Something I looked up, after reading a thread that included this concern.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16828231&query_hl=1&itool=pubmed_docsumIn addition to low-protein diets and drugs that suppress angiotensin II activity, a variety of other agents and measures may have potential for impeding the process of glomerulosclerosis. These include vitamin E, which blunts the rise in mesangial diacylglycerol levels induced by hyperglycemia; statins and (possibly) policosanol, which down-regulate NADPH oxidase activity by diminishing isoprenylation of Rac1; lipoic acid, whose potent antioxidant activity antagonizes the impact of oxidant stress on TGF-beta expression; pyridoxamine, which inhibits production of advanced glycation endproducts; arginine, high-dose folate, vitamin C, and salt restriction, which may support glomerular production of nitric oxide; and estrogen and soy isoflavones, which may induce nitric oxide synthase in glomerular capillaries while also interfering with TGF-beta signaling. Further research along these lines may enable the development of complex nutraceuticals which have important clinical utility for controlling and preventing glomerulosclerosis and renal failure. Most of these measures may likewise reduce risk for left ventricular hypertrophy in hypertensives, inasmuch as the signaling mechanisms which mediate this disorder appear similar to those involved in glomerulosclerosis.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16716285&query_hl=1&itool=pubmed_docsumAn apparent rise in the activities of N-acetyl-beta-d-glucosaminidase, beta-glucuronidase and cathepsin D were seen in the renal tissue of CsA given rats, which were reversed upon treatment with LA. CsA administration induced significant elevation in lipid peroxidation along with abnormal levels of enzymic (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase) and non-enzymic antioxidants (glutathione, vitamins C and E) in the rat kidney. LA administration improved renal function, by bringing about a significant decrease in peroxidative levels and increase in antioxidant status. CONCLUSION: These results indicate that LA has a protective action against CsA nephrotoxicity and suggest that the LA may find clinical application against a variety of toxins where cellular damage is a consequence of reactive oxygen species.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16236146&query_hl=1&itool=pubmed_docsumCo-administration of alpha-lipoic acid, Ginkgo biloba extract, melatonin or amrinone with vancomycin prevented the increases in the urea, creatinine and melondialdehyde levels and also resulted in higher superoxide dismutase and GSH peroxidase activities. The antioxidants and AMR improved the renal pathology compared to rats treated with vancomycin alone (P<0.05). These results indicate that the three antioxidants and amrinone have potential protective effects against vancomycin-induced nephrotoxicity, which might in part be due to inhibition of free oxygen radical production. Amrinone was the most effective drug as judged on the basis of the pathological findings.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=15526909&query_hl=1&itool=pubmed_docsumAttenuation of chloroquine-induced renal damage by alpha-lipoic acid: possible antioxidant mechanism.
* Murugavel P,
* Pari L.
Department of Biochemistry, Faculty of Science, Annamalai University, Tamil Nadu, India.
The toxic effect of chloroquine (CQ) has been attributed to oxidative stress with the consequences of lipid peroxidation. This study investigates the effects of alpha-lipoic acid (LA) on CQ-induced nephrotoxicity in rats. A single oral administration of CQ (970 mg/kg)-induced nephrotoxicity, manifested biochemically by a significant increase in serum creatinine and blood urea nitrogen concentrations. In addition, renal tissue from CQ-treated rats showed a significant increase in lipid peroxides measured as thiobarbituric acid reactive substances and hydroperoxides, along with significant decrease in nonenzymic antioxidants (vitamin C, vitamin E, and reduced glutathione) and enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase) levels. Oral administration of LA (10, 30, or 100 mg/kg) in different doses for 10 days produced a significant protection against nephrotoxicity induced by CQ. Treatment with LA markedly reduced the elevated lipid peroxidation, restored the depleted renal antioxidant defense system. LA at 100 mg/kg was effective when compared with other doses (10 and 30 mg/kg). This was accompanied by the histopathological observations in kidney tissue. The results suggest that LA ameliorate the lipid peroxidation and the loss of cellular antioxidants, thereby protecting the CQ-induced oxidative damage in kidney.