ORLANDO, Fla.—Low serum 25-hydroxyvitamin D (25-D) levels may play a role in bone disease among renal transplant recipients, researchers reported here at the National Kidney Foundation’s Spring Clinical Meetings.
Investigators at the State University of New York Upstate Medical University in Syracuse retrospectively studied 419 renal transplant recipients and found preliminary evidence suggesting that vitamin D deficiency may aggravate secondary hyperparathyroidism (SHPT) and lead to a subsequent decrease in bone mineralization.
It has been shown that kidney transplantation causes a reduction in parathyroid hormone (PTH) concentration, helps correct hyperphosphatemia, and improves production of 1,25-dihydroxyvitamin D3. However, persistent SHPT is common after transplantation, and renal osteodystrophy remains an ongoing, clinically significant problem.
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Julie Ann Linatoc, MD, and her colleagues conducted a retrospective study of all adult renal transplant patients attending a renal transplant clinic from January 1999 to July 2009 who had 25-D, PTH, and bone mineral density (BMD) measured.
Of the 419 recipients, only 33 patients had vitamin D levels measured. All 33 had low levels of vitamin D, with vitamin D insufficiency present in 54%, deficiency in 45%, and severe deficiency in 1%. In addition, 82% had hyperparathyroidism. Of the 10 patients who had BMD measurements, three had osteoporosis and four had osteopenia.
“This is a wake-up call that we need to measure vitamin D levels and bone mineral density,” said Dr. Linatoc, a medical resident, in an interview with Renal & Urology News. “Right now, there is no consensus in this area about monitoring these levels. So this needs to be extensively studied.”
