Diabetes and hyperglycaemia in patients post-transplantation

Organ transplantation is associated with an increased risk of the development of post-transplant diabetes and, in patients with pre-existing diabetes, may lead to difficulty in achieving glycaemic targets. Ideally, transplant patients without pre-existing diabetes should be screened for diabetes before and after a transplant, and diabetes should be managed in consultation with the multidisciplinary transplant team.

The development of post-transplant diabetes is associated with increased mortality and morbidity. Drugs used post-transplant can contribute to diabetes development; however, the immunosuppressant regimens shown to provide the best outcomes for patient and graft survival should be used, regardless of post-transplant diabetes risk. Major contributors to glucose disturbance after a transplant include the immunosuppressants (particularly calcineurin inhibitors [ciclosporin, tacrolimus], everolimus and sirolimus) and glucocorticoids.

Tailoring of immunosuppressants for a patient with glucose intolerance is the responsibility of the transplant specialist—withholding glucocorticoids or calcineurin inhibitors may precipitate acute rejection. If the transplant team adjusts the dose of immunosuppressants, the antihyperglycaemic drug dosage may also need adjustment—for example, if the glucocorticoid dose is reduced then insulin doses may also need to be reduced to avoid hypoglycaemia. Conversely, improved kidney function post–kidney transplant may result in increased insulin requirement due to enhanced clearance of endogenous insulin by the kidneys.

Insulin treatment is the same as for nontransplant patients with type 2 diabetes who are being treated with glucocorticoids (see Management of acute glucocorticoid-induced hyperglycaemia in patients with type 2 diabetes).

In the immediate post-transplant period caution is required with use of noninsulin antihyperglycaemic drugs, especially for post–kidney transplant patients or patients with kidney impairment.

For patients with kidney impairment, avoid metformin and long-acting sulfonylureas (glibenclamide, glimepiride). The shorter-acting sulfonylureas (gliclazide, glipizide) can be used. When kidney function has stabilised metformin is an effective option for post-transplant diabetes. Dipeptidyl peptidase-4 (DPP-4) inhibitors are sometimes used in transplant patients, but doses (except linagliptin) need adjustment for patients with kidney impairment.

Be aware of possible interactions between antihyperglycaemic drugs and immunosuppressants—for example sitagliptin may be associated with a long QT interval when combined with ciclosporin.

Data are lacking on the safety and efficacy of glucagon-like peptide-1 (GLP-1) receptor agonist use in post-transplant diabetes.

Avoid thiazolidinediones in post-transplant patients due to their adverse effect profile.

Avoid sodium-glucose co-transporter 2 (SGLT2) inhibitors in the early management of post-transplant diabetes as there is no evidence of safety and efficacy. SGLT2 inhibitors can cause volume depletion, increased risk for genitourinary infections, and have been associated with an increased risk of diabetic ketoacidosis.

In the longer term management of post-transplant diabetes is similar to type 2 diabetes in the nontransplant setting (including lifestyle modification); see Type 2 diabetes in adults. As well as glycaemic management, cardiovascular disease risk must be considered; see Cardiovascular disease risk modification for management of cardiovascular disease risk factors.