# Immediate Glycemic Outcomes Following Simultaneous Pancreas–Kidney Transplantation: Equivalent Early Metabolic Profiles in Type 1 and Type 2 Diabetes

**Authors:** Mojgan Jalalzadeh, Zahidul Mondal, Nooruddin Hashmi, Sonalis Bunin, Mital Shah, Jing Shen, Daniel P Pieloch, Steve Khalil, Neeraj Singh, Advaith Bongu, Ronald P Pelletier

PMC · DOI: 10.7759/cureus.102422 · Cureus · 2026-01-27

## TL;DR

The study finds that early blood sugar control after pancreas-kidney transplants is similar in type 1 and type 2 diabetes patients.

## Contribution

It demonstrates that standardized glycemic protocols can be safely applied to both type 1 and type 2 diabetes SPKT recipients.

## Key findings

- Early postoperative glucose levels were similar between T1DM and T2DM SPKT recipients.
- Rates of insulin use and dextrose administration were comparable between the two groups.
- Short-term graft outcomes and hospital stays were not significantly different between T1DM and T2DM recipients.

## Abstract

Background and objective: Simultaneous pancreas-kidney transplantation (SPKT) is increasingly performed in both type 1 and carefully selected type 2 diabetes mellitus recipients. Although long-term outcomes are well described, early postoperative glycemic behavior remains poorly defined. Persistent hyperglycemia during the early postoperative phase raises concerns regarding potential technical complications or acute rejection after SPKT. In contrast, early normalization of glucose levels suggests pancreas graft viability and sufficient functional beta-cell mass. Despite extensive long-term data, comparative evidence between T1DM and T2DM recipients is limited. This study compares early glycemic trajectories, perioperative glycemic management, and short-term outcomes between these groups.

Methods: We conducted a single-center retrospective study of adult SPKT recipients from January 2018 to December 2025. Exclusion criteria were multiorgan transplantation beyond SPKT, pancreas graft loss or patient death within 24 hours, and incomplete early postoperative glucose data. Perioperative glucose interventions, pancreatic enzyme markers, and glucose values obtained at predefined postoperative time points (6, 12, and 24 hours; POD 7, 14, and 28) were analyzed. Primary outcomes included early glucose levels and insulin independence at one month, a clinically meaningful indicator of endocrine graft function. Secondary outcomes included delayed graft function, postoperative complications, return to the operating room, pancreatic enzyme levels, and length of hospital stay.

Results: Among 80 SPKT recipients, 31 (38.8%) had T1DM and 49 (61.2%) had T2DM. T2DM recipients were older (50.3 ± 9.3 vs. 41.3 ± 9.3 years, p = 0.001) and had a higher body mass index (27.0 ± 3.5 vs. 24.9 ± 4.0 kg/m², p = 0.016). T1DM recipients, in contrast, had a longer duration of diabetes and lower C-peptide levels (both p < 0.001). Early postoperative glucose values at 6, 12, and 24 hours, as well as on postoperative days 7, 14, and 28, were similar between groups (all p > 0.05). Rates of intravenous insulin use (T1DM: 3/31 [9.7%] vs. T2DM: 7/49 [14.3%]; p = 0.732) and intravenous dextrose administration (23/31 [74.2%] vs. 26/49 [53.1%], p = 0.191) were comparable. No significant differences were observed in pancreatic enzyme levels, insulin dependence at one month, delayed graft function, postoperative complications, or length of hospital stay.

Conclusions: Early postoperative glycemic control and short-term graft outcomes are comparable between type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) SPKT recipients, supporting the safety and applicability of standardized perioperative glycemic protocols across both populations.

## Linked entities

- **Diseases:** type 1 diabetes mellitus (MONDO:0005147), type 2 diabetes mellitus (MONDO:0005148)

## Full-text entities

- **Genes:** HLA-A (major histocompatibility complex, class I, A) [NCBI Gene 3105] {aka HLAA}, CABIN1 (calcineurin binding protein 1) [NCBI Gene 23523] {aka CAIN, KB-318B8.7, PPP3IN}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** abdominal infection (MESH:D000007), enteric leak (MESH:D004751), T2DM (MESH:D003924), Insulin dependence (MESH:D003922), dysfunction (MESH:D006331), urinary tract complications (MESH:D014570), pancreatic or duodenal complications (MESH:D010182), sepsis (MESH:D018805), reperfusion injury (MESH:D015427), vascular thrombosis (MESH:D013927), death (MESH:D003643), gastrointestinal (MESH:D005767), end-stage renal disease (MESH:D007676), immunologic injury (MESH:D007154), hypoglycemia (MESH:D007003), infection (MESH:D007239), insulin resistance (MESH:D007333), wound infection (MESH:D014946), brain death (MESH:D001926), bleeding (MESH:D006470), bladder leak (MESH:D001745), hypoglycemic (MESH:C000721848), ischemia (MESH:D007511), hematoma (MESH:D006406), hyperglycemia (MESH:D006943), circulatory (MESH:D012769), diabetes (MESH:D003920), intra-abdominal infection (MESH:D059413), pancreatic leak (MESH:D010195), ureteral leak (MESH:D014515)
- **Chemicals:** prednisone (MESH:D011241), Dextrose (MESH:D005947), creatinine (MESH:D003404), SPKT (-), methylprednisolone (MESH:D008775), blood glucose (MESH:D001786), C-peptide (MESH:D002096)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12945400/full.md

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12945400/full.md

## References

16 references — full list in the complete paper: https://tomesphere.com/paper/PMC12945400/full.md

---
Source: https://tomesphere.com/paper/PMC12945400