The epidemiology of age-related macular degeneration

Klein, Ronald; Pető, Tünde; Bird, Alan C.; VanNewkirk, Mylan R.

doi:10.1016/j.ajo.2003.11.069

Cited by 808 publications

(548 citation statements)

References 100 publications

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“…8 Oxidative stress has also been implicated in AMD pathogenesis. 7 As CKD accelerates, the progression of atherosclerosis and increases propensity to oxidative stress 6 ; these processes may potentially explain the increased risk of AMD. Additionally, microvascular disease involving smaller vessels in both the renal and retinal circulations may also potentially play a role in explaining our findings, particularly as the microstructure at the interface of the capillary tuft, glomerular basement membrane, and the glomerular epithelial cells in the kidney is similar to the interface involving choriocapillaris, Bruch's membrane, and retinal pigment epithelium in the eye (the sites where AMD pathology occurs).…”

Section: Discussionmentioning

confidence: 99%

CKD Increases the Risk of Age-Related Macular Degeneration

Liew

Mitchell

Wong³

et al. 2008

Journal of the American Society of Nephrology

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Age-related macular degeneration is the leading cause of irreversible blindness in the United States and often coexists with chronic kidney disease. Both conditions share common genetic and environmental risk factors. A total of 1183 participants aged 54ϩ were examined in the population-based, prospective cohort Blue Mountains Eye Study (Australia) to determine if chronic kidney disease increases the risk of age-related macular degeneration. Moderate chronic kidney disease (estimated glomerular filtration rate Ͻ 60 ml/min per 1.73 m 2 based on the Cockcroft-Gault equation) was present in 24% of the population (286 of 1183). The 5-yr incidence of early age-related macular degeneration was 3.9% in participants with no/mild chronic kidney disease (35 of 897) and 17.5% in those with moderate chronic kidney disease (50 of 286). After adjusting for age, sex, cigarette smoking, hypertension, complement factor H polymorphism, and other risk factors, persons with moderate chronic kidney disease were 3 times more likely to develop early age-related macular degeneration than persons with no/mild chronic kidney disease (odds ratio ϭ 3.2; 95% confidence interval, 1.8 to 5.7, P Ͻ 0.0001). Each SD (14.8 ml/min per 1.73 m 2 ) decrease in Cockcroft-Gault estimated glomerular filtration rate was associated with a doubling of the adjusted risk for early age-related macular degeneration (odds ratio ϭ 2.0; 95% confidence interval, 1.5 to 2.8, P Ͻ 0.0001). In conclusion, persons with chronic kidney disease have a higher risk of early age-related macular degeneration, suggesting the possibility of shared pathophysiologic mechanisms between the two conditions. 19: 806 -811, 200819: 806 -811, . doi: 10.1681 Chronic kidney disease (CKD) is a relatively common condition whose prevalence rises rapidly with age. CKD is estimated to affect over 50% of older persons in the United States 1 and has important extrarenal systemic consequences, such as cardiovascular, metabolic, and hematologic abnormalities. However, the effects of CKD on the sensory organs, such as the eye, are not well understood. J Am Soc NephrolAge-related macular degeneration (AMD) is another relatively common condition in older persons and is the leading cause of blindness and low vision in the United States. 2 CKD and AMD may share common risk factors and pathophysiologic mechanisms. 3 For example, vascular risk factors, such as hypertension and cigarette smoking, may increase risk of both conditions. 4 -7 CKD is known to accelerate the progression of atherosclerosis and increase propensity to oxidative stress, 6 both of which are implicated in AMD pathogenesis. 8,9 Systemic in-

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Section: Discussionmentioning

confidence: 99%

CKD Increases the Risk of Age-Related Macular Degeneration

Liew

Mitchell

Wong³

et al. 2008

Journal of the American Society of Nephrology

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“…2 The prevalence of AMD has been reported across a range of populations and measures as high as 25% for the over 75-year age group. 3 Stereoscopic fundus fluorescein angiography (FFA) is the current gold standard for the diagnosis of neovascular AMD (nAMD)and its use is recommended by the Royal College of Ophthalmologists in the UK. 4 It permits a functional assessment of the retinal and choroidal circulation as well as identification of a breakdown in the blood retinal barrier.…”

Section: Introductionmentioning

confidence: 99%

The diagnostic accuracy of spectral-domain optical coherence tomography for neovascular age-related macular degeneration: a comparison with fundus fluorescein angiography

Wilde

Patel²,

Lakshmanan

et al. 2015

Eye

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“…[1][2][3][4] An estimated 13 million Americans have some degree of AMD and unless better preventive treatments emerge, this number is expected to climb and even reach epidemic proportions with the overall aging demographics. Although the cause of AMD has not yet been fully determined, this complex multifactorial disease clearly results from the interplay of multiple genetic and environmental risk factors 2,5 that lead to progressive destruction of retinal pigment epithelial (RPE) cells and photoreceptors and ultimately to vision loss.…”

mentioning

confidence: 99%

Cigarette Smoke-Related Hydroquinone Induces Filamentous Actin Reorganization and Heat Shock Protein 27 Phosphorylation through p38 and Extracellular Signal-Regulated Kinase 1/2 in Retinal Pigment Epithelium

Pons

Cousins

Csaky

et al. 2010

The American Journal of Pathology

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Retinal pigment epithelium (RPE)-derived membranous debris named blebs, may accumulate and contribute to sub-RPE deposit formation, which is the earliest sign of age-related macular degeneration (AMD). Oxidative injury to the RPE might play a significant role in AMD. However, the underlying mechanisms are unknown. We previously reported that hydroquinone (HQ), a major pro-oxidant in cigarette smoke, foodstuff, and atmospheric pollutants, induces actin rearrangement and membrane blebbing in RPE cells as well as sub-RPE deposits in mice. Here, we show for the first time that phosphorylated Heat shock protein 27 (Hsp27), a key regulator of actin filaments dynamics, is up-regulated in RPE from patients with AMD. Also, HQ-induced nonlethal oxidative injury led to Hsp27mRNA up-regulation, dimer formation , and Hsp27 phosphorylation in ARPE-19 cells. Furthermore, we found that a cross talk between p38 and extracellular signal-regulated kinase (ERK) mediates HQ-induced Hsp27 phosphorylation and actin aggregate formation, revealing ERK as a novel upstream mediator of Hsp27 phosphorylation. Finally, we demonstrated that Hsp25, p38, and ERK phosphorylation are increased in aging C57BL/6 mice chronically exposed to HQ, whereas Hsp25 expression is decreased. Our data suggest that phosphorylated Hsp27 might be a key mediator in AMD and HQ-induced oxidative injury to the RPE, which may provide helpful insights into the early cellular events associated with actin reorganization and bleb formation involved in sub-RPE deposits formation relevant to the pathogenesis of AMD.

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The epidemiology of age-related macular degeneration

Cited by 808 publications

References 100 publications

CKD Increases the Risk of Age-Related Macular Degeneration

CKD Increases the Risk of Age-Related Macular Degeneration

The diagnostic accuracy of spectral-domain optical coherence tomography for neovascular age-related macular degeneration: a comparison with fundus fluorescein angiography

Cigarette Smoke-Related Hydroquinone Induces Filamentous Actin Reorganization and Heat Shock Protein 27 Phosphorylation through p38 and Extracellular Signal-Regulated Kinase 1/2 in Retinal Pigment Epithelium

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