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Hypocalcemia immediately after renal transplantation
Author(s) -
Nobata Hironobu,
Tominaga Yoshihiro,
Imai Hirokazu,
Uchida Kazuharu
Publication year - 2013
Publication title -
clinical transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 76
eISSN - 1399-0012
pISSN - 0902-0063
DOI - 10.1111/ctr.12221
Subject(s) - hypophosphatemia , medicine , endocrinology , transplantation , tacrolimus , urinary system , parathyroid hormone , excretion , calcineurin , urinary calcium , kidney , secondary hyperparathyroidism , kidney transplantation , calcium
Background After renal transplantation ( RTX ), hypercalcemia, mainly due to persistent hyperparathyroidism, and hypophosphatemia, caused by the improved ability to excrete phosphorus in the renal tubules, are expected. However, immediately after RTX , a transient reduction in serum calcium (Ca) levels has been previously reported, the reason for which is not clear. Patients and Methods In 21 patients receiving ABO compatible living donor kidney transplants, serum levels of Ca, phosphorus, intact parathyroid hormone (iPTH), 1,25‐dihydroxyvitamin D, and tacrolimus were measured within three wk after RTX , along with urinary Ca and phosphorus excretion. The immunosuppressive regimen consisted of a three‐drug combination including a glucocorticoid, a calcineurin inhibitor, and an antimetabolite agent. Results Serum Ca levels declined significantly during the first post‐operative week. Urinary Ca excretion increased immediately after RTX and gradually normalized. Increased urinary Ca excretion did not correlate with serum levels of iPTH and tacrolimus. Conclusions Immediately after RTX, regardless of serum iPTH and tacrolimus levels, transient increases in urinary Ca excretion and hypocalcemia were observed. Administration of glucocorticoids is one potential cause of inappropriate urinary Ca wasting.