Oral hydrogen water prevents chronic allograft nephropathy in rats.

Abstract

Reactive oxygen species (ROS) are implicated in the interstitial fibrosis and tubular atrophy characteristic of chronic allograft nephropathy (CAN). Using an orthotopic kidney transplantation model (Lewis-to-Brown Norway rat), animals received hydrogen-rich water (HW) or regular water from day 0 through day 150 post-transplant. Recipients given regular water progressively developed proteinuria and declining creatinine clearance, culminating in graft failure. By contrast, HW-treated animals maintained better allograft function, showed slower CAN progression, exhibited reduced oxidative damage and inflammatory mediator levels, and achieved higher overall survival rates. Activation of mitogen-activated protein kinase inflammatory signaling cascades was markedly lower in renal allografts from HW-treated animals. These findings indicate that orally administered molecular hydrogen exerts antioxidant and anti-inflammatory effects capable of preserving transplanted kidney function in this experimental model.

Mechanism

Molecular hydrogen scavenges ROS, thereby reducing oxidative damage and dampening MAPK-mediated inflammatory signaling, which collectively limits interstitial fibrosis and tubular atrophy in renal allografts.