Abstract
AimIn this work we estimated the contribution of the fluorescence of 4-pyridoxic acid (4-PA) to the total fluorescence of spent dialysate with the aim of evaluating the on-line monitoring of removal of this vitamin B-6 metabolite from the blood of patients with end-stage renal disease (ESRD).MethodsSpectrofluorometric analysis of spent dialysate, collected from hemodialysis and hemodiafiltration sessions of 10 patients receiving regularly pyridoxine injections after dialysis treatment, was performed in the range of Ex/Em 220–500 nm. 4-PA in dialysate samples was identified and quantified using HPLC with fluorescent and MS/MS detection.ResultsAveraged HPLC chromatogram of spent dialysate had many peaks in the wavelength region of Ex320/Em430 nm where 4-PA was the highest peak with contribution of 42.2±17.0% at the beginning and 47.7±18.0% in the end of the dialysis. High correlation (R = 0.88–0.95) between 4-PA concentration and fluorescence intensity of spent dialysate was found in the region of Ex310-330/Em415-500 nm, respectively.Conclusion4-PA elimination from the blood of ESRD patients can be potentially followed using monitoring of the fluorescence of the spent dialysate during dialysis treatments.
Highlights
Vitamin deficiency is common in chronic kidney disease (CKD) patients
High correlation (R = 0.88–0.95) between 4-pyridoxic acid (4-PA) concentration and fluorescence intensity of spent dialysate was found in the region of Ex310-330/Em415-500 nm, respectively
As vitamin B6 is commonly used in the treatment of patients of chronic kidney disease, the monitoring of the vitamin status of the patient is important
Summary
Vitamin deficiency is common in chronic kidney disease (CKD) patients. One vitamin that CKD patients are lacking is vitamin B-6 (B6) which is the term for a group of interconvertible molecules containing pyridoxine, pyridoxal, pyridoxamine and their phosphates. Many studies have pointed out that lower vitamin B-6 concentrations increase the risk of coronary artery disease [7,8,9] as well as renal dysfunction [10]. Concerning uremia it is essential to consider metabolic link between urea accumulation in uremic tissues and inactivation of pyridoxal-5’-phosphate (PLP) by carbamoyl phosphate, the very first product of condensation of carbonate with ammonia in the metabolic pathway of urea biosynthesis [11] leading to symptoms of B6 deficiency [12]. Levine et al have found that decreased excretion of pyridoxine and its metabolites might increase the likelihood to pyridoxine toxicity [16] and status of pyridoxine monitoring would be beneficial
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
