New-Onset Diabetes Mellitus in the Kidney Recipient

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.

The direct effects of tacrolimus and cyclosporin A on isolated human islets: A functional, survival and gene expression study

“…These findings support the results from studies 10,12 demonstrating more marked (although not significantly so) islet morphological changes in pancreatic biopsies of patients treated with tacrolimus, and reduced insulin secretion release from isolated human islets, and contribute to the understanding of the clinical observation that new-onset diabetes after transplantation is more common when this immunosuppressant is used. [1][2][3] In fact, after transplantation, insulin secretion dysfunction, rather than insulin resistance, plays a major causative role in new-onset diabetes. 15,16 The effects of calcineurin inhibitors on b-cells are not surprising, since the calcineurin/NFAT signaling pathway has been described in these cells, and is important in b-cell function and turnover.…”

“…[1][2][3][4][5] Among the several factors that have an impact on the increased risk of CVD in graft recipients, new-onset diabetes after transplantation (NODM) plays a major role, and has been associated with reduced graft function, diminished patient survival and increased risk of graft loss. [1][2][3][4][5] Chronic immunusoppression is a common cause leading to NODM in susceptible patients, including the use of calcineurin inhibitors, that is associated with decreased insulin secretion and possible toxic effects on pancreatic b-cells. [1][2][3][4][5][6] The direct action of tacrolimus and cyclosporin A on the b-cell has been investigated in a few studies.…”

“…[1][2][3][4][5] Chronic immunusoppression is a common cause leading to NODM in susceptible patients, including the use of calcineurin inhibitors, that is associated with decreased insulin secretion and possible toxic effects on pancreatic b-cells. [1][2][3][4][5][6] The direct action of tacrolimus and cyclosporin A on the b-cell has been investigated in a few studies. Both molecules have been shown to impair glucose stimulated insulin release and reduce b-cell mass in b-cell lines and rodent islets.…”

Glikokortykosteroidy a zaburzenia metabolizmu glukozy

“…Dlatego w dostępnej literaturze istnieje duża rozbieżność w tym zakresie. Według różnych danych cukrzycę posteroidową rozpoznaje się u 1,5-47% pacjentów leczonych GS [21][22][23][24]. Więk-szość badań oceniających efekt działania hormonów steroidowych analizuje tylko wartości glikemii na czczo, mimo że hormony te wpływają przede wszystkim na glikemie w ciągu dnia, głównie poposiłkowe.…”

Diabetes mellitus – an overview

“…SUs reduce HbA 1c levels by 0.8-2.0% and FPG concentrations by 60-70 mg/dl (3.3-3.9 mmol/l) [81]. The use of the fi rstgeneration SUs has been replaced by newer-generation SUs (glipizide, glyburide (glibenclamide) and glimepiride) with more favourable side effect profi les [82]. SUs differ mainly in their potency and their duration of action [83].…”