α-Tocopherol Ameliorates Redox Equilibrium Disorders and Reduces Inflammatory Response Caused by Diclofenac-Induced Nephrotoxicity in Male Wistar Rats.

Background Diclofenac (DCF), a nonsteroidal anti-inflammatory drug (NSAID), is widely used for its analgesic and anti-inflammatory properties, but it can also be nephrotoxic. Vitamin E (α-tocopherol) has been shown to protect against renal toxicity caused by various agents, including NSAIDs. This study aims to evaluate the pathophysiology of renal damage and the nephroprotective effect of vitamin E against DCF-induced renal damage in male Wistar rats. Animal and methods Twenty-four male Wistar rats, divided into six equal groups, were used for the study. Group 1 (control group) was treated with distilled water only, while the other groups received either high or low doses of DCF with or without a fixed dose of vitamin E. Renal function was assessed by measuring serum urea, creatinine, and kidney injury molecule-1 (KIM-1). Oxidative damage and renal antioxidant levels were also assessed. Additionally, the expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), renal cytokine tumor necrosis factor-α (TNF-α), and histopathological changes were evaluated. Results DCF caused a significant increase in serum urea, creatinine, KIM-1, TNF-α, NF-κB, and malondialdehyde levels compared to the control group. However, in the groups treated with DCF plus vitamin E, a significant reduction (P<0.05) in the levels of pro-inflammatory cytokines and malondialdehyde was observed, along with improvement in renal function indices, superoxide dismutase, catalase, and glutathione peroxidase levels comparable to the control group. The observed renal histopathological changes were consistent with the results of the biochemical parameters between the treated groups and the normal control rats. Conclusion Findings from this investigation suggested that DCF can be nephrotoxic at a certain dose when used for a prolonged duration. Co-administration of vitamin E suppressed the elevated inflammatory cytokines and led to changes in the cell redox-sensitive signaling pathways induced by DCF, with eventual amelioration of the nephrotoxicity.

Burden of end-stage renal disease in sub-Saharan Africa.

Chronic kidney disease (CKD) particularly in its most severe form, end-stage renal disease (ESRD), is highly prevalent globally. Although both the incidence and prevalence appears to be increasing, the rate of increase is far higher in developing countries, probably as a result of underdevelopment, high incidence of communicable and noncommunicable diseases, poverty as well as inaccessible, unavailable, or unaffordable treatment modalities. The epidemiology differs remarkably between developing and developed economies - it afflicts the young and middle-aged in the former and older individuals in the latter. The etiologies also differ significantly, and the outcome is mainly determined by accessibility and availability of renal replacement therapies. While the three modalities of treatment namely hemodialysis, peritoneal dialysis, and kidney transplantation are available in sub-Saharan Africa, affordability of care remains a major challenge due to nonavailability of healthcare insurance in many of the countries, and where state support is available, dialysis and transplant rationing based on certain criteria remains a major limitation. Data on CKD and ESRD are largely unreliable because of a lack of renal registries in most countries, but the reactivation of the South African Renal Registry and its extension to cover other African countries may improve data quality.
.