Israel Medical Association Journal

Background: Vitamin B6 is an essential cofactor in amino acid metabolism. Its deficiency is linked to neuropathy, anemia, and cardiovascular risk. Deficiency is common among hemodialysis patients due to dialytic losses and restrictive diets; however, data related to high-flux (HF) dialysis membranes and Mediterranean dietary patterns are scarce.

Objectives: To assess the prevalence and determinants of deficiency in unsupplemented Israeli hemodialysis patients.

Methods: This retrospective chart review, utilizing a cross-sectional design, was conducted in August 2024. We included 27 chronic hemodialysis patients not receiving vitamin B6 supplementation, representing the available unsupplemented cohort from a unit of approximately 150 patients. Vitamin B6 status was assessed by measuring plasma pyridoxal-5'-phosphate (PLP); deficiency < 20 ng/ml. Clinical and nutritional parameters were evaluated to identify deficiency.

Results: Vitamin B6 deficiency was noted in 63% of patients (median PLP 18 ng/ml, interquartile range 13–23). The cohort was 67% male, median age 74 years. All patients were treated with HF dialyzers. No significant correlations were found between PLP levels and nutritional indices or laboratory markers. A non-significant trend was observed between older age and lower PLP levels (r = -0.35, P = 0.098).

Conclusions: Vitamin B6 deficiency was common among Israeli hemodialysis patients treated with HF dialyzers, despite a presumed Mediterranean diet. It was not associated with nutritional status, suggesting dialysis-related losses, potentially augmented by high-flux membranes, may outweigh intake. Given the high prevalence of deficiency and low cost, routine low-dose vitamin B6 supplementation may be warranted, particularly in older patients.

A 55-year-old male with a history of Dubin-Johnson syndrome (DJS), obesity, and smoking presented to the emergency department with generalized weakness and jaundice. On admission, he was hypotensive (blood pressure 87/56 mmHg), and profound jaundice was noted. Laboratory investigations revealed severe acute kidney injury with a creatinine level of 5.53 mg/dl and blood urea nitrogen of 92 mg/dl. Liver function tests were mildly elevated, and his lipid profile was within normal limits. Total bilirubin was markedly elevated at 52.5 mg/dl, predominantly direct (40.9 mg/dl). The patient was anuric at the time of catheter insertion.

A non-contrast abdominal computed tomography scan showed normal kidney size and appearance without hydronephrosis. The liver was normal size with sharp borders. The patient was treated with intravenous fluids, inotropic support, and intravenous antibiotics. Despite these interventions, he remained anuric with worsening hyperkalemia, necessitating urgent hemodialysis.

Within 10 minutes of initiating hemodialysis, a yellowish discoloration appeared in the effluent tubing of the dialysate. Simultaneously, the dialyzer fibers, which are typically pinkish in color, began to develop a yellowish tint. By the end of the session, the dialyzer appeared distinctly yellow, likely due to bilirubin deposition [Figure 1A–1C].