全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

Chronic Kidney Disease in Disadvantaged Populations

DOI: 10.1155/2012/469265

Full-Text   Cite this paper   Add to My Lib

Abstract:

Disadvantaged populations across the globe exhibit a disproportionate burden of chronic kidney disease (CKD) because of differences in CKD occurrence and outcomes. Although many CKD risk factors can be managed and modified to optimize clinical outcomes, the prevailing socioeconomic and cultural factors in disadvantaged populations, more often than not, militate against optimum clinical outcomes. In addition, disadvantaged populations exhibit a broader spectrum of CKD risk factors and may be genetically predisposed to an earlier onset and a more rapid progression of chronic kidney disease. A basic understanding of the vulnerabilities of the disadvantaged populations will facilitate the adaptation and adoption of the kidney disease treatment and prevention guidelines for these vulnerable populations. The purpose of this paper is to examine recent discoveries and data on CKD occurrence and outcomes in disadvantaged populations and explore strategies for the prevention and treatment of CKD in these populations based on the established guidelines. 1. Background and Epidemiology The global prevalence of chronic kidney disease (CKD) is increasing and creating enormous socioeconomic burdens for patients, families, society, and the health care system across the globe. Data from the third National Health and Nutrition Examination Survey (NHANES 1999–2004) suggest that about 1 out of 8 adult Americans exhibit evidence of CKD [1]. Comparable estimates have been reported in Asia [2], Australia [3], and across Europe [4–6]. The lack of national registries and limited representative national surveys in developing countries make the estimation of the burden of CKD in these countries difficult. However, the risk factors for CKD are known to be just as prevalent in many developing countries as in the developed countries. Therefore, the burden of CKD in those developing countries may be comparable to those of the developed countries. In addition, developing countries exhibit a disproportionate burden of infectious and environmental factors that broaden the spectrum of CKD risk factors and is apt to increase CKD burden. A greater understanding of CKD onset and progression among racial/ethnic minorities and socioeconomically disadvantaged persons in the US may provide insights into CKD burdens in similar populations globally. The Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines by the National Kidney Foundation in 2002 defined CKD as functional and structural abnormalities of the kidneys that persist for more than three months. This widely publicized and

