Introduction: Albuminuria is commonly observed in renal transplant recipients and its etiology varies widely. It is associated with poorer graft function and worse patient and graft survival. Furthermore, there is a high prevalence of vitamin D deficiency in renal transplant recipients. It has been hypothesized that vitamin D deficiency is linked to renal damage and microalbuminuria. Our goal was to 1) examine if vitamin D deficiency is associated with albuminuria; 2) determine if inflammatory cytokines are correlated in this pathophysiology.
Methods: One hundred and fifty prevalent renal transplant recipients with stable graft function were enrolled in this cross-sectional analysis. Inflammatory markers were measured in eighty patients and included CCL (1-5, 8, 11, 13, 15, 17, 21, 26, 27), CXCL (5, 10, 12, 13), IL (1a, 1b, 2, 4-10, 12, 13, 15-17, 19-21, 23, 28a, 33), G-CSF, GM-CSF, INFg, LIF, SCF, TNFa, TPO, TRAIL, TSLP, VEGF, PDGF-bb, PTX3, HMGB1, ADRENO. Other biochemical measurements included serum creatinine, calcium, parathyroid hormone, 25OH vitamin D, albumin, magnesium, phosphate, hemoglobin, hs-CRP, fasting lipid profile, hemoglobin A1C and urine microalbumin.
Results: Mean age of the cohort was 50 ± 15 years and 57% were males. Most patients (75%) were Caucasian. Mean time since date of transplant was 7.9 ± 4.9 years and eGFR was 54.7 ± 25.2 ml/min. Vitamin D status was negatively correlated to microalbuminuria (r = -0.23, p=0.015) but not to serum creatinine or eGFR. Vitamin D was associated negatively with PTH (r=-0.44, p<0.0001) but not to serum calcium or phosphate. There was no association between vitamin D status and inflammatory markers. Microalbuminuria was associated with CCL 15 (r=0.27, p=0.02), 27 (r=0.26, p=0.024), SCF (r=0.26, p=0.025) and TPO (r=0.31, p=0.008). Microalbuminuria was associated negatively with eGFR (r=-0.31, p<0.0001), ejection fraction (r=-0.24, p=0.03) and positively with PTH (r=0.27, p=0.005), systolic and diastolic blood pressure (r=0.32, p<0.0001 and r=0.27, p=0.001, respectively) and FRS (r=0.18, p=0.03).
Conclusion: We present data that further elucidates the pathophysiology of microalbuminuria in renal transplant recipients. Although vitamin D deficiency may be hypothesized as mediating microalbuminuria, this mechanism is independent of inflammatory cytokines.
To cite this abstract in AMA style:Mainra R, Hassan A, Moser M, Luo Y, Shoker A. Association of Vitamin D and Albuminuria in Renal Transplant Recipients, The [abstract]. Am J Transplant. 2013; 13 (suppl 5). https://atcmeetingabstracts.com/abstract/association-of-vitamin-d-and-albuminuria-in-renal-transplant-recipients-the/. Accessed October 30, 2020.
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