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Pregnancy and Sarcoidosis*: An Insight Into the Pathogenesis of Hypercalciuria

Padmanabhan Subramanian, DM; Hithaishi Chinthalapalli, DM; Murali Krishnan, DM; Susan M. Tarlo, MBBS, FCCP; Thierry Lobbedez, MD; Maria Elsa Pineda, MD; Dimitrios G. Oreopoulos, MD, PhD
Author and Funding Information

*From the Division of Nephrology (Drs. Subramanian, Chinthalapalli, Krishnan, Lobbedez, Pineda, and Oreopoulos) and Respirology (Dr. Tarlo), University Health Network and University of Toronto, Toronto, ON, Canada.

Correspondence to: Dimitrios G. Oreopoulos, MD, PhD, University Health Network, 399 Bathurst St, Toronto, ON, M5T 2S8, Canada; e-mail: dgo@teleglobal.ca



Chest. 2004;126(3):995-998. doi:10.1378/chest.126.3.995
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Hypercalciuria with or without hypercalcemia is a well-known complication of sarcoidosis, the pathogenesis of which is not fully understood. Pregnancy is associated with physiologic alterations in calcium metabolism. These changes can further alter the derangement of calcium metabolism that occurs in sarcoidosis, if the two conditions coexist. We had the opportunity to study prospectively the changes in serum and urine calcium along with all the hormonal changes that occur during pregnancy in a young woman with sarcoidosis, who had hypercalciuria at presentation. We believe that an increased level of calcitriol is central to the calcium abnormalities in our patient. In her case, the increased calcitriol is derived from sarcoid granulomas and renal sources enhanced by the effect of estradiol and prolactin on the conversion of 25(OH)D to 1,25(OH)2 D. She acquired hypoparathyroidism, with normal serum calcium, which probably was due to the direct suppression of parathyroid hormone (PTH) secretion by calcitriol. Finally, hypercalciuria is the result of the combined effect of hyperabsorption of calcium from the gut (the result of increased calcitriol levels leading to increased filtration of calcium) and decreased tubular reabsorption of calcium, as a result of undetectable PTH.


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