Phase-specific intraoperative glycemic control in simultaneous pancreas-kidney transplantation

Table 1 Biological pathways linking intraoperative glycemic variability to early pancreas graft complications[5,22-25,27-40]

Domain	Pathophysiologic effect	Clinical consequence
Endothelium	Oxidative stress, nitric oxide disruption	Microvascular injury
Coagulation	Platelet activation, procoagulant signaling	Graft thrombosis
Innate immunity	Impaired neutrophil function	Infection
β-cell adaptation	Insulin hypersecretion followed by instability	Hypoglycemia

Table 2 Comparison of perioperative glycemic management paradigms across transplant settings[7-16,42,43,45,50-52]

Setting	Primary focus	Timing emphasized	Limitation for SPKT
General surgery	Threshold avoidance	Intra-/postoperative	Ignores endocrine recovery
ICU protocols	Tight control	Postoperative	Assumes metabolic stability
Kidney transplantation	Long-term control	Postoperative	Limited intraoperative detail
Liver transplantation	Infection reduction	Peri-/postoperative	Endocrine effects indirect
Phase-specific SPKT approach	Metabolic stability	Intraoperative	Requires validation

ICU: Intensive care unit; SPKT: Simultaneous pancreas-kidney transplantation.