Simultaneous Pancreas-Kidney Transplant Outcomes Stratified by Autoantibodies Status and Pretransplant Fasting C-peptide

Abstract

Backgrounds: Pancreatic beta cell function and islet autoantibodies classically distinguish types of diabetes (type 1 diabetes mellitus [DM] or type 2 DM). Here, we sought to evaluate simultaneous pancreas-kidney (SPK) transplant outcomes stratified by the presence or absence of beta cell function and autoantibodies.

Methods: SPK recipients were eligible if pretransplant autoantibodies were measured against insulin, islet cell, or glutamic acid decarboxylase 65-kD isoform. Recipients were categorized as A⁺ or A^- based on the detection of ≥1 autoantibodies. Recipients were similarly categorized on the basis of detectable pretransplant fasting C-peptide of ≥2 ng/mL (β⁺) or <2 ng/mL (β^-). Thus, recipients were categorized into 4 groups: A⁺β^-, A^-β^-, A^-β⁺, and A⁺β⁺. Outcomes of interest were overall pancreas graft failure (non-death-censored), death-censored pancreas, or kidney graft failure (death-censored pancreas graft failure [DCGF]; kidney DCGF), composite outcomes with any of the 3 outcomes as pancreas DCGF, use of an antidiabetic agent, or hemoglobin A1c >6.5.

Results: One hundred eighty-three SPK recipients were included: A⁺β^- (n = 72), A^-β^- (n = 42), A^-β⁺ (n = 49), and A⁺β⁺ (n = 20). We did not detect a statistical difference in non-death-censored pancreas graft failure for A⁺β^- recipients compared with other groups: A^-β^- (adjusted hazard ratio [aHR]: 0.44; 95% confidence interval [CI], 0.14-1.42), A^-β⁺ (aHR: 1.02; 95% CI, 0.37-2.85), and A⁺β⁺ (aHR: 0.67; 95% CI, 0.13-3.33) in adjusted analyses. Similar outcomes were observed for other outcomes.

Conclusions: In SPK recipients, outcomes were similar among recipients with classic features of type 1 DM and various other types of DM.

FIGURE 1.

Comparison of outcomes among 4 SPK recipient groups stratified by pretransplant fasting C-peptide and presence or absence of autoantibodies. No significant difference was observed in the pancreas non–death-censored graft survival (A; P = 0.56), pancreas death-censored graft survival (B; P = 0.47), pancreas compositive outcome-free survival (C; P = 0.13), or kidney death-censored graft survival (D; P = 0.92). SPK, simultaneous pancreas and kidney.

FIGURE 2.

Comparison of outcomes among SPK recipient groups stratified by the presence or absence of autoantibodies. No significant difference was observed in the pancreas non–death-censored graft survival (A; P = 0.45), pancreas death-censored graft survival (B; P = 0.51), pancreas compositive outcome-free survival (C; P = 0.87), or kidney death-censored graft survival (D; P = 0.79). SPK, simultaneous pancreas and kidney.

FIGURE 3.

Comparison of outcomes among SPK recipients stratified by pretransplant fasting C-peptide. No significant difference was observed in the pancreas non–death-censored graft survival (A; P = 0.87), pancreas death-censored graft survival (B; P = 0.66), or kidney death-censored graft survival (D; P = 0.64). However, pancreas compositive outcome-free survival was significantly lower in the high C-peptide group (C; P = 0.04). SPK, simultaneous pancreas and kidney.