Thesis (M. Phil.)--University of Hong Kong, 2000. / Includes bibliographical references (leaves 127-144).

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MMed (Paediatrics), Faculty of Health Sciences,University of the Witwatersrand / IgA (Immunoglobulin A) nephropathy is reported as the most common form of primary glomerulonephropathy worldwide. Despite this there is limited research on IgA nephropathy in African children. This study reviewed IgA and Henoch-Schonlein Purpura (HSP) nephropathies, as it is believed that they are variants of the same pathological process. This study hypothesized that IgA and HSP nephropathies occur in South African black children and that disease progression is worse in this population group and compares them to their international counterparts. Methods: The study was a retrospective review of the records of children that presented to the paediatric renal clinics at two academic hospitals in Johannesburg. It reviewed the epidemiology and progression in South African children. These results were then compared to appropriate international reviews. There were a total of 1835 paediatric renal biopsies between 1985 and 2008. Of these 51 were confirmed to be IgA nephropathy (3%) of which one was excluded. Children were reviewed as a whole and then divided into a HSP and an IgA nephropathy group. Results: The average age at presentation was 9.5 years old. There was a male predominance with a male to female ratio of 2.2:1. Racial differences were noted, and when reviewed in the light of the demographics of the area, there was a higher “prevalence” in Caucasian and Indian patients. The most common presenting symptom in the study population was haematuria. Nephrotic range proteinuria occurred in more than half of all patients. Presentation in acute renal iii dysfunction was uncommon. Predictors of a poor prognosis were found to be nephrotic range proteinuria, and a lower GFR at presentation. The study hypothesis that black African children with IgA or HSP nephropathy have a poorer prognosis than other children with similar presentations, was disproved.

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

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.

No description available.

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.

No description available.