Disorders of Phosphorus

The Effects of Acid on Calcium and Phosphate Metabolism

“…Additionally, PTH production is inhibited by 1,25(OH) 2 D 3 [35]. At the tubular level, PTH enhances distal calcium reabsorption through the upregulation of TRPV5, leading to increased serum calcium levels [36].…”

“…Additionally, PTH production is inhibited by 1,25(OH)2D3 [35]. At the tubular level, PTH enhances distal calcium reabsorption through the upregulation of TRPV5, leading to increased serum calcium levels [36]. Phosphate is essential for many physiological needs, including cellular energy production, cell signaling and structure, oxygen delivery to tissues and bone mineralization, among others.…”

“…Most phosphate exists as hydroxyapatite in the mineralized bone matrix (85%), and 14% intracellularly [34], of which 70% occurs as organic (phospholipids, phosphoproteins, nucleic acids, adenosine triphosphate (ATP) and cyclic adenosine monophosphate (cAMP)) and 30% as inorganic phosphate. Only 1% of total body phosphate exists as non-osseous extracellular serum phosphate [36] in the serum, of which 15% is found to be protein bound, 14% is complexed to cations [35], and 47% is ionized as divalent (HPO 4 2− ) and monovalent (H 2 PO 4 − ) phosphate in a 4:1 ratio at pH 7.4 [36]. Phosphate homeostasis is balanced through three major systems: intestinal uptake, bone release/incorporation and renal excretion.…”

“…Phosphaturia occurs when maximal tubular phosphate reabsorption becomes saturated. The regulatory mechanisms of renal phosphate reabsorption adapt to the body's needs, [36] including the parathyroid hormone (PTH), Fibroblast Growth Factor-23 (FGF-23) and αKlotho [42]. FGF-23 and PTH promote the retrieval and degradation of NaPi-IIa [43], NaPi-Iic [41,44] and PiT2 (Figure 3) [8].…”

“…FGF-23 and PTH promote the retrieval and degradation of NaPi-IIa [43], NaPi-Iic [41,44] and PiT2 (Figure 3) [8]. Additionally, in a phosphate depletion state, there is a reduction in the phosphaturic effect of PTH [36] due to the augmentation of the tubular reabsorption of phosphate [45]. It has been recently described that the calcium-sensing receptor (CaSR) represents a phosphatesensing mechanism in the parathyroid gland, since raising the extracellular phosphate concentration significantly inhibited CaSR activity via non-competitive antagonism and stimulated PTH secretion in murine models [46].…”