Secondary Hyperparathyroidism Ups Risk of Kidney Allograft Loss

Increased fractional excretion of phosphate also found to increase risk of allograft loss.
Increased fractional excretion of phosphate also found to increase risk of allograft loss.

Secondary hyperparathyroidism and increased fractional excretion of phosphate predict allograft loss in kidney transplant (KT) recipients, according to a new study.

Following kidney transplantation, fibroblast growth factor-23 (FGF-23) normally returns to baseline within 1 year, but hyperparathyroidism persists in most KT patients, Sinee Disthabanchong, MD, and colleagues at Mahidol University in Bangkok, Thailand. Consequently, serum phosphate remains relatively low in association with increased serum calcium and urinary phosphate excretion when compared with patients who have chronic kidney disease.

Dr Disthabanchong's team prospectively followed 273 kidney transplant patients for an average of 71.4 months. Death censored graft loss occurred in 41 patients (15%). After adjusting for cardiovascular disease risk factors, donor type, dialysis vintage, serum albumin, and allograft function, only increased parathyroid hormone (PTH) and fractional excretion of phosphate (FePi) remained associated allograft failure, the investigators reported online ahead of print in Clinical and Experimental Nephrology.

Adjusted survival curves showed that PTH levels above 90 pg/mL and FePi above 20% was associated with a significantly higher risk of graft loss compared with lower values.

“This study is the first to describe an independent association between FePi and adverse graft outcome in long-term KT recipients,” the investigators noted.

Reference

1. Prakobsuk S, Sirilak S, Vipattawat K, et al. Hyperparathyroidism and increased fractional excretion of phosphate predict allograft loss in long-term kidney transplant recipients. Clin Exp Nephrol 2016; published online ahead of print.

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