Calcification Propensity (T50) Predicts a Rapid Decline of Renal Function in Kidney Transplant Recipients

J Clin Med. 2023 Jun 10;12(12):3965. doi: 10.3390/jcm12123965.

Abstract

Background: Serum creatinine level, proteinuria, and interstitial fibrosis are predictive of renal prognosis. Fractional excretion of phosphate (FEP)/FGF23 ratio, tubular reabsorption of phosphate (TRP), serum calcification propensity (T50), and Klotho's serum level are emerging as determinants of poor kidney outcomes in CKD patients. We aimed at analysing the use of FGF23, FEP/FGF23, TRP, T50, and Klotho in predicting the rapid decline of renal function in kidney allograft recipients.

Methods: We included 103 kidney allograft recipients in a retrospective study with a prospective follow-up of 4 years. We analysed the predictive values of FGF23, FEP/FGF23, TRP, T50, and Klotho for a rapid decline of renal function defined as a drop of eGFR > 30%.

Results: During a follow-up of 4 years, 23 patients displayed a rapid decline of renal function. Tertile of FGF23 (p value = 0.17), FEP/FGF23 (p value = 0.78), TRP (p value = 0.62) and Klotho (p value = 0.31) were not associated with an increased risk of rapid decline of renal function in kidney transplant recipients. The lower tertile of T50 was significantly associated with eGFR decline >30% with a hazard ratio of 3.86 (p = 0.048) and remained significant in multivariable analysis.

Conclusion: T50 showed a strong association with a rapid decline of renal function in kidney allograft patients. This study underlines its role as an independent biomarker of loss of kidney function. We found no association between other phosphocalcic markers, such as FGF23, FEP/FGF23, TRP and Klotho, with a rapid decline of renal function in kidney allograft recipients.

Keywords: decline of renal function; kidney transplant; phosphocalcic markers; prediction.

Grants and funding

This work was funded by grants from NCCR kidney.ch to S.d.S. and A.P. and Swiss National Foundation to S.d.S. (320030_204187/1) and to LB (PZ00P3_208670). L.B was funded by a grant Projet de Recherche et développement (PRD) from the University hospital of Geneva (PRD 19-2018) and by the research fund of the department of Internal Medicine of the University Hospital and the Faculty of Medicine of Geneva.