Lab findings include ↑ PTH (response to low calcium), ↓ serum calcium (renal failure), ↑ serum phosphate (renal failure), and ↑ alkaline phosphatase (PTH activating osteoBlasts).
haliburtonalso remember that in renal failure, 1-alpha-hydroxylase activity is down, so there will be less activation of 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol, which is a key mechanism causing hypocalcemia.+12019-05-22T19:39:55Z
crwhy not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain+2019-06-15T17:50:55Z
nala_ulaIncreased phosphate, since the kidneys aren't working well, leads to the release of fibroblast growth factor 23 from bone, which decreases calcitriol production and decreased calcium absorption. The increase in phosphate and the decrease in calcium lead to secondary hyperparathyroidism. +12019-06-16T20:38:35Z
privatejokerProbably a dumb question but how do we definitively know that the ALP is elevated if they give us no reference range in the lab values or Q stem? Everything stated above definitely makes sense from a physiological standpoint, I was just curious.+2019-07-18T03:22:29Z
why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain +
usmle11ai believe increase 25OHcholecalciferol indicates the storage capacity of vit D, which wont be affected in case of CKD.
it goes like this, kidneys wont respond to regular PTH, loses Ca and cant execrete PO4, PTH gets made and tries to burn bone to produce Ca, resulting in elevated levels of Ca and PO4, Ca will bind the calcium and go to kidneys, yet same story all over.
add to that the fact that 1 oh hydroxylase wont be able to function in a dead kidney.+2019-07-04T16:21:34Z
to snoo-finity ... and beyond!
submitted by hayayah(416), 2019-05-19T22:51:40Z
Secondary hyperparathyroidism (usually d/t chronic renal failure).
Lab findings include ↑ PTH (response to low calcium), ↓ serum calcium (renal failure), ↑ serum phosphate (renal failure), and ↑ alkaline phosphatase (PTH activating osteoBlasts).