Hypophosphatemic Rickets (HPR) – Pathophysiology Explained

Hypophosphatemic rickets (HPR) is a classic example of how disordered phosphate homeostasis, rather than calcium deficiency, leads to rickets, bone deformities, and impaired growth. Understanding its pathophysiology is essential for correct diagnosis and rational therapy. In this MedEClasses session, we break down the pathophysiology of HPR step by step, linking molecular mechanisms to clinical and biochemical patterns using a clear, clinician-friendly framework. What this video covers Normal phosphate physiology and its role in bone mineralization Renal phosphate handling and NaPi transporters The central role of FGF23 in phosphate regulation How excess FGF23 causes: Renal phosphate wasting Reduced 1,25(OH)₂D synthesis Defective bone mineralization Pathophysiological basis of XLH and other FGF23-mediated disorders Why calcium may be normal but rickets still develops Linking mechanisms to lab patterns: low phosphate, high ALP, normal/low calcium Clinical implications: growth failure, bone pain, deformities, poor response to vitamin D alone Learning format Conceptual explanation with clinical correlation Case-based reasoning Clear take-home mechanisms relevant for practice Who should watch Pediatric endocrinologists Pediatricians Fellows and residents Clinicians managing rickets and metabolic bone disease Disclaimer: Educational content for healthcare professionals. Clinical decisions must be individualized. Hashtags #HypophosphatemicRickets #HPR #FGF23 #PhosphateMetabolism #Rickets #BoneHealth #PediatricEndocrinology #MedEClassesLearn about the intricacies of Pediatric Endocrinology. MedEClasses Online Fellowship in Pediatric Endocrinology. https://learning.growsociety.in/learning-opportunities