References

[1]  J. Coresh, E. Selvin, L. A. Stevens et al., “Prevalence of chronic kidney disease in the United States,” Journal of the American Medical Association, vol. 298, no. 17, pp. 2038–2047, 2007.
[2]  J. Chen, R. P. Wildman, D. Gu et al., “Prevalence of decreased kidney function in Chinese adults aged 35 to 74 years,” Kidney International, vol. 68, no. 6, pp. 2837–2845, 2005.
[3]  S. J. Chadban, E. M. Briganti, P. G. Kerr et al., “Prevalence of kidney damage in Australian adults: The AusDiab kidney study,” Journal of the American Society of Nephrology, vol. 14, no. 2, pp. S131–S138, 2003.
[4]  O. Viktorsdottir, R. Palsson, M. B. Andresdottir, T. Aspelund, V. Gudnason, and O. S. Indridason, “Prevalence of chronic kidney disease based on estimated glomerular filtration rate and proteinuria in Icelandic adults,” Nephrology Dialysis Transplantation, vol. 20, no. 9, pp. 1799–1807, 2005.
[5]  A. Otero, P. Gayoso, F. Garcia, and A. L. de Francisco, “Epidemiology of chronic renal disease in the Galician population: results of the pilot Spanish EPIRCE study,” Kidney international. Supplement., no. 99, pp. S16–S19, 2005.
[6]  M. Cirillo, M. Laurenzi, M. Mancini, A. Zanchetti, C. Lombardi, and N. G. De Santo, “Low glomerular filtration in the population: prevalence, associated disorders, and awareness,” Kidney International, vol. 70, no. 4, pp. 800–806, 2006.
[7]  A. S. Levey, J. Coresh, K. Bolton et al., “K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification,” American Journal of Kidney Diseases, vol. 39, no. 2, supplement 1, pp. S1–S266, 2002.
[8]  S. I. Hallan, J. Coresh, B. C. Astor et al., “International comparison of the relationship of chronic kidney disease prevalence and ESRD risk,” Journal of the American Society of Nephrology, vol. 17, no. 8, pp. 2275–2284, 2006.
[9]  S. Wild, G. Roglic, A. Green, R. Sicree, and H. King, “Global prevalence of diabetes: estimates for the year 2000 and projections for 2030,” Diabetes Care, vol. 27, no. 5, pp. 1047–1053, 2004.
[10]  R. Correa-Rotter and L. González-Michaca, “Early detection and prevention of diabetic nephropathy: a challenge calling for mandatory action for Mexico and the developing world,” Kidney International, Supplement, vol. 68, no. 98, pp. S69–S75, 2005.
[11]  A. M. Cusumano, G. G. Garcia, C. Di Gioia, O. Hermida, and C. Lavorato, “The Latin American dialysis and transplantation registry (RLDT) annual report 2004,” Ethnicity and Disease, vol. 16, no. S2, pp. 10–13, 2006.
[12]  F. A. M. Shaheen and A. A. Al-Khader, “Preventive strategies of renal failure in the Arab world,” Kidney International, Supplement, vol. 68, no. 98, pp. S37–S40, 2005.
[13]  A. S. Go, G. M. Chertow, D. Fan, C. E. McCulloch, and C. Y. Hsu, “Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization,” New England Journal of Medicine, vol. 351, no. 13, pp. 1296–1370, 2004.
[14]  “United States Renal Data System (USRDS) 2000 Annual Data”.
[15]  R. S. Barsoum, “End-stage renal disease in North Africa,” Kidney International, Supplement, vol. 63, no. 83, pp. S111–S114, 2003.
[16]  V. Kher, N. E. Madias, J. T. Harrington et al., “End-stage renal disease in developing countries,” Kidney International, vol. 62, no. 1, pp. 350–362, 2002.
[17]  US Renal Data System, USRDS 2010 annual data report: atlas of end-stage renal disease in the United States, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Disease, Bethesda, Md, USA, 2010.
[18]  K. C. Norris and L. Y. Agodoa, “Unraveling the racial disparities associated with kidney disease,” Kidney International, vol. 68, no. 3, pp. 914–924, 2005.
[19]  W. Rosamond, K. Flegal, K. Furie et al., “Heart disease and stroke statistics-2008 Update: a report from the American heart association statistics committee and stroke statistics subcommittee,” Circulation, vol. 117, no. 4, pp. e25–e46, 2008.
[20]  R. Turner, R. Holman, I. Stratton et al., “Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38,” British Medical Journal, vol. 317, no. 7160, pp. 703–713, 1998.
[21]  B. M. Egan, Y. Zhao, and R. N. Axon, “US trends in prevalence, awareness, treatment, and control of hypertension, 1988–2008,” Journal of the American Medical Association, vol. 303, no. 20, pp. 2043–2050, 2010.
[22]  F. A. McAlister, K. Wilkins, M. Joffres et al., “Changes in the rates of awareness, treatment and control of hypertension in Canada over the past two decades,” CMAJ, vol. 183, no. 9, pp. 1007–1013, 2011.
[23]  W. H. L. Kao, M. J. Klag, L. A. Meoni et al., “MYH9 is associated with nondiabetic end-stage renal disease in African Americans,” Nature Genetics, vol. 40, no. 10, pp. 1185–1192, 2008.
[24]  G. Genovese, D. J. Friedman, M. D. Ross et al., “Association of trypanolytic ApoL1 variants with kidney disease in African Americans,” Science, vol. 329, no. 5993, pp. 841–845, 2010.
[25]  B. I. Freedman, J. B. Kopp, C. D. Langefeld et al., “The Apolipoprotein L1 (APOL1) gene and nondiabetic nephropathy in African Americans,” Journal of the American Society of Nephrology, vol. 21, no. 9, pp. 1422–1426, 2010.
[26]  B. J. Materson, D. J. Reda, W. C. Cushman et al., “Single-drug therapy for hypertension in men—a comparison of six antihypertensive agents with placebo,” New England Journal of Medicine, vol. 328, no. 13, pp. 914–921, 1993, Erratum in: New England Journal of Medicine, vol. 330, no. 23, p. 1689, 1994.
[27]  K. C. Norris, N. Tareen, D. Martins, and N. D. Vaziri, “Implications of ethnicity for the treatment of hypertensive kidney disease, with an emphasis on African Americans,” Nature Clinical Practice Nephrology, vol. 4, no. 10, pp. 538–549, 2008.
[28]  P. E. de Jong, M. van der Velde, R. T. Gansevoort, and C. Zoccali, “Screening for chronic kidney disease: where does Europe go?” Clinical Journal of the American Society of Nephrology, vol. 3, no. 2, pp. 616–623, 2008.
[29]  E. L. Knight, H. M. Kramer, and G. C. Curhan, “High-normal blood pressure and microalbuminuria,” American Journal of Kidney Diseases, vol. 41, no. 3, pp. 588–595, 2003.
[30]  K. C. Norris and L. Y. Agodoa, “Unraveling the racial disparities associated with kidney disease,” Kidney International, vol. 68, no. 3, pp. 914–924, 2005.
[31]  A. V. Chobanian, G. L. Bakris, H. R. Black et al., “The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report,” Journal of the American Medical Association, vol. 289, no. 19, pp. 2560–2572, 2003.
[32]  C. Baigent, K. Burbury, and D. Wheeler, “Premature cardiovascular disease in chronic renal failure,” Lancet, vol. 356, no. 9224, pp. 147–152, 2000.
[33]  F. C. Luft, C. E. Grim, N. Fineberg, and M. C. Weinberger, “Effects of volume expansion and contraction in normotensive whites, blacks, and subjects of different ages,” Circulation, vol. 59, no. 4, pp. 643–650, 1979.
[34]  G. Chandramohan, Y. Bai, K. Norris, B. Rodriguez-Iturbe, and N. D. Vaziri, “Effects of dietary salt on intrarenal angiotensin system, NAD(P)H oxidase, COX-2, MCP-1 and PAI-1 expressions and NF-κB activity in salt-sensitive and -resistant rat kidneys,” American Journal of Nephrology, vol. 28, no. 1, pp. 158–167, 2007.
[35]  H. Hayakawa, K. Coffee, and L. Raij, “Endothelial dysfunction and cardiorenal injury in experimental salt-sensitive hypertension: effects of antihypertensive therapy,” Circulation, vol. 96, no. 7, pp. 2407–2413, 1997.
[36]  J. T. Wright Jr., G. Bakris, T. Greene et al., “Effect of blood pressure lowering and antihypertensive drug class on progression of hypertensive kidney disease: results from the AASK trial,” Journal of the American Medical Association, vol. 288, no. 19, pp. 2421–2431, 2002, Erratum in: Journal of the American Medical Association, vol. 295, no. 23, p. 2726, 2006.
[37]  L. J. Appel, J. T. Wright Jr., T. Greene et al., “Intensive blood-pressure control in hypertensive chronic kidney disease,” New England Journal of Medicine, vol. 363, no. 10, pp. 918–929, 2010.
[38]  “K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Executive summary,” American Journal of Kidney Diseases, vol. 42, supplement 1, pp. 16–33, 2004.
[39]  J. Lea, T. Greene, L. Hebert et al., “The relationship between magnitude of proteinuria reduction and risk of end-stage renal disease: results of the African American study of kidney disease and hypertension,” Archives of Internal Medicine, vol. 165, no. 8, pp. 947–953, 2005.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133