Can someone please explain how does vitamin D toxicity lead to impaired concentration of urine in DCT leading to polydipsia and polyuria?
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Step I Vitamin D toxicity
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Vit D toxicity --> Hypercalcemia --> Nephrogenic DI through incompletely understood mechanisms. Possibly by tubulointerstitial injury or inhibition of loop sodium chloride reabsorption.
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?
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.
Thank you very much dfib slim and Phloston for the explanation! 🙂
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.
http://www.the-aps.org/mm/publications/journals/pim/sands-pdf.pdf
http://www.the-aps.org/mm/publications/journals/pim/sands-pdf.pdf
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?
