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Glucose homeostasis after simultaneous pancreas and kidney transplantation: a comparison of subjects with C ‐peptide‐positive non‐type 1 diabetes mellitus and type 1 diabetes mellitus
Author(s) -
Chakkera Harini A.,
Kudva Yogish C.,
Chang YuHui H.,
Heilman Raymond L.,
Singer Andrew L.,
Mathur Amit K.,
Hewitt Winston R.,
Khamash Hasan A.,
Huskey Janna L.,
Katariya Nitin N.,
Moss Adyr A.,
Behmen Senaida,
Reddy Kunam S.
Publication year - 2016
Publication title -
clinical transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 76
eISSN - 1399-0012
pISSN - 0902-0063
DOI - 10.1111/ctr.12658
Subject(s) - medicine , insulin resistance , type 1 diabetes , glucose homeostasis , endocrinology , insulin , diabetes mellitus , transplantation , homeostasis , pancreas transplantation , type 2 diabetes mellitus , type 2 diabetes , kidney transplantation
Background While simultaneous pancreas kidney transplant ( SPKT x) is a therapeutic option for patients with type 1 diabetes (T1 DM ) and renal failure, few centers offer SPKT x to “select” non‐T1 DM patients. To address concerns that existing insulin resistance may limit the benefits of the pancreas allograft among non‐T1 DM , we compared several indices of glucose homeostasis, in “select” non‐T1 DM and T1 DM patients who received SPKT x. Methods Criteria for “select” non‐T1 DM included the following: positive C‐peptide, BMI <30 kg/m 2 , treatment with oral agents before insulin initiation, and insulin at <1 unit/kg/d. We compared several indices of glucose homeostasis within 1 yr post‐ SPKT x among seven “select” patients with non‐T1 DM and nine patients with T1 DM with similar age, BMI , and immunosuppression. Measurements of insulin resistance included the following: homeostatic model, insulin sensitivity index, and insulin–glucose ratio; insulin secretion measures included the following: corrected insulin response. Results Non‐T1 DM had similar pre‐transplant metabolic (fasting glucose, HbA1c, blood pressure, and lipid) parameters to the T1 DM cohort. There were no significant differences in the various measures of insulin resistance and secretion between T1 DM and “select” non‐T1 DM patients. Conclusion Our results suggest SPKT x should be considered in the therapeutic armamentarium among carefully select non‐T1 DM with features of minimal insulin resistance; however, a larger cohort with longer follow‐up is needed to confirm our results.