In people with type 2 diabetes, higher levels of vitamin D-binding protein in the blood are consistently observed as kidney function worsens, with measurable increases from 93.6 ng/mL to 132.8 ng/mL...
Mechanism
Synthesis from 1 study
When kidneys stop working well, they can't remove a protein called vitamin D-binding protein, so it builds up in the blood. The body also makes more of this protein because low calcium and low active vitamin D signal the liver to produce it. More of this protein traps vitamin D, making it harder...
Most probable mechanism
When the kidneys fail, they can no longer filter out vitamin D-binding protein effectively, so it builds up in the blood. At the same time, low calcium and low active vitamin D signal the liver to make more of this protein, which traps vitamin D and prevents it from working properly. This causes more vitamin D-binding protein to accumulate as kidney damage gets worse.
The kidneys lose the ability to filter and excrete vitamin D-binding protein due to reduced glomerular filtration rate and tubular dysfunction.
Hypocalcemia and reduced production of active vitamin D trigger increased hepatic synthesis of vitamin D-binding protein as a compensatory response.
Elevated vitamin D-binding protein binds a larger proportion of circulating vitamin D and its active metabolite, reducing the concentration of free, biologically available vitamin D.
Reduced bioavailability of active vitamin D impairs intestinal calcium absorption and renal calcium reabsorption, sustaining hypocalcemia and further stimulating hepatic vitamin D-binding protein production.
The persistent elevation of vitamin D-binding protein in serum correlates directly with the severity of kidney dysfunction, creating a progressive increase in serum levels as kidney function declines.
Evidence from Studies
Supporting (1)
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