Hydrogen sulfide (H2S) is constitutively synthesized in the kidney. Recent investigations suggest a role for H2S in the regulation of fundamental kidney physiological events including arterial blood flow, glomerular filtration, and electrolyte and water transport. Deficiency of H2S generation has been implicated in acute kidney injury brought on by ischemia, administration of nephrotoxic medications, and obstruction. A role for impaired H2S expression has been shown in chronic kidney injury seen with chronic heart failure, obesity, and diabetes. Deficient H2S generation by the kidney could contribute to blood pressure dysregulation in models of hypertension and preeclampsia. Aging induced chronic kidney impairment is associated with inadequate H2S generation in the kidney. The mechanistic pathways regulated by H2S include but not limited to transcription, mRNA translation, signaling, inflammation, and oxidative stress demonstrating the versatility of the gasotransmitter. In the aforementioned conditions amelioration of kidney injury has been reported by the administration of agents that provide H2S. In renal cancer H2S may participate as an injurious agent. Overall, research on H2S in the kidney is in its early stages, and it is becoming evident that it has a context-dependent nuanced role in various kidney pathologies. There is an urgent need for exploration of H2S in physiology and pathology of the kidney including its role in oxygen sensing and glomerulonephritis. H2S may prove to be a novel therapeutic agent in some kidney disease states.
Keywords: Acute kidney injury; Chronic kidney disease; Gasotransmitter; Hypertension; Signaling.
© 2021. Springer Nature Singapore Pte Ltd.