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Retired NBME 24 Answers

 +9  upvote downvote
submitted by โˆ—radshopeful(19)
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chronic kidney disease --> decreased EPO --> decreased hematocrit chronic kidney disease --> decreased PO4- excretion --> increased PTH chronic kidney disease --> decreased 1,25 dihydrovitD (calcitriol) --> increased PTH

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jotajota94  she is also volume overloaded. more fluid leads to a decrease in Hematocrit. +6
h0odtime  I thought PTH increases 1-alpha-hydroxylase which increases levels of 1 ,25? +1
batmane  it's supposed to in the setting of proper kidney fxn +2
h0odtime  Whoops +1
avocadotoast  The decrease in GFR leads to decreased delivery of 25 dihydro vit D to the PCT and the decrease in functional renal mass limits production of 1a-hydroxylase. The increase in PO4 also stimulates FGF-23 from bone, which inhibits PO4 reabsorption and 1a-hydroxylase. +1



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submitted by โˆ—avicenna(12)
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got it from osmosis

Finally, thereโ€™s renal osteodystrophy.

This happens for a number of reasons and itโ€™s important to memorize all of them.

First, the kidneys canโ€™t excrete phosphate, leading to hyperphosphatemia.

Next, the kidneys are needed to convert 25- hydroxyvitamin D to active 1,25 dihydroxyvitamin D, or calcitriol, which is the active form of vitamin D which helps with intestinal calcium reabsorption.

As a result, there will be hypocalcemia.

Now, since thereโ€™s too much phosphate and too little calcium, this can affect the bones and they can become thinner and more prone to break.

Hyperphosphatemia and hypocalcemia also triggers the parathyroid glands to release more parathyroid hormone, a hormone that causes increased bone break down to release more calcium.

Finally, the extra phosphate in the blood can also bind to calcium and they can deposit in various tissues, such as the vascular tissue.

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