The changes in serum leptin, body fat mass and insulin resistance after renal transplantation.

BACKGROUND: In this prospective-controlled study, we aimed to investigate the effect of changes in insulin resistance and anthropometrical parameters on serum leptin levels (SLL) after renal transplantation (Tx). PATIENTS AND METHODS: Thirty-four patients (M/F: 19/15, mean age: 29 +/- 9 yr) and 30 age and sex-matched healthy controls (C) were included. Body weight, subscapular, suprailiac, periumbilical, biceps and triceps skinfold thicknesses, neck, wrist, hip and waist circumferences, as well as body mass index and body fat mass were measured as anthropometrical parameters. In order to measure the serum glucose, insulin and SLL, blood samples were obtained before and 1 wk, 1 and 6 months after Tx. Homeostasis Model Assessment (HOMA) values were calculated as an index of insulin resistance. RESULTS: Serum leptin levels (SLL) of the patients at pre-Tx were significantly higher than C (21.5 +/- 3.5 vs. 7.8 +/- 0.9 ng/mL, p = 0.002) and decreased at first week after Tx (from 21.5 +/- 3.5 to 8.4 +/- 1.5 ng/mL, p < 0.001). Thereafter, it gradually increased to 12.8 +/- 2.1 ng/mL in the first month and to 14.4 +/- 2.1 ng/mL in the sixth month after Tx. Serum leptin levels at sixth month were significantly higher than C (p = 0.005). Serum insulin and HOMA values changed similar to SLL after Tx. Correlations between SLL and HOMA persisted during the study period [pre-Tx (r: 0.40) and at first (r: 0.38) and sixth (r: 0.47) months]. In linear regression analysis, HOMA and fat mass were found as independent variables for predicting SLL at the sixth month after Tx. CONCLUSION: Serum leptin levels dramatically decreased immediately after Tx and significantly correlated with serum insulin levels and HOMA during the entire study. Increase in SLL at sixth months was probably because of increase in fat mass, insulin resistance and steroid use in renal transplant recipients.

Association between hepatitis C virus infection and development of posttransplantation diabetes mellitus in renal transplant recipients.

BACKGROUND: Posttransplantation diabetes mellitus (PTDM) is a metabolic complication of renal transplantation. A high prevalence of DM has been recently reported in patients with chronic hepatitis C virus (HCV) infection in the nontransplant population. The aim of this study was to investigate possible factors that may have a role in the development of DM, including HCV infection in renal transplant recipients. PATIENTS AND METHODS: This case-control study included 43 patients with PTDM (36 men, 7 women; mean age, 44+/-10 years) and 43 consecutive transplant patients who did not develop PTDM (30 men, 13 women; mean age, 37+/-11 years). Age, body mass index, high-dose steroid use, family history for DM and HCV, and presence of HLA-DR2, -DR3, and -DR4 were considered as possible factors for predicting PTDM. