Endocrine Abstracts

We describe a patient who was treated for hypercalcaemia with inadvertent ramifications. A 59 year old gentleman with a background history of chronic kidney disease stage (CKD) 4, type 2 diabetes mellitus, hypertension, congestive cardiac failure and bilateral lower limb below knee amputations, presented with hypercalcemia of 3.30 mmol/l (reference range 2.20–2.60) and suppressed PTH at 12 ng/l (reference range 15–65), from a previously raised PTH level of 162 due to CKD. Investigations showed raised ACE levels of 106 U/l (reference range 10–52), enlarged mediastinal and hilar lymph nodes on CT. A presumptive diagnosis of sarcoidosis was made in view of patient’s reluctance to undergo invasive biopsy. He was treated with oral prednisolone 60 mg.od. Calcium normalised to 2.56 mmol/l within one week and continued to drop further leading to symptomatic hypocalcaemia at 1.87 mmol/l in 3 weeks. The PTH rose to 268 ng/l. This was treated with alfacalcidol and the calcium normalised. His was weaned off prednisolone and patient stopped alfacalcidol in few months and the calcium remains normal with a raised PTH.

Discussion: The likely explanation for the above findings is, renal 1-alpha-hydroxylase in the proximal tubule is inhibited in chronic kidney disease, leading to calcitriol deficiency. Extra renal 1-alpha-hydroxylase is upregulated in the sarcoid granulomas which produces calcitriol leading to hypercalcemia. On administering the prednisolone, the inhibition of calcitriol synthesis in macrophages, effectively leads to vitamin D deficiency induced hypocalcemia. The above presentation demonstrates the complex interactions between renal and extra renal 1-alpha-hydroxylases and their clinical significance. On performing a literature review, we were unable to any case report describing the above phenomenon. This case highlights the need for vigilance and close monitoring in treating hypercalcemia of sarcoidosis in the presence of preexisting renal disease.