Ryuzaky et al. showed that in the non-clipped kidneys at 12 weeks after 2K1C surgery, activated prorenin levels, Ang II levels, and transforming growth factor (TGF)-β mRNA levels of HRP-treated rats were prevented as compared to 2K1C rats, suggesting again that PRR-dependent activation of prorenin contributes to the pathogenesis of slowly progressive nephropathy in the contralateral kidney in a rat model of renovascular hypertension [56]. The gene discussed is ATP6AP2; the disease is renovascular hypertension.