Hydrogen Therapy Shows Promise for Treating Nighttime Frequent Urination

Authors
Journal
Biochemistry and Biophysics Reports
Year
DOI
10.1016/j.bbrep.2025.101923
Study Type
Mouse
Outcome
Positive
Peer Reviewed
Yes
Country
Japan
Health Condition
Nocturnal Polyuria
Body System
Urinary

TL;DR

A new study suggests that an antioxidant made from silicon could help treat frequent nighttime urination by reducing kidney stress and regulating salt handling in the body.

Key Finding

Oxidative stress in the kidney activates the NCC pathway, driving nocturnal polyuria in mice, and a silicon-based hydrogen-releasing agent reduced this oxidative stress and improved nighttime urination symptoms.

Summary

Nocturnal polyuria is a condition where people urinate excessively at night, disrupting sleep and quality of life. This mouse study found that excess oxidative stress (cellular damage from unstable molecules) in the kidneys activates a protein called NCC, which causes the body to retain sodium during the day and then excrete it excessively at night, leading to nighttime urination. When researchers treated the mice with a new silicon-based agent that releases hydrogen and reduces oxidative stress, the NCC activation decreased and nighttime urination improved.

Practical Takeaway

This is early research in mice only, so findings cannot yet be applied to humans. The study suggests that targeting oxidative stress in the kidneys may be a promising approach for nocturnal polyuria, but human clinical trials would be needed to determine if hydrogen-releasing agents could help people with this condition. The specific silicon-based agent tested here is not yet available for consumer use.

Abstract

Nocturnal polyuria is a prevalent condition associated with significant deterioration in quality of life and increased risk of mortality. Despite its clinical relevance, the underlying pathogenesis is poorly understood, and existing therapies have limited efficacy. A recent study in mouse model revealed that overactivation of the intrarenal SPAK (STE20/SPS1-related proline-alanine rich protein kinase)-sodium chloride co-transporter (NCC) pathway in the distal renal tubule is a crucial mechanism contributing to nocturnal polyuria. Here, we demonstrate that increased oxidative stress in the kidney activates the NCC, leading to insufficient sodium excretion during the active period and compensatory sodium excretion during the inactive period, resulting in polyuria during the inactive period. In addition, we show that a newly developed antioxidant-a silicon component agent-reduced oxidative stress and inhibited NCC activation, resulting in the amelioration of polyuria during the inactive period. These findings highlight the critical contributions of intrarenal oxidative stress to the pathogenesis of nocturnal polyuria and suggest that silicon-based agent holds promise for clinical application as a novel treatment for nocturnal polyuria.