Hyperphosphatemia in Kidney Failure: Pathophysiology, Challenges and Critical Role of Phosphorus Management

作者：Swetha Raju, Ramesh Saxena · 发表于：Preprints.org · 年份：2025 · DOI：10.20944/preprints202503.2193.v2 · 被引用次数：4 · 研究领域：Parathyroid Disorders and Treatments、Hemoglobinopathies and Related Disorders、Electrolyte and hormonal disorders

Phosphorus is one of the most abundant minerals in the body and plays a pivotal role in numerous cellular processes, including maintenance of skeletal health, integrity of phospholipid bilayers, cell signaling, and synthesis of nucleic acid and adenosine triphosphate (ATP). About 85% of total phosphate is deposited in bone as hydroxyapatite crystals, 14% is present in soft tissues as various organic phosphates, and the remaining 1% is found in extracellular space mainly as inorganic phosphate. The plasma inorganic phosphorus concentration is tightly maintained between 2.5 - 4.5 mg/dL by intertwined interactions between fibroblast growth factor 23 (FGF-23), parathyroid hormone (PTH) and vitamin D that tightly regulate the precise balance in the phosphorus trafficking across the gastrointestinal tract, kidneys and bones. Disruption of the tight hemostatic control of phosphorus balance can lead to altered cellular and organ functions that are associated with high morbidity and mortality. In the past three decades, there has been a steady increase in the prevalence of kidney failure (KF) population needing various kidney replacement therapies. The individuals with KF have unacceptably high mortality, and well over half of deaths are related to cardiovascular disease. Abnormal phosphorus metabolism is one of the major factors that is independently associated with vascular calcification and cardiovascular mortality in KF. While overt hyperphosphatemia is observed late during the pr...