New-onset diabetes after kidney transplantation: Incidence, risk factors, and outcomes

Abstract

Many patients develop new-onset diabetes after kidney transplantation (NODAT). Its incidence and epidemiology are unknown in the Saudi population. We aimed to study the incidence, epidemiology, and outcomes of kidney transplant recipients who developed NODAT. This is a retrospective study of all adults who received kidney transplant between January 2003 and December 2009. NODAT was defined according to the criteria outlined in the 2003 International Consensus guidelines. A total of 500 patients were included in this study, 54% were male patients. One hundred thirty-six patients (27%) developed diabetes (NODAT group). In the univariate analysis, patients were older in the NODAT group (P <0.001), were of higher weight (P = 0.006), and had positive family history of diabetes (P = 0.002). Similarly, more patients in this group had impaired glucose tolerance before transplant (P = 0.01) and history of hepatitis C infection (P = 0.005). In the multivariate analysis, older age [odds ratio (OR) 1.06], family history of diabetes (OR 1.09), hepatitis C infection (OR 1.92), and impaired fasting glucose (OR 1.79) were significant risk factors for the development of NODAT. Mortality was 6% in the NODAT group and 0.5% in the non-diabetic group had died (P <0.001). Graft survival was not different between the groups (P = 0.35). In conclusion, there is a significant risk of developing diabetes after renal transplantation. Patients are at higher risk if they are older, have a family history of diabetes, pre-transplant impaired fasting/random glucose, and hepatitis C virus infection.

<p>Immunogenetics of new onset diabetes after transplantation in Kuwait</p>

“…It is more common in African Americans and Hispanics than Caucasians and Asians. 6 Currently, aside from a few epidemiological studies, there is a dearth of information about NODAT in Arab populations 7–12. These studies suggest that around 25–30% of KTR develop NODAT in Arab countries.…”

“…These studies suggest that around 25–30% of KTR develop NODAT in Arab countries. More specifically, the incidence of NODAT after kidney transplantation is 27% in Saudi Arabia,7,8 30% in Bahrain, 9 22.2% in Egypt10 and recently it was reported as 25.6% in Kuwait 11,12…”

Effects of preoperative hepatitis B virus infection, hepatitis C virus infection, and coinfection on the development of new‐onset diabetes after kidney transplantation

“…17 Considering the adverse consequences following NODAT, it is important that the association between HBV and HCV infection and incident NODAT in KTRs is well established. However, limited studies on HBV infection and incident NODAT are available to establish a reliable association between the two; it remains contentious whether HCV infection increases the risk of NODAT, with some studies reporting a significant correlation between the two, 2,4,[18][19][20][21] and others indicating no consistent association. [22][23][24][25][26] Moreover, whether coinfection with HBV and HCV exerts a greater effect on the development of NODAT than infection with each virus individually remains unclear due to the scarcity of relevant information.…”

Analysis of the frequency of single nucleotide polymorphisms in cytokine genes in patients with New Onset Diabetes After Transplant

“…scarce, with the exception of few epidemiologic studies [9][10][11] suggesting that 25-30% of KTRs eventually develop NODAT [9][10][11][12] . Specifically, the incidence rate of NODAT, following kidney transplantation, has been found in to be as high as 27% in Saudi Arabia 9 , 30% in Bahrain 10 , 22.2% in Egypt 11 , and 25.6% in Kuwait 12,13 .…”

“…Given the critical role of cytokines in regulating immune responses, subtle differences in cytokine expression may have a major effect on the outcomes of those responses 20 . Single nucleotide polymorphisms (SNP) in the regulatory region of the cytokine genes have been shown to correlate with individual variations in cytokine production [9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] . Thus, variations in susceptibility to NODAT may be influenced by inter-individual genetic variations of cytokine genes [19][20][21][22][23] .…”