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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Chronic kidney disease–mineral and bone disorder (CKD-MBD) is a well-known complication of progressive CKD. In early CKD, phosphate excretion is maintained through reduced tubular reabsorption driven by elevated parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23). As CKD advances, this mechanism fails, leading to hyperphosphatemia. Kidney transplantation, a form of renal replacement therapy, often causes a marked drop in serum phosphate early post-transplant, sometimes resulting in transient hypophosphatemia. This is attributed to ongoing renal phosphate wasting driven by elevated PTH and FGF23 levels. Although some patients develop severe hypophosphatemia, few studies have examined its incidence, duration, complications, or risk factors. This study aimed to investigate the clinical features of early post-transplant severe hypophosphatemia following living donor kidney transplantation.
We retrospectively analyzed 206 patients who underwent living donor kidney transplantation and developed hypophosphatemia between 2016 and 2021. Changes in serum phosphate levels during the first month after kidney transplantation were evaluated. Based on the lowest serum phosphate level, patients were categorized as having severe (<1.0 mg/dL), moderate (1.0–1.5 mg/dL), or mild (1.5–2.5 mg/dL) hypophosphatemia. We assessed the incidence, time to nadir, duration of severe hypophosphatemia, and short- and long-term outcomes including symptoms, treatment requirements, bone mineral density at 1 year, kidney function, and trends in mineral metabolism. Associations with pre-transplant recipient and donor characteristics, early post-transplant kidney function, and postoperative dietary intake were also analyzed.
Among 206 patients, 23 (11.2%) developed severe hypophosphatemia. No overt symptoms directly attributable to hypophosphatemia were observed. Bone mineral density at 1 year post-transplant did not differ significantly among groups. The severe group tended to show better post-transplant kidney function. Among pre-transplant recipient factors, sex, prior transplantation, and corrected calcium differed significantly across groups. Dialysis vintage and PTH levels showed no significant differences. Donor age, sex, and renal function also did not differ. Compared with the moderate and mild groups, the severe group had significantly higher estimated glomerular filtration rate (eGFR) and had lower food intake one week after transplantation. When patients were stratified by median eGFR and dietary intake at one week after transplantation, the subgroup with higher eGFR and lower dietary intake had the highest incidence of severe hypophosphatemia.
Severe hypophosphatemia in the early post-transplant period may be influenced not only by pre-transplant factors such as corrected calcium and dialysis vintage but also by favorable early graft function and reduced dietary intake.
