What are some conditions that would affect one’s ability to produce the active form of Vitamin D?

What are some conditions that would affect one’s ability to produce the active form of Vitamin D?
I’m going to mention factors that both increase calcitriol (active form of vitamin D) and decrease it. There are 2 steps in activating vitamin D (1):

1^st: in liver, Provitamin D (from forms and sources you mentioned) is converted to 25(OH)D via enzyme 25-hydroxylase.

2^nd: in kidneys, 25(OH)D converted to 1,25 (OH)₂D via enzyme the enzyme 1-hydroxylase. The 1,25 (OH)₂D is calcitriol and considered the active form of vitamin D.

Renal disease may impact step 2 above and reduce the availability of active form of vitamin D. Inducers of the renal enzyme that form calcitriol are PTH and hypophosphatemia, whereas repressors are calcium and calcitriol itself (2). Pathological states, such as lymphoma may see rise in levels of calcitriol as the enzyme 1-hydroxylase is present in circulating macrophages and more active vitamin D is produced (2). In lymphoma, unlike in kidneys, the enzyme is NOT repressed by calcium or calcitriol, so hypercalcemia may result (2). Medications such as glucocorticoid, ketoconazole or chloroquine repress the enzyme 1-hydroxylase reducing levels of calcitriol. Sarcoidosis also results in hypercalcemia as the enzyme 1-hydroxylase is present in granuloma (2).

Fibroblast growth factor 23 (FGF23) normally suppresses renal enzyme 1-hydroxylase which may result in hypocalcemia when elevated (3). FGF-23 is produced by osteocytes when phosphate or calcitriol increases in serum (2,3). Thus in renal disease that results in higher phosphate levels in serum will prompt higher levels of FGF23 which in turn inhibits renal enzyme 1-hydroxylase resulting in hypocalcemia and increased phosphate in urine (3). Mutations that lead to higher levels of FDG23 exist which lead to chronic vitamin D deficiency (2). 

Step 1 of active vitamin D production can be impaired with liver disease, or medications that inhibit liver hydroxylases, such as barbiturates, phenytoin, rifampin or isoniazid (2). Inhibitors of liver conversion of provitamin D to storage form of vit D lead to decreased levels of calcitrol due to decreased supply of 25(OH)D.

Sources:
1/ Gropper et al. Advanced Nutrition in Human Metabolism. 7th Ed. Cengage. 2018.
2/ Bringhurst F, Demay MB, Kronenberg HM. Bone and Mineral Metabolism in Health and Disease. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. Harrison's Principles of Internal Medicine, 20e New York, NY: McGraw-Hill`
3/ Jüppner, H., 2011. Phosphate and FGF-23. Kidney Int. Suppl. S24-27. https://doi.org/10.1038/ki.2011.27