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Can someone please explain how does vitamin D toxicity lead to impaired concentration of urine in DCT leading to polydipsia and polyuria?
Thanks
 

dfib slim

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Can someone please explain how does vitamin D toxicity lead to impaired concentration of urine in DCT leading to polydipsia and polyuria?
Thanks
Vit D toxicity --> Hypercalcemia --> Nephrogenic DI through incompletely understood mechanisms. Possibly by tubulointerstitial injury or inhibition of loop sodium chloride reabsorption.
 

Saxappeal1

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Ehh, if the mechanism isn't completely understood I guess we aren't expected to understand it; but tubulointerstitial injury makes sense I guess-- is it possible for the hypercalcemia to cause calcium deposits to solidify in the DCT, resulting in some sort of physical injury to the receptors in the DCT?
 
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Phloston

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dfib slim has pretty much nailed it. Hypercalcemia, through debated mechanisms, can cause "direct tubular damage" (what I remember from questions) and a lack of response to ADH.
 

lymphocyte

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Clinically there's a distinction between partial and complete nephrogenic DI (and one extremely annoying UWorld question I still remember 2 years later). Hypercalcemic crisis causes partial nephrogenic DI, so you still maintain some capacity to concentrate urine. The mechanism isn't that controversial. Down-regulation of aquaporin-2 channels in the medulla.

upload_2016-8-16_21-49-13.png

http://www.the-aps.org/mm/publications/journals/pim/sands-pdf.pdf
 

Saxappeal1

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Lymphocyte so the hypercalcemia down regulates the ADH receptors in the medulla, but only partially? What sort of condition or causes would cause a complete nephrogenic DI?
 
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