Post-renal transplantation hypophosphatemia: a review and novel insights.
OBJECTIVE
This review intends to elucidate the pathophysiologic mechanism of renal phosphorus loss in the post-renal transplantation population. This review will provide new insight in to the pathophysiologic mechanism(s) responsible for the development of this phenomenon and will also explore the pathogenetic role of persistent phosphorus wasting in the development of post-renal transplantation osteodystrophy.


RESULTS
Recently, the phosphaturic hormone, fibroblast growth factor-23, has been ascertain to be increased in the sera of patients with chronic kidney and end-stage renal disease. There is new evidence that a non-PTH humoral factor is persistently present in post-renal transplantation patients that is likely responsible for the observed persistent renal phosphorus loss. We offer that fibroblast growth factor-23 (and/or other phosphatonins) is the culprit factor responsible for the phenomenon of persistent hypophosphatemia in post-renal transplantation patients. Moreover, we believe that the phenomenon of persistent renal phosphorus wasting is an important but overlooked cause of osteodystrophy and increased fracture risk in this patient population.


CONCLUSIONS
The pathophysiology of post-renal transplantation phosphorus wasting is complex and to date is still not fully recognized. Further studies of the regulatory mechanism of fibroblast growth factor-23 and its metabolism may offer additional insights into phosphorus homeostasis and its clinical application in the post-renal transplantation population.
Department of Internal Medicine and Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Hrishikesh
H
Ghanekar
Brian J
BJ
Welch
Orson W
OW
Moe
Khashayar
K
Sakhaee
D000818:Animals; D015415:Biomarkers / Q000032:analysis; D015519:Bone Density / Q000502:physiology; D012080:Chronic Kidney Disease-Mineral and Bone Disorder / Q000209:etiology* / Q000503:physiopathology; D015232:Dinoprostone / Q000235:genetics / Q000378:metabolism; D005260:Female; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000378:metabolism; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D017674:Hypophosphatemia / Q000209:etiology* / Q000378:metabolism*; D007676:Kidney Failure, Chronic / Q000175:diagnosis / Q000601:surgery; D016030:Kidney Transplantation / Q000009:adverse effects* / Q000379:methods; D008297:Male; D010281:Parathyroid Hormone / Q000378:metabolism; D011379:Prognosis; D018570:Risk Assessment; D012680:Sensitivity and Specificity
D015415:Biomarkers; D010281:Parathyroid Hormone; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23; D015232:Dinoprostone