Abstract: TH-PO945

Relationship of Magnesium and Insulin Resistance in Living Donor Kidney Transplant Recipients

Session Information

Category: Transplantation

  • 1702 Transplantation: Clinical and Translational

Authors

  • Nolte, Joy V, Houston Methodist Hospital, Houston, Texas, United States
  • Workeneh, Biruh, MD Anderson Cancer Center, Houston, Texas, United States
  • Moore, Linda W., Houston Methodist Hospital, Houston, Texas, United States
  • Gabour, Marie Christine, UMASS Boston, Lexington, Massachusetts, United States
  • Gaber, Ahmed Osama, Houston Methodist Hospital, Houston, Texas, United States
  • Mitch, William E., Baylor College of Medicine, Houston, Texas, United States
Background

Magnesium (Mg) is an important cofactor for blood glucose control and energy metabolism. Decreased Mg stores have been correlated with increased insulin resistance (IR) in diabetes and chronic kidney disease. It is difficult to assess total magnesium stores because serum Mg does not necessarily correlate with total body magnesium. Dietary intake of Mg before and after kidney transplant (KT) has not been heretofore described.

Methods

We sought to determine differences in Mg intake before and after KT. We analyzed 31 subjects who completed the ASA24 24hr dietary recall and oral glucose tolerance tests (OGTT) <1 month prior to transplant and 3 months post-transplant. Subjects were noninsulin dependent at KT, mostly male (84%) and an average age of 48yo. IR was indicated by Matsuda Index (MI). Spearman’s correlation (ρ) and mixed model statistics were used.

Results

Dietary recalls revealed most subjects consumed inadequate Mg pre- and post-KT(Table 1); however, serum Mg (SMg) remained within range for 83% pre-KT and 90% post-KT. Mean SMg decreased 0.23mg/dL despite increased dietary intake. Neither calcinuerin dose nor trough correlated with SMg post-KT. SMg, but not dietary Mg, correlated with fasting insulin and MI at baseline but did not reach significance (ρ= -0.346, P=0.056 and ρ=0.332, P=0.068). IR significantly correlated with weight (PE= -0.087, P=0.0003), waist circumference (PE= -0.096, P<0.0001), and BMI (PE= -0.119, P=0.032) over time but not serum or dietary Mg intake (ρ=0.001, P=0.61).

Conclusion

We found that pre-KT patients do not consume sufficient dietary Mg and a significant number were insulin resistant. Post-KT insulin resistance worsened despite increased Mg intake, but we speculate that treatment with calcinuerin inhibitors and other undetermined mechanisms could be depleting total Mg stores and potentially contributing to the insulin resistance observed post-KT. More accurate biomarkers for total body Mg and overall dietary Mg intake are needed to further examine magnesium's role in IR.

 Pre-KTPost-KTp-value†
Met Recommended Dietary Allowance, n (%)3 (10%)9 (34%)--
Serum Mg, mg/dL (SD)2.0 (0.43)1.77 (0.17)0.004
Total Mg intake*, mg (SD)321 (238)501 (433)0.006
Matsuda Index, (SD)4.35 (3)3.54 (2.5)0.09

*Total Mg intake includes prescription Mg dose. †Wilcoxon