Abstract
Background: The perturbation of phosphate homeostasis portends unfavorable outcomes in chronic kidney disease (CKD). However, the absence of randomized clinical trials (RCT) fuels the discussion of whether phosphate or some other phosphorous-related factor(s) such as fibroblast growth factor 23 (FGF-23) mediates the cardiovascular and systemic toxicity. We herein test whether the fractional excretion of phosphate (FeP) as a marker of renal stress to excrete phosphorous predicts unfavorable outcomes in CKD patients. Methods: Retrospective, cross-sectional observational study. For current analysis, an historical cohort of 407 records of CKD stage 3b-5 patients attending between January 2010 and October 2015 at the Nephrology Unit of Solofra (AV), Italy were utilized. Demographic, clinical, laboratory, and outcome data were identified through the subjects’ medical records. We tested whether quartiles of FeP are associated with the risk of CKD progression or all causes of death. Parametric as well as non-parametric tests, linear and logistic regression, as well as survival analysis were utilized. Results: Overall, we investigated middle-age (mean 66.0, standard deviation 12.3 years) men and women (male 43%) with CKD stage 3b to 5 (creatinine clearance 32.0 (13.3) mL/min). Older age, lower diastolic blood pressure, poor renal function, as well as higher serum phosphate were associated with FeP. Patients with higher FeP were at an increased risk of starting dialysis or dying (hazard ratio 2.40; 95% confidence interval (1.44, 3.99)). Notably, when the two endpoints were analyzed separately, FeP was associated with renal but not all-cause survival. Conclusion: FeP is associated with ESRD, but not all-cause mortality risk in a large cohort of moderate to advanced CKD patients. Future efforts are required to validate FeP as a marker of nephron stress and risk factor for CKD progression in this high-risk population.
Highlights
The perturbation of phosphate homeostasis portends unfavorable outcomes in chronic kidney disease (CKD) [1]
We examined the association of fractional excretion of phosphate (FeP) and three outcomes: (i) the occurrence of the composite event of all-cause mortality and CKD progression to end-stage renal disease (ESRD), whichever came first; (ii) the occurrence of CKD progression to ESRD; and (iii) the occurrence of all-cause mortality
The risk of ESRD associated with serum phosphate was progressively attenuated by greater degree of 24-h proteinuria [14]
Summary
The perturbation of phosphate homeostasis portends unfavorable outcomes in chronic kidney disease (CKD) [1]. In vitro evidence demonstrates that vascular smooth muscle cells exposed to progressively higher concentrations of phosphate differentiate, acquire an osteoblastic-like phenotype, and prompt vascular calcification deposition and progression by secreting a bone matrix within the context of the arterial wall [8,9]. This hypothesis is corroborated by the observation of a strong association of serum phosphate and cardiovascular calcification, as well as arterial stiffness in different stages of CKD [10,11,12].
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