This paper defines the structural architecture of the Lantern of Sulfur (LoS) framework, a translational model for understanding hyperchloremia as a system-level signal rather than an isolated electrolyte abnormality. Persistent hyperchloremia is typically interpreted within renal or acid–base frameworks. However, it frequently appears in the absence of intrinsic kidney dysfunction and does not respond predictably to standard interventions. This work reframes hyperchloremia as a regulatory terrain signal—an output of upstream conditions involving hydration state, bile flow, neuroendocrine signaling, and metabolic coordination. The model maps how upstream regulatory dynamics shape downstream terrain and signal expression across RAAS, HPA, and mitochondrial systems. It positions the kidney as an execution layer responding to upstream conditions rather than a primary driver of dysfunction. This paper represents Concept A (Structure) within the Lantern of Sulfur framework. It establishes the system architecture that underlies companion papers describing mechanistic execution (Concept B), failure dynamics (Directional Pressure Failure), clinical pattern expression (Concept C), and application. Derived from longitudinal observation across repeated collapse–recovery cycles, this framework is presented as a pattern-based, testable model intended to organize existing physiological signals into a coherent system for clinical evaluation and further research. This work is part of the Lantern of Sulfur (LoS) framework, a systems-level model of electrolyte balance, RAAS signaling, and physiological coordination. For the complete master index of related works, see concept DOI: 10.5281/zenodo.17915492
Beth Ann Martell (Wed,) studied this question.