The roles of hydrogen sulfide in renal physiology and disease states

Hydrogen sulfide (H(2)S), an endogenous gaseous signaling transmitter, has gained recognition for its physiological effects. In this review, we aim to summarize and discuss existing studies about the roles of H(2)S in renal functions and renal disease as well as the underlying mechanisms. H(2)S is mainly produced by four pathways, and the kidneys are major H(2)S–producing organs. Previous studies have shown that H(2)S can impact multiple signaling pathways via sulfhydration. In renal physiology, H(2)S promotes kidney excretion, regulates renin release and increases ATP production as a sensor for oxygen. H(2)S is also involved in the development of kidney disease. H(2)S has been implicated in renal ischemia/reperfusion and cisplatin–and sepsis–induced kidney disease. In chronic kidney diseases, especially diabetic nephropathy, hypertensive nephropathy and obstructive kidney disease, H(2)S attenuates disease progression by regulating oxidative stress, inflammation and the renin–angiotensin–aldosterone system. Despite accumulating evidence from experimental studies suggesting the potential roles of H(2)S donors in the treatment of kidney disease, these results need further clinical translation. Therefore, expanding the understanding of H(2)S can not only promote our further understanding of renal physiology but also lay a foundation for transforming H(2)S into a target for specific kidney diseases.