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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Pediatr+Nephrol
2010 ; 25
(2
): 213-20
Nephropedia Template TP
Pediatr Nephrol
2010[Feb]; 25
(2
): 213-20
PMID19603188
show ga
An understanding of the pathophysiologic mechanisms of post-renal transplant
(PRT) bone disease is of important clinical significance. Although bone disease
occurs after all solid organ transplantation, the cumulative skeletal fracture
rate remains high in PRT subjects while reaching a plateau with other
transplantations. One major difference in the pathophysiology of PRT bone disease
is, perhaps, due to persistent renal phosphorus (Pi) wasting. Novel phosphaturic
agents have recently been suggested to participate in the development of bone
disease in PRT subjects. However, it is unclear as of yet whether these factors
alone or in conjunction with excess parathyroid hormone (PTH) secretion play a
key role in the development of negative Pi balance and consequent bone disease in
this population. In this review, I present a natural history of PRT
hypophosphatemia and persistent renal Pi leak, provide pathophysiologic insight
into these developments, and discuss the difficulty in diagnosing these
phenotypes in both adult and pediatric populations.
|Adult
[MESH]
|Child
[MESH]
|Chronic Kidney Disease-Mineral and Bone Disorder/blood/*etiology/physiopathology
[MESH]
free
free
free
