Date: Tuesday, May 2, 2017
Session Name: Poster Session D: Kidney: Cardiovascular and Metabolic
Session Time: 6:00pm-7:00pm
Presentation Time: 6:00pm-7:00pm
Location: Hall D1
- Provision of Highly Specialized Aftercare by the Transplant Center Strongly Improves Patient and Allograft Survival in Long-Term Follow-Up After Kidney Transplantation.
- Nephrectomy of the Failed First Kidney Allograft Predisposes Kidney Transplant Recipients to Presensitization with Alloreactive T-Cells and Inferior Allograft Survival After Retransplantation.
Significant variations in posttransplant phosphate levels are recognized after kidney transplantation, and associated with more favorable allograft outcomes. Although posttransplant hypophosphatemia may be associated with severe chronic kidney disease mineral bone disorder (CKD-MBD), these markers failed to provide a link towards superior allograft outcomes.
We studied 561 first deceased-donor and 297 living-donor kidney transplant recipients (KTRs) at our transplant center between 2005 and 2015. Measurements of phosphate levels posttransplantation were correlated to CKD-MBD, long-term patient and allograft outcomes. In addition, a paired difference testing was performed in 87 left/right deceased donor kidney pairs to account for donor characteristics.
KTRs with persistent hypophosphatemia showed superior death-censored allograft survival and function compared to KTRs without persistent hypophosphatemia (p<0.05). This difference, however, was observed among deceased-donor KTRs only (p<0.05). The incidence of posttransplant persistent hypophosphatemia was comparable between deceased donor (29%) and living-donor KTRs (32%). Persistent hypophosphatemia was associated with higher levels of PTH pre- and posttransplantation among deceased-donor and living-donor KTRs (p<0.05). No differences were observed for recipient/donor age, gender, BMI, cold ischemia time, HLA-match, and time on dialysis between KTRs with persistent hypophosphatemia and those without. In addition, no differences were observed for delayed allograft function, acute cellular rejection or any infectious complications (p>0.05). In the analysis of left/right deceased-donor kidney pairs, persistent hypophosphatemia was most likely detected in both kidney pairs than one pair only (p<0.05). Among those pairs with persistent hypophosphatemia no differences were observed for PTH (p>0.05).
Our results suggest that persistent hypophosphatemia among living-donor KTRs marks PTH-mediated hypophosphatemia that becomes visible due to less ischemia/reperfusion injury and tubular integrity. In contrast, posttransplant persistent hypophosphatemia among deceased-donor KTRs is associated with superior allograft outcomes. Here, our paired kidney analysis suggests that hypophosphatemia is linked to donor factors most likely associated with less ischemia/reperfusion injury and better tubular integrity, that in turn account for superior allograft outcomes.
CITATION INFORMATION: Otto N, Schachtner T, Reinke P. Persistent Hypophosphatemia Among Deceased-Donor Kidney Transplant Recipients Is Donor-Dependent and Associated with Superior Long-Term Allograft Outcomes. Am J Transplant. 2017;17 (suppl 3).
To cite this abstract in AMA style:Otto N, Schachtner T, Reinke P. Persistent Hypophosphatemia Among Deceased-Donor Kidney Transplant Recipients Is Donor-Dependent and Associated with Superior Long-Term Allograft Outcomes. [abstract]. Am J Transplant. 2017; 17 (suppl 3). https://atcmeetingabstracts.com/abstract/persistent-hypophosphatemia-among-deceased-donor-kidney-transplant-recipients-is-donor-dependent-and-associated-with-superior-long-term-allograft-outcomes/. Accessed October 29, 2020.
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