Tubular Dysfunction following Kidney Transplantation

Better, Ori S.

doi:10.1159/000181840

Cited by 35 publications

(13 citation statements)

References 18 publications

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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%

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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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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

et al. 2006

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“…39. 40], Second, intrinsic tubular dysfunction follow ing kidney transplantation [13], Third, increased tubular sensitivity to PTH [12. 41], Such undue sensitivity could explain the high frequency of PTH-unrelated renal P loss after kidney transplantation, even in patients without hyperparathyroidism [14,15], Fourth, the presence of 242 Dumoulin/Hory/Nguyen/Henriet/Bresson/ Parathyroid Suppression by Oral Calcium Rcgnard/Saint-Hillier after Renal Transplantation only one kidney.…”

Section: Abnormal P Metabolismmentioning

confidence: 99%

“…mostly a consequence of urinary P leakage [13][14][15]. Although this inappropriate phosphaturia might like ly be linked to persistent hyperparathyroidism, the role of PTH in posttransplant renal P loss remains unclear since this disorder has also been ascribed to PTH-independent mechanisms [7,12,15].…”

Section: Introductionmentioning

confidence: 99%

Acute Oral Calcium Load Decreases Parathyroid Secretion and Suppresses Tubular Phosphate Loss in Long-Term Renal Transplant Recipients

Dumoulin¹,

Hory

Nguyen³

et al. 1995

Am J Nephrol

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Persistent hyperparathyroidism and impaired tubular reabsorption of phosphate (P) are common after kidney transplantation. In order to assess the suppressibility of these abnormalities, we studied the effects of a single oral calcium (Ca) load (1 g) in 7 healthy subjects (HS) and in 14 normocalcemic long-term renal transplant recipients with good renal function (RT). In HS and RT, serum and urinary Ca were similar at baseline, and increased (p < 0.001) to the same extent after Ca ingestion. Serum parathyroid hormone (PTH) and nephrogenic cAMP (NcAMP) levels were higher at baseline in RT than HS (mean ± SEM; respectively, PTH 7.8 ± 0.8 vs. 3.5 ± 0.6 pmol/l, p < 0.001, and NcAMP 24.8 ± 2.3 vs. 13.9 ± 2.3 nmol/lGFRp < 0.01). After Ca, PTH (p < 0.001) and NcAMP (p < 0.01) decreased markedly in both RT and HS. Maximal changes in PTH and NcAMP were larger in RT than HS (PTH -3.3 ± 0.4 vs. -2.1 ± 0.03 pmol/l, p < 0.01, and NcAMP -18.2 ± 3.3 vs. -8.1 ± 2.6 nmol/l GFR, p < 0.05). Although PTH levels remained significantly higher in RT than HS from baseline to the end of the study (p < 0.001), PTH decreased to the normal range in RT after Ca load. Moreover, NcAMP reached similar values in RT and HS after Ca (16.0 ± 3.2 vs. 13.2 ± 2.8 nmol/l GFR at the end of the survey, NS). At baseline, RT had higher phosphaturia than HS (246 ± 25 vs. 127 ± 19 µmol/l, p < 0.01), and Ca ingestion lowered phosphaturia to similar values in both RT and HS (116 ± 13 vs. 95 ± 7 µmol/l GFR, NS). Renal P threshold expressed as TmP/GFR and tubular reabsorption rate of P were lower in RT than HS at baseline, and resumed normal values after Ca. To summarize, in normocalcemic long-term kidney transplant recipients, a single oral Ca intake acutely blunted the excessive PTH secretion and increased tubular reabsorption of P up to a normal range. We conclude therefore, that PTH is a main factor of tubular P loss in these patients.

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“…It should be taken into account that the transplanted kidney might not function normally. It has been reported that transplanted kidneys maintained glomerular function relatively well, but the function of the renal tubule was sometimes severely disturbed [4]. The renal tubular function of the transplanted patient in this report might be relatively well maintained, because his urinary BMG and NAG levels before surgery were the same as those of the two control patients.…”

Section: Discussionmentioning

confidence: 47%