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Review
. 2024 Mar 27;13(7):1928.
doi: 10.3390/jcm13071928.

New-Onset Diabetes Mellitus after Kidney Transplantation

Salah Alajous  1 , Pooja Budhiraja  1
Affiliations
Review

New-Onset Diabetes Mellitus after Kidney Transplantation

Salah Alajous et al. J Clin Med. .

Abstract

New-Onset Diabetes Mellitus after Transplantation (NODAT) emerges as a prevalent complication post-kidney transplantation, with its incidence influenced by variations in NODAT definitions and follow-up periods. The condition's pathophysiology is marked by impaired insulin sensitivity and β-cell dysfunction. Significant risk factors encompass age, gender, obesity, and genetics, among others, with the use of post-transplant immunosuppressants intensifying the condition. NODAT's significant impact on patient survival and graft durability underscores the need for its prevention, early detection, and treatment. This review addresses the complexities of managing NODAT, including the challenges posed by various immunosuppressive regimens crucial for transplant success yet harmful to glucose metabolism. It discusses management strategies involving adjustments in immunosuppressive protocols, lifestyle modifications, and pharmacological interventions to minimize diabetes risk while maintaining transplant longevity. The importance of early detection and proactive, personalized intervention strategies to modify NODAT's trajectory is also emphasized, advocating for a shift towards more anticipatory post-transplant care.

Keywords: GLP1 AR; HbA1c; NODAT; kidney; metformin; transplant.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
The figure illustrates the risk factors and the main pathophysiological mechanisms implicated in the pathogenesis of NODAT.
Figure 2
Figure 2
This figure illustrates the cascading effects of NODAT on various physiological processes, particularly hypertension, inflammation, and oxidative stress, ultimately leading to cardiac complications. NODAT is state of hyperglycemia caused by β-Cell dysfunction and increaseed insulin resistance, leads to elevated blood pressure and systemic inflammation. These interconnected factors heighten oxidative stress levels, exerting detrimental effects on cardiac function and health.
See this image and copyright information in PMC

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Grants and funding

This research received no external funding.