We read with interest the Lancet Series on Global Kidney Disease. Valerie Luyckx and colleagues describe the economics and medical management of chronic kidney disease in sub-Saharan Africa.1 We note clear similarities with patients in Peru. Indeed, in Peru, the Ministry of Health (MINSA)—which covers 70% of the population—does not have a comprehensive programme for the management of patients with chronic kidney disease, including renal replacement therapies. However, the Social Security System (Essalud)—which covers 20% of the population—has a chronic kidney disease programme. / Revisión por pares

Thesis (Ph. D.)--Virginia Commonwealth University, 2006. / Prepared for: Dept. of Biomedical Engineering. Bibliography: leaves 202-220. Also available online.

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Title from PDF of title page (University of Missouri--Columbia, viewed on Feb. 20, 2010). The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file. Dissertation advisor: Charlotte L. Phillips. Vita. Includes bibliographical references.

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Hyperhomocysteinemia, a condition of elevated blood homocysteine (Hcy) level, is an independent risk factor for cardiovascular disease. Folic acid supplementation can effectively reduce blood Hcy levels. Recent studies have demonstrated that hyperhomocysteinemia is also associated with kidney disease. However, the underlying mechanisms remain unclear. The overall objective of the study was to investigate the biochemical and molecular mechanisms of Hcy-induced kidney injury and the effect of folic acid supplementation on Hcy-induced kidney injury. Hyperhomocysteinemia was induced in Sprague-Dawley rats by feeding a high-methionine diet for 12 weeks. An elevation of serum total Hcy level was observed in hyperhomocysteinemic rats. Hyperhomocysteinemia-induced superoxide anion production via nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation resulted in oxidative stress in the kidney. Reduction of oxidative stress by inhibiting superoxide anion production effectively ameliorated hyperhomocysteinemia-induced kidney injury. Inflammatory responses such as increased chemokine expression have been implicated as one of the mechanisms of kidney disease. Monocyte chemoattractant protein-1 (MCP-1) is a potent chemokine that is involved in the inflammatory response in kidney disease. Nuclear factor-kappa B (NF-kappaB) plays an important role in upregulation of MCP-1 expression. We investigated the effect of hyperhomocysteinemia on MCP-1 expression and the molecular mechanism responsible for such an effect in rat kidneys as well as in human kidney proximal tubular cells.

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