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Review
. 2008 Mar;3 Suppl 2(Suppl 2):S38-48.
doi: 10.2215/CJN.02650707.

New-onset diabetes mellitus in the kidney recipient: diagnosis and management strategies

Affiliations
Review

New-onset diabetes mellitus in the kidney recipient: diagnosis and management strategies

Roy D Bloom et al. Clin J Am Soc Nephrol. 2008 Mar.

Abstract

Advancing care has markedly improved survival after kidney transplantation, leaving patients susceptible to the effects of chronic transplant-associated morbidities. New-onset diabetes mellitus (NODM) is common in kidney recipients, threatening health and longevity by predisposing to microvascular and cardiovascular disease and by reducing graft survival. A strong rationale therefore exists for the aggressive treatment of NODM in kidney recipients to limit these complications. Screening for diabetes should be systematic and should span the pre- and posttransplantation periods. Once NODM is diagnosed in the kidney transplant patient, a comprehensive plan of therapy should be used to achieve treatment targets. As in the general population, treatment includes lifestyle modification and drug therapy as needed, but transplant-specific factors add complexity to the care of kidney recipients. Among these, minimizing immunosuppression-related toxicity without compromising graft outcomes is of paramount importance. Preexisting allograft functional impairment and the potential for significant interactions with immunosuppressive agents mandate that the expanding armamentarium of hypoglycemic agents be used with care. A team-oriented treatment approach that capitalizes on the collective expertise of transplant physicians, diabetologists, nurse-educators, and dieticians will optimize both glycemic control and the overall health of hyperglycemic kidney recipients.

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Figure 1.
Figure 1.
Illustration of the pathogenic mechanisms that lead to transplant-associated hyperglycemia (TAH) in kidney recipients. Bulleted blue text represents potential therapeutic interventions depicted at sites where their effects may be optimally mediated. *Nonmodifiable risk factors for TAH. CNIs, calcineurin inhibitors; DPP-IV, dipeptidyl peptidase-IV; GLP-1, glucagon-like peptide-1; HCV, hepatitis C virus; HTN, hypertension; IFG, impaired fasting glucose; Srl, sirolimus; TZDs, thiazolidinediones.

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References

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