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. 2018 Jan;41(1):79-87.
doi: 10.2337/dc17-1042. Epub 2017 Nov 16.

N-Glycan Profile and Kidney Disease in Type 1 Diabetes

Mairead L Bermingham  1 , Marco Colombo  2 , Stuart J McGurnaghan  3 , Luke A K Blackbourn  3 , Frano Vučković  4 , Maja Pučić Baković  4 , Irena Trbojević-Akmačić  4 , Gordan Lauc  4 , Felix Agakov  5 , Anna S Agakova  5 , Caroline Hayward  6 , Lucija Klarić  2   6 , Colin N A Palmer  7 , John R Petrie  8 , John Chalmers  9 , Andrew Collier  10 , Fiona Green  11 , Robert S Lindsay  8 , Sandra Macrury  12 , John A McKnight  13 , Alan W Patrick  14 , Sandeep Thekkepat  15 , Olga Gornik  16 , Paul M McKeigue  2   5 , Helen M Colhoun  3   17 ; SDRN Type 1 Bioresource Investigators
Affiliations

N-Glycan Profile and Kidney Disease in Type 1 Diabetes

Mairead L Bermingham et al. Diabetes Care. 2018 Jan.

Abstract

Objective: Poorer glycemic control in type 1 diabetes may alter N-glycosylation patterns on circulating glycoproteins, and these alterations may be linked with diabetic kidney disease (DKD). We investigated associations between N-glycans and glycemic control and renal function in type 1 diabetes.

Research design and methods: Using serum samples from 818 adults who were considered to have extreme annual loss in estimated glomerular filtration rate (eGFR; i.e., slope) based on retrospective clinical records, from among 6,127 adults in the Scottish Diabetes Research Network Type 1 Bioresource Study, we measured total and IgG-specific N-glycan profiles. This yielded a relative abundance of 39 total (GP) and 24 IgG (IGP) N-glycans. Linear regression models were used to investigate associations between N-glycan structures and HbA1c, albumin-to-creatinine ratio (ACR), and eGFR slope. Models were adjusted for age, sex, duration of type 1 diabetes, and total serum IgG.

Results: Higher HbA1c was associated with a lower relative abundance of simple biantennary N-glycans and a higher relative abundance of more complex structures with more branching, galactosylation, and sialylation (GP12, 26, 31, 32, and 34, and IGP19 and 23; all P < 3.79 × 10-4). Similar patterns were seen for ACR and greater mean annual loss of eGFR, which were also associated with fewer of the simpler N-glycans (all P < 3.79 × 10-4).

Conclusions: Higher HbA1c in type 1 diabetes is associated with changes in the serum N-glycome that have elsewhere been shown to regulate the epidermal growth factor receptor and transforming growth factor-β pathways that are implicated in DKD. Furthermore, N-glycans are associated with ACR and eGFR slope. These data suggest that the role of altered N-glycans in DKD warrants further investigation.

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