Stanniocalcin supports the functional adaptation of adult-sized kidneys transplanted into the pediatric recipients.

BACKGROUND

The functional adaptation of adult-sized kidney (ASK) grafts to the recipient's size is not completely reversible and is associated with irreversible histologic damage in the smallest recipients. The aim of the study was to unveil the molecular mechanisms underlying the functional adaptation of ASK transplants to small pediatric recipients.

METHODS

Because physiologic and functional adaption of ASK in infants is seen maximally at 3 months after transplantation, we selected 21 pediatric recipients of an ASK with protocol biopsies at engraftment and 3 and 6 months, without delayed graft function or interval rejection, and we conducted whole-genome expression profiles of the renal allograft biopsies at 3 months and correlated results with subsequent absolute glomerular filtration rate (aGFR).

RESULTS

Seven hundred twenty-four unique genes correlated significantly with aGFR (q value <5%). Canonical pathway analysis identified overrepresentation of relevant pathways involved in regulation of tubular salt reabsorption and enzymatic pathways for organ development and hypertrophy. The single gene that correlated best with aGFR was stanniocalcin 1 (STC1). STC1 expression also correlated with the recipient's size at the time of transplantation and the chronic allograft damage index at 6 months.

CONCLUSIONS

Functional adaptation of adult-sized grafts to the pediatric recipient is associated with molecular adaptation for normal-volume homeostasis of the recipient. Our finding also suggests that stanniocalcin (STC1) plays an important role on functional adaption in pediatric kidney transplantation.