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Abstract: PO2501

Iron Deficiency in Kidney Transplant Recipients: Impact on Cognitive Functioning

Session Information

Category: Transplantation

  • 1902 Transplantation: Clinical

Authors

  • Vinke, Joanna Sophia Jacoline, University Medical Center Groningen, Department of Nephrology, Groningen, Netherlands
  • Ziengs, Aaltje Lisanne, University Medical Center Groningen, Department of Neuropsychology, Groningen, Netherlands
  • van Sonderen, Lisanne, University Medical Center Groningen, Department of Neuropsychology, Groningen, Netherlands
  • Gomes Neto, Antonio Wouter, University Medical Center Groningen, Department of Neuropsychology, Groningen, Netherlands
  • Buunk, Anne, University Medical Center Groningen, Department of Neuropsychology, Groningen, Netherlands
  • Berger, Stefan P., University Medical Center Groningen, Department of Nephrology, Groningen, Netherlands
  • Bakker, Stephan J.L., University Medical Center Groningen, Department of Nephrology, Groningen, Netherlands
  • Eisenga, Michele F., University Medical Center Groningen, Department of Nephrology, Groningen, Netherlands
  • De Borst, Martin H., University Medical Center Groningen, Department of Nephrology, Groningen, Netherlands
Background

Cognitive function impairment is common in kidney transplant recipients (KTRs). Brain functioning requires energy, for which iron is essential at the level of oxygen delivery and mitochondrial function. Iron deficiency (ID) has been linked to compromised cognitive functioning in premenopausal women. We aimed to investigate whether ID could be a potentially modifiable risk factor for cognitive function impairment in KTRs.

Methods

In a prospective study among KTRs participating in the TransplantLines Biobank and Cohort study, we analyzed KTRs >1 yr post-transplant with data on iron status. All participants underwent neurocognitive testing to measure memory (Digit Span Forward, Immediate and Delayed Recall of the 15 Word Test), attention and mental speed (Symbol Digit Modalities Test, Trail Making Test-A) and executive functioning (Trail Making Test-B, Digit Span Backward). ID was defined as ferritin <100 µg/mL or 100-299 µg/mL with transferrin saturation (TSAT) ≤20%. We used multivariable linear regression analyses to assess associations between ID and neurocognitive outcomes. Analyses were adjusted for hemoglobin, CRP, age, sex, eGFR, BMI, smoking, alcohol intake, time since transplantation, dialysis duration, donor type, educational level and immunosuppressives.

Results

We included 398 KTRs (age 56±14 yrs, 62% male, eGFR 52±14 mL/min/1.73 m2). ID was present in 289 KTRs (73%). Associations of plasma ferritin, TSAT and ID with neurocognitive scores are presented in the table.

Conclusion

ID, low ferritin and low TSAT are consistently associated with poor performance on neurocognitive tasks measuring verbal memory, executive functioning, mental speed and attention in KTRs, independent of hemoglobin and other potential confounders. Future studies should address whether ID correction restores cognitive function.

N=398FerritinTSATIron Deficiency
Memory
○Digit Span Forwardst.β=0.12, P=0.022st.β=0.05, P=0.358st.β=-0.09, P=0.074
○15 Word Test, immediate recallst.β=0.18, P<0.001st.β=0.08, P=0.09st.β=-0.08, P=0.089
○15 Word Test, delayed recallst.β=0.31, P<0.001st.β=0.17, P=0.001st.β=-0.22, P<0.001
Attention & Mental Speed
○Symbol Digit Modalities Testst.β=0.16, P=0.001st.β=0.17, P<0.001st.β=-0.14, P=0.002
○Trail Making Test-Ast.β=-0.20, P<0.001st.β=-0.08, P=0.115st.β=0.15, P=0.001
Executive Functioning
○Trail Making Test-Bst.β=-0.04, P=0.47st.β=0.08, P=0.118st.β=0.002, P=0.961
○Trail Making Test–B/A ratiost.β=0.14, P=0.009st.β=0.18, P=0.001st.β=-0.15, P=0.004
○Digit Span Backwardst.β=0.18, P<0.001st.β=-0.03, P=0.515st.β=-0.14, P=0.006