Tags

Type your tag names separated by a space and hit enter

Renal phosphate loss in long-term kidney transplantation.
Clin J Am Soc Nephrol. 2012 Feb; 7(2):323-31.CJ

Abstract

BACKGROUND AND OBJECTIVES

Renal phosphate wasting occurs early postkidney transplantation as a result of an accumulation of parathyroid hormone and fibroblast growth factor 23 from the CKD period. Serum phosphate, parathyroid hormone, and fibroblast growth factor 23 return to baseline 1 year postkidney transplantation. What happens beyond this period is unknown.

DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS

Mineral parameters were obtained from 229 kidney transplant recipients at least 1 year posttransplantation; 46 normal subjects and 202 CKD patients with similar GFR served as controls. Factors associated with phosphate metabolism were analyzed.

RESULTS

Despite the reduced graft function, most kidney transplant recipients had lower serum phosphate than normal subjects accompanied by renal phosphate loss. Fibroblast growth factor 23 was mostly lower or comparable with normal subjects, whereas parathyroid hormone was elevated in most patients. Hyperparathyroidism is also more common among kidney transplant recipients compared with CKD patients. Both parathyroid hormone and fibroblast growth factor 23 showed relationships with renal phosphate excretion, but only parathyroid hormone displayed an independent association. Parathyroid hormone showed the highest area under the curve in predicting renal phosphate leak. When patients were categorized according to parathyroid hormone and fibroblast growth factor 23 levels, only subset of patients with high parathyroid hormone had an increased renal phosphate excretion.

CONCLUSIONS

Relatively low serum phosphate from renal phosphate leak continued to present in long-term kidney transplantation. Both parathyroid hormone and fibroblast growth factor 23 participated in renal tubular phosphate handling, but persistent hyperparathyroidism seemed to have a greater influence in this setting.

Authors+Show Affiliations

Division of Nephrology, Department of Medicine, Ramathibodi Hospital, Mahidol University, Phayathai, Bangkok, 10400 Thailand.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22134626

Citation

Sirilak, Supinda, et al. "Renal Phosphate Loss in Long-term Kidney Transplantation." Clinical Journal of the American Society of Nephrology : CJASN, vol. 7, no. 2, 2012, pp. 323-31.
Sirilak S, Chatsrisak K, Ingsathit A, et al. Renal phosphate loss in long-term kidney transplantation. Clin J Am Soc Nephrol. 2012;7(2):323-31.
Sirilak, S., Chatsrisak, K., Ingsathit, A., Kantachuvesiri, S., Sumethkul, V., Stitchantrakul, W., Radinahamed, P., & Disthabanchong, S. (2012). Renal phosphate loss in long-term kidney transplantation. Clinical Journal of the American Society of Nephrology : CJASN, 7(2), 323-31. https://doi.org/10.2215/CJN.06380611
Sirilak S, et al. Renal Phosphate Loss in Long-term Kidney Transplantation. Clin J Am Soc Nephrol. 2012;7(2):323-31. PubMed PMID: 22134626.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Renal phosphate loss in long-term kidney transplantation. AU - Sirilak,Supinda, AU - Chatsrisak,Kamonwan, AU - Ingsathit,Atiporn, AU - Kantachuvesiri,Surasak, AU - Sumethkul,Vasant, AU - Stitchantrakul,Wasana, AU - Radinahamed,Piyanuch, AU - Disthabanchong,Sinee, Y1 - 2011/12/01/ PY - 2011/12/3/entrez PY - 2011/12/3/pubmed PY - 2012/6/13/medline SP - 323 EP - 31 JF - Clinical journal of the American Society of Nephrology : CJASN JO - Clin J Am Soc Nephrol VL - 7 IS - 2 N2 - BACKGROUND AND OBJECTIVES: Renal phosphate wasting occurs early postkidney transplantation as a result of an accumulation of parathyroid hormone and fibroblast growth factor 23 from the CKD period. Serum phosphate, parathyroid hormone, and fibroblast growth factor 23 return to baseline 1 year postkidney transplantation. What happens beyond this period is unknown. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Mineral parameters were obtained from 229 kidney transplant recipients at least 1 year posttransplantation; 46 normal subjects and 202 CKD patients with similar GFR served as controls. Factors associated with phosphate metabolism were analyzed. RESULTS: Despite the reduced graft function, most kidney transplant recipients had lower serum phosphate than normal subjects accompanied by renal phosphate loss. Fibroblast growth factor 23 was mostly lower or comparable with normal subjects, whereas parathyroid hormone was elevated in most patients. Hyperparathyroidism is also more common among kidney transplant recipients compared with CKD patients. Both parathyroid hormone and fibroblast growth factor 23 showed relationships with renal phosphate excretion, but only parathyroid hormone displayed an independent association. Parathyroid hormone showed the highest area under the curve in predicting renal phosphate leak. When patients were categorized according to parathyroid hormone and fibroblast growth factor 23 levels, only subset of patients with high parathyroid hormone had an increased renal phosphate excretion. CONCLUSIONS: Relatively low serum phosphate from renal phosphate leak continued to present in long-term kidney transplantation. Both parathyroid hormone and fibroblast growth factor 23 participated in renal tubular phosphate handling, but persistent hyperparathyroidism seemed to have a greater influence in this setting. SN - 1555-905X UR - https://www.unboundmedicine.com/medline/citation/22134626/Renal_phosphate_loss_in_long_term_kidney_transplantation_ L2 - https://cjasn.asnjournals.org/cgi/pmidlookup?view=long&pmid=22134626 DB - PRIME DP - Unbound Medicine ER -