Abstract
New-onset diabetes mellitus after transplantation (NODAT) is a frequent complication in kidney allograft recipients. It may be caused by modifiable and non-modifiable factors. The non-modifiable factors are the same that may lead to the development of type 2 diabetes in the general population, whilst the modifiable factors include peri-operative stress, hepatitis C or cytomegalovirus infection, vitamin D deficiency, hypomagnesemia, and immunosuppressive medications such as glucocorticoids, calcineurin inhibitors (tacrolimus more than cyclosporine), and mTOR inhibitors. The most worrying complication of NODAT are major adverse cardiovascular events which represent a leading cause of morbidity and mortality in transplanted patients. However, NODAT may also result in progressive diabetic kidney disease and is frequently associated with microvascular complications, eventually determining blindness or amputation. Preventive measures for NODAT include a careful assessment of glucose tolerance before transplantation, loss of over-weight, lifestyle modification, reduced caloric intake, and physical exercise. Concomitant measures include aggressive control of systemic blood pressure and lipids levels to reduce the risk of cardiovascular events. Hypomagnesemia and low levels of vitamin D should be corrected. Immunosuppressive strategies limiting the use of diabetogenic drugs are encouraged. Many hypoglycemic drugs are available and may be used in combination with metformin in difficult cases. In patients requiring insulin treatment, the dose and type of insulin should be decided on an individual basis as insulin requirements depend on the patient’s diet, amount of exercise, and renal function.
Highlights
Among the many complications that may occur during the post-transplant course, new-onset diabetes mellitus after transplantation (NODAT)
Even though the criteria for New-onset diabetes mellitus after transplantation (NODAT) proposed by the International Congress Guidelines and by the American Diabetes Association (ADA) are basically the same as for the general population, this specific form of type 2 diabetes is due to a progressive loss of adequate β-cell insulin secretion frequently on the background of insulin resistance
Attempts to reduce the toxicity of glucocorticoids in Kidney transplantation (KT) recipients included steroid-free regimens, usually based on the association of one calcineurin inhibitor (CNI) with a purine synthesis inhibitor, steroidsparing regimens, based on low-dose prednisone (5–10 mg per day), or steroid-withdrawal after the first months after transplant
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Significant advances in surgical techniques and medical care, as well as the development of new and more powerful immunosuppressive agents, have led to a progressive reduction of transplant-related mortality and morbidity [1]. Deserves special consideration as it is commonly associated to metabolic disorders or infections and may result in diabetic kidney disease with nephrotic syndrome, impaired renal function or even premature allograft loss. In combination with pre- or co-existing conditions [4,5,6,7], NODAT may contribute to the development and aggravation of major adverse cardiovascular events (MACE), which represent a leading cause of morbidity and mortality in this specific group of patients [8,9,10]
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