The patient, suffering from chronic renal failure, has hyperparathyroidism secondary to decreased production of active vitamin D (loss of renal 1-alpha-hydroxylase activity). 1-alpha hydroxylase activity as well as 25-hydroxylase are required to make the active form of vitamin D, 1,25 dihydrocholecalciferol. 25-hydroxylase is produced in the liver and in end stage liver disease you would be unable to produce active 1,25 vitamin D.
Secondary hyperparathyroidism is the increase in parathyroid hormone (PTH) as a result of decreased calcium. This may occur due to decreased calcium intake, hyperphosphatemia, as well as decreased serum levels of vitamin D (i.e., renal failure, liver failure). When vitamin D levels are decreased, there is decreased Ca absorption from the GI tract, leading to decreased serum Ca levels -- resulting in increased PTH release.
Taniegra notes the common lab findings seen in secondary hyperparathyroidism. The author notes that serum PTH is increased and that Ca levels may be low; the low serum Ca is opposite to what is seen in primary hyperparathyroidism (high serum Ca). The causes of low Ca can be due to lack of adequate vitamin D or decrease of Ca ingestion. Furthermore, deficiencies may result from malabsorption of Ca/vitamin D.
Lips discusses how vitamin D deficiency-mediated secondary hyperparathyroidism may result in the elderly due to age-related changes in their skin response to UV light. The author notes that UV light-mediated formation of vitamin D is decreased in this patient population and if their diet does not contain adequate vitamin D, this can result in vitamin D deficiency. Treatment centers around increasing intake of foods fortified with vitamin D and also intake of vitamin supplements.
Illustration A depicts how calcium is regulated in the body. Note how if the kidneys and liver are unable to produce the active form of vitamin D, there will be decreased Ca absorption from the gut.
Illustration B is a table showing the different calcium, phosphorous, and alkaline phosphatase levels in primary, secondary, and tertiary hyperparathyroidism.
Answer 2: Though insufficient Ca intake can lead to hyperparathyroidism, the mechanism is not driven by decreased levels of vitamin D.
Answer 3: Parathyroid adenomas cause hyperparathyroidism due to increased secretion of PTH from the mass -- primary hyperparathyroidism.
Answer 4: Decreased functioning of the CASR can cause increased release of PTH from chief cells, however this is not driven by low vitamin D levels.
Answer 5: Sarcoidosis granulomas contain 1-alpha-hydroxylase, and would be associated with an increase in vitamin D and no hyperparathyroidism.
Taniegra ED. Hyperparathyroidism. Am Fam Physician. 2004 Jan 15;69(2)
PMID:14765772 (Link to Abstract)
Lips P. Vitamin D deficiency and secondary hyperparathyroidism in the elderly: consequences for bone loss and fractures and therapeutic implications. Endocr Rev. 2001 Aug;22(4)
PMID:11493580 (Link to Abstract)