Decreased phosphate reabsorption after renal transplantation: Evidence for a mechanism independent of calcium and parathyroid hormone

Rosenbaum, Robert; Hruska, Keith A.; Korkor, Adel B.; Anderson, Charles B.; Slatopolsky, Eduardo

doi:10.1038/ki.1981.54

Cited by 76 publications

(29 citation statements)

References 34 publications

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“…Morgan et al (39) reported that transplantation of a normal kidney into a patient with XLH resulted in continued hypophosphatemia and decreased renal reabsorption of phos-phorus. This evidence is tempered by the tendency of transplanted kidneys in humans to function abnormally and exhibit low renal retention of phosphate (40). Further, at the time of study in the posttransplantation period, an abnormal hormonal milieu secondary to renal failure likely persisted, and may have influenced phosphate homeostasis.…”

Section: Discussionmentioning

confidence: 99%

Crosstransplantation of kidneys in normal and Hyp mice. Evidence that the Hyp mouse phenotype is unrelated to an intrinsic renal defect.

Nesbitt¹,

Coffman²,

Griffiths³

et al. 1992

J. Clin. Invest.

209

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Although deranged phosphate transport is the fundamental abnormality in X-linked hypophosphatemic (XLH) rickets, it remains unknown if this defect is the consequence of an intrinsic kidney abnormality or aberrant production of a humoral factor. To discriminate between these possibilities, we examined phosphate homeostasis in normal and Hyp mice, subjected to renal crosstransplantation. We initially evaluated the effects of uninephrectomy on the indices of phosphate metabolism that identify the mutant biochemical phenotype. No

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Section: Discussionmentioning

confidence: 99%

Crosstransplantation of kidneys in normal and Hyp mice. Evidence that the Hyp mouse phenotype is unrelated to an intrinsic renal defect.

Nesbitt¹,

Coffman²,

Griffiths³

et al. 1992

J. Clin. Invest.

209

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“…Post-transplant bone disease has been attributed to a variety of factors, including hyperparathyroidism, pre-transplant bone disease, steroids, immunosuppressive medications and hypophosphatemia [58,59,60,61]. …”

Section: Discussionmentioning

confidence: 99%

“…If plasma phosphorus concentrations control phosphatonin expression, it is likely that their expression is also altered in other disease entities where phosphate dysregulation is evident. Post-renal transplantation hypophosphatemia is seen commonly, and has clinical importance due to its linkage with post transplant bone disease [58,59,60,61,62]. The present study examines the impact of hyperphosphatemia and CKD on FGF-23 and sFRP-4, and the potential role of these phosphatonins in post transplantation hypophosphatemia.…”

Section: Introductionmentioning

confidence: 99%

FGF-23 and sFRP-4 in Chronic Kidney Disease and Post-Renal Transplantation

et al. 2006

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Background: The phosphatonins fibroblast growth factor-23 (FGF-23) and FRP-4 are inhibitors of tubular phosphate reabsorption that may play a role in the hyperphosphatemia associated with chronic kidney disease (CKD) or in the hypophosphatemia associated with renal transplants. Methods: Plasma FGF-23, FRP-4, phosphorus and parathyroid hormone were measured in patients at all stages of CKD. Phosphate regulation of FGF-23 and secreted frizzled related protein-4 (sFRP-4) was examined in end-stage renal disease patients in the presence and absence of therapeutic phosphate binder usage. In renal transplant patients, plasma FGF-23, sFRP-4 and phosphorus concentrations were determined before and 4–5 days after transplantation. Results: Plasma FGF-23 correlated with creatinine clearance (r² = –0.584, p < 0.0001) and plasma phosphorus (r² = 0.347, p < 0.001) in CKD patients and with plasma phosphorus (r² = 0.448, p < 0.001) in end-stage renal disease patients. Phosphate binder withdrawal increased FGF-23 levels. In kidney transplant patients, dramatic decreases in FGF-23 (–88.8 ± 5.4%) and phosphorus (–64 ± 10.2%) were observed by 4–5 days post-transplantation. In patients with post-transplant hypophosphatemia, FGF-23 levels correlated inversely with plasma phosphorus (r² = 0.661, p < 0.05). sFRP-4 levels did not change with creatinine clearance or hyperphosphatemia in CKD or end-stage renal disease patients, and no relation was noted between post-transplant sFRP-4 levels and hypophosphatemia. Conclusions: In CKD, FGF-23 levels rose with decreasing creatinine clearance rates and increasing plasma phosphorus levels, and rapidly decreased post-transplantation suggesting FGF-23 is cleared by the kidney. Residual FGF-23 may contribute to the hypophosphatemia in post-transplant patients.

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“…Decreased renal tubular reabsorption may occur, despite low levels of PTH, and hypophosphatemia can persist even after elevated PTH levels have normalized (4)(5)(6)(7). Furthermore, even if hypophosphatemia and hyperparathyroidism stimulate calcitriol (1,25-(OH) 2 -D 3 ) synthesis, calcitriol levels are often inappropriately low following renal transplantation, despite normal or mildly impaired allograft function.…”

Section: Introductionmentioning

confidence: 99%

Early post-transplantation hypophosphatemia is associated with elevated FGF-23 levels

Trombetti¹,

Richert²,

Hadaya³

et al. 2011

European Journal of Endocrinology

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Background: We examined the hypothesis that high FGF-23 levels early after transplantation contribute to the onset of hypophosphatemia, independently of parathyroid hormone (PTH) and other factors regulating phosphate metabolism. Methods: We measured serum phosphate levels (sPi), renal tubular reabsorption of Pi (TmPi/GFR), estimated GFR (eGFR), intact PTH (iPTH), calcitriol, intact (int) and C-terminal (Cter) FGF-23, dietary Pi intake and cumulative doses of glucocorticoids in 69 patients 12 days (95% confidence interval, 10-13) after renal transplantation. Results: Hypophosphatemia was observed in 43 (62%) of the patients 12 days after transplantation. Compared with non-hypophosphatemic subjects, their post-transplantation levels of intact and CterFGF-23 were higher (195 (108-288) vs 48 (40-64) ng/l, P!0.002 for intFGF-23; 205 (116-384) vs 81 (55-124) U/ml, P!0.002, for CterFGF-23). In all subjects, Cter and intFGF-23 correlated inversely with sPi (rZK0.35, P!0.003; K0.35, P!0.003, respectively), and TmPi/GFR (rZK0.50, P!0.001; K0.54, P!0.001, respectively). In multivariate models, sPi and TmPi/GFR were independently associated with FGF-23, iPTH and eGFR. Pre-transplant iPTH levels were significantly higher in patients developing hypophosphatemia after renal transplantation. Pretransplant levels of FGF-23 were not associated with sPi at the time of transplantation. Conclusion: In addition to PTH, elevated FGF-23 may contribute to hypophosphatemia during the early post-renal transplant period.

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Decreased phosphate reabsorption after renal transplantation: Evidence for a mechanism independent of calcium and parathyroid hormone

Cited by 76 publications

References 34 publications

Crosstransplantation of kidneys in normal and Hyp mice. Evidence that the Hyp mouse phenotype is unrelated to an intrinsic renal defect.

Crosstransplantation of kidneys in normal and Hyp mice. Evidence that the Hyp mouse phenotype is unrelated to an intrinsic renal defect.

FGF-23 and sFRP-4 in Chronic Kidney Disease and Post-Renal Transplantation

Early post-transplantation hypophosphatemia is associated with elevated FGF-23 levels

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