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A more important effect of PTH on the kidney is, however, its inhibition of the reabsorption of phosphate (HPO 4 2−) from the tubular fluid, resulting in a decrease in the plasma phosphate concentration. Phosphate ions form water-insoluble salts with calcium.
PTH acts on the distal convoluted tubule and collecting duct to increase calcium reabsorption in the nephron. [28] PTH also acts on the proximal convoluted tubule to decrease phosphate reabsorption to lower the serum phosphate. [28] This decreases formation of insoluble calcium phosphate salts leading to an increase in serum ionized calcium.
PTH increases gastrointestinal calcium absorption by activating vitamin D, and promotes calcium conservation (reabsorption) by the kidneys. [12] Phosphate. PTH is the major regulator of serum phosphate concentrations via actions on the kidney. It is an inhibitor of proximal tubular reabsorption of phosphorus.
Therefore, without enough PTH there is more reabsorption of the phosphate leading to a high phosphate level in the blood. [citation needed] Chronic kidney failure: When the kidneys are not working well, there will be increased phosphate retention. [citation needed] Drugs: hyperphosphatemia can also be caused by taking oral sodium phosphate ...
phosphate: approximately 80%: Parathyroid hormone reduces reabsorption of phosphate in the proximal tubules, but, because it also enhances the uptake of phosphate from the intestine and bones into the blood, the responses to PTH cancel each other out, and the serum concentration of phosphate remains approximately the same. citrate: 70%–90% [12]
Continued elevation of PTH levels increases the abundance of osteoclasts. This leads to a greater resorption of calcium and phosphate ions. [4] High levels of calcium in the blood, on the other hand, leads to decreased PTH release from the parathyroid gland, decreasing the number and activity of osteoclasts, resulting in less bone resorption.
[4] phosphate diabetes is a condition that falls under the category of tubulopathies, which refers to the pathologies of the renal tubules. [5] The mutated PHEX gene causes pathological elevations in fibroblast growth factor 23 (FGF23), [1] a hormone that regulates phosphate homeostasis by decreasing the reabsorption of phosphate in the kidneys ...
PTH will inhibit phosphate reabsorption. AT II stimulates Na +, H 2 O and HCO 3 − reabsorption. Thin descending loop of Henle: H 2 O: Reabsorbs via medullary hypertonicity and makes urine hypertonic. Thick ascending loop of Henle: Na + (10–20%), K +, Cl −; indirectly induces para cellular reabsorption of Mg 2+, Ca 2+
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