reducing oxidative/nitrative stress in a rat-CKD model. Subtotally nephrectomized (Nx) rats aged 17 weeks were divided into two groups: control rats and rats orally treated with AST-120. Two weeks after initiation of AST-120, serum and urinary IS levels, renal histological scores and endothelium-dependent vascular responses (EDVRs) in the aorta were investigated. EDVR in 5-h incubation with 250 lg ml À1 IS was also examined in normal rat aortas. Nitrotyrosine content, mRNA expression of p47phox, a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase component, and expression and phosphorylation (serine-1177) of endothelial nitric oxide synthase (eNOS) in the aorta were examined in untreated and treated Nx rats. At the end of treatment, renal function and histological scores were not different in the two groups. AST-120 prevented the elevation of serum IS level in Nx rats, reducing urinary IS excretion, and ameliorated decreased EDVR in Nx rats. Incubation with IS tended to reduce EDVR in normal aortas, albeit insignificantly. AST-120 also suppressed nitrotyrosine accumulation and inhibited p47phox expression in Nx rats. The eNOS expression and phosphorylation were similar in the two groups. In conclusion, AST-120 ameliorated endothelial dysfunction and alleviated oxidative/nitrative stress in the aorta through reduced accumulation of IS, independent of renal function, in a rat CKD model.

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“…The prevalence of CKD in Western populations is high (1)(2)(3), and the number of patients with ESRD has increased dramatically in the past few decades. This rise is expected to continue, particularly in developing countries, where smoking and other cardiovascular risk factors are increasing substantially (4,5), and will be paralleled by rising CKD-and ESRD-related costs (6,7).…”

mentioning

confidence: 99%

Smoking

Orth

Hallan²

2008

Clinical Journal of the American Society of Nephrology

256

174

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Although it is beyond any doubt that smoking is the number one preventable cause of death in most countries, smoking as an independent progression factor in renal disease has been questioned against the background of evidence-based criteria. This is because information from large, randomized, prospective studies that investigate the effects of smoking on renal function in healthy individuals as well as in patients with primary or secondary renal disease are lacking. Since 2003, a substantial number of clinical and experimental data concerning the adverse renal effects of smoking have been published, including large, prospective, population-based, observational studies. These more recent data together with evidence from experimental studies clearly indicate that smoking is a relevant risk factor, conferring a substantial increase in risk for renal function deterioration. This review summarizes the present knowledge about the renal risks of smoking as well as the increased cardiovascular risk caused by smoking in patients with chronic kidney disease. The conclusion is that smoking is an important renal risk factor, and nephrologists have to invest more efforts to motivate patients to stop smoking.

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The Chronic Kidney Disease Epidemic

Cited by 56 publications

References 63 publications

Association of Visceral and Subcutaneous Adiposity with Kidney Function

Association of Visceral and Subcutaneous Adiposity with Kidney Function

Oral adsorbent AST-120 ameliorates endothelial dysfunction independent of renal function in rats with subtotal nephrectomy

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