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I know that PTH serves to endocytose Na-Phosphate symporters from the apical surface of renal tubular cells into the cytoplasm. I realize in chronic renal failure the kidney isn't working as well in general, however, if there is increased PTH, then there would be an increase in endocytosis of these symporters and you would think that more phosphate would be wasted in CRF. So why do we see hyperphosphatemia? If your answers is, because less is filtered by the kidneys, well fair, except then why dont we also see hypercalcemia as well?
to put the question another way, even if PTH can't act on the kidney tubular cells because they are messed up, then it follows that there would be phosphate reabsorption (because the tubular cells are messed up). Either way, logic would argue that you should be hypophosphatemic in CRF.
to put the question another way, even if PTH can't act on the kidney tubular cells because they are messed up, then it follows that there would be phosphate reabsorption (because the tubular cells are messed up). Either way, logic would argue that you should be hypophosphatemic in CRF.