Mechanisms of herb-induced nephrotoxicity.

Herbal therapies gained much popularity among the general public, but compared to therapies approved by official authorities, toxicological studies are frequently not available for them. Hence, there may be inherent risks and the kidneys may be especially vulnerable to toxic effects. Herbs may induce nephrotoxicity by induction of apoptosis. High oxalate contents in Star fruit (Averrhoa carambola L.) may induce acute nephropathy. Triptolide from Thunder God Vine (Triperygium wilfordii Hook) is a diterpenoid epoxide with induces reactive oxygen species and nephrotubular apoptosis. Cranberry juice is discussed as promoter of kidney stone formation (nephrolithiasis). Abuse of guaifenesin from Roughbark (Guaicum officinale L.) increases stone formation. Aristolochia acids from Aristolochia fangchi Y.C.Wu ex L.D. Chow & S.M. Hwang causes the well-known aristolochic acid nephropathy and carcinogenesis by DNA adduct formation. Carboxyatractyloside from Impila (Callilepsis laureola DC.) inhibits mitochondrial ATP synthesis. Acute allergic interstitial nephritis was diagnosed after intake of Peruvian Cat's claw (Uncaria tomentosa Willd. DC.). Whether or not Willow Bark (Salix alba L.) induces analgesic nephropathwy is a matter of discussion. Other herbal therapies are considered to affect the rennin-angiotensisn-aldosterone (RAA) system Ephedra sinica Stapf with its ingredient ephedrine. Devil's Claw (Harpagophytum procumbens DC. Ex Meisn.) and licorice (Glycyrrhiza glabra L.) may inhibit major renal transport processes needed for filtration, secretion, and absorption. Strategies to minimize nephrotoxicity include (1) quality control and standardization of herbal products, (2) research on the molecular modes of action to better understand pathophysiological mechanisms of herbal products as well as (3) clinical trials to demonstrate efficacy and safety.