Maleic acid (MA)-induced nephropathy that is characterized by proteinuria, glycosuria, phosphaturia and a deficient urinary acidification and concentration. Sulforaphane (SF) is an indirect antioxidant that shows nephroprotective effects. The aim of the present work was to test the pre-treatment with SF against the MA-induced nephropathy.

Wistar rats (230–260 g) were separated in the following groups: control, MA (which received 400 mg/kg of MA), SF + MA (which received MA and 1 mg/kg of SF each day for four days) and SF (which only received SF). MA induced proteinuria, an increase in urinary excretion of N-acetyl-β-d-glucosaminidase, and a decrease in plasma glutathione peroxidase activity, renal blood flow, and oxygenation and perfusion of renal cortex. All these impairments correlated with higher levels of oxidative damage markers and exacerbated superoxide anion production on renal cortex. Moreover, MA impaired mitochondrial bioenergetics associated to complex I, mitochondrial membrane potential and respiratory control index and increased the mitochondrial production of hydrogen peroxide. Further it disrupted mitochondrial morphology. SF prevented all the above-described alterations.

In conclusion, the protective effect of SF against MA-induced nephropathy is associated with preservation of mitochondrial bioenergetics, amelioration of oxidative stress and improvement of renal hemodynamics and renal cortex oxygenation.

马来酸（MA）诱导的肾病，其特征在于蛋白尿，糖尿，血尿和尿液酸化和浓度不足。萝卜硫素（SF）是一种间接抗氧化剂，具有肾保护作用。当前工作的目的是测试针对MA引起的肾病的SF预处理。

Wistar大鼠（230–260 g）分为以下几组：对照组，MA（接受400 mg / kg的MA），SF + MA（接受4天每天接受MA和1 mg / kg的SF）和SF（仅收到SF）。MA引起蛋白尿，N-乙酰基-β- d尿排泄增加-氨基葡萄糖苷酶，并降低血浆谷胱甘肽过氧化物酶活性，肾血流量以及肾皮质的充氧和灌注。所有这些损伤都与较高水平的氧化损伤标记物和肾皮质上加剧的超氧阴离子产生有关。此外，MA损害了与复合物I，线粒体膜电位和呼吸控制指数相关的线粒体生物能，并增加了过氧化氢的线粒体产生。此外，它破坏了线粒体的形态。SF阻止了所有上述更改。

总之，SF对MA诱导的肾病的保护作用与线粒体生物能的保存，氧化应激的改善以及肾血流动力学和肾皮质氧合的改善有关。