Table 2.

Proposed Igls criteria 2.0

Treatment outcome	Glycemic control		Hypoglycemia		Treatment success
	HbA1c, % (mmol/mol)a	CGM, % time-in-range	Severe hypoglycemia, events per y	CGM, % time < 54 mg/dl (3.0 mmol/L)
Optimal	≤6.5 (48)	≥80	None	0	Yes
Good	<7.0 (53)	≥70	None	<1	Yes
Marginal	≤Baseline	>Baseline	<Baselineb	<Baseline	Noc
Failure	~Baseline	~Baseline	~Baselined	~Baseline	No
β-cell graft functione	C-peptide, ng/mL (nmol/L) f		Insulin use or noninsulin antihyperglycemic therapy
Optimal	Any		None
Good	>0.5 (0.17) stimulated ≥0.2 (0.07) fasting		Any
Marginal	0.3-0.5 (0.10-0.17) stimulated 0.1-<0.2 (0.04-<0.07) fasting		Any
Failure	<0.3 (0.10) stimulated <0.1 (0.04) fasting		Any

Baseline, pretransplant assessment (not applicable to total pancreatectomy with islet autotransplantation patients).

Abbreviations: CGM, continuous glucose monitoring; HbA_1c, glycated hemoglobin.

^a Mean glucose should be used to provide an estimate of the HbA_1c, termed the glucose management indicator, in the setting of disordered red blood cell life span.

^b Should severe hypoglycemia occur following treatment, then continued benefit may require assessment of hypoglycemia awareness, exposure to serious hypoglycemia (<54 mg/dL [3.0 mmol/L]), and/or glycemic variability/lability with demonstration of improvement from baseline.

^c Clinically, benefits of maintaining and monitoring β-cell graft function may outweigh risks of maintaining immunosuppression.

^d If severe hypoglycemia was not present before β-cell replacement therapy, then a return to baseline measures of glycemic control used as the indication for treatment (6, 7) may be consistent with β-cell graft failure.

^e Categorization of β-cell graft function must first meet treatment outcome based on measures of glucose regulation.

^f May not be reliable in uremic patients and/or in those patients with evidence of C-peptide production before β-cell replacement therapy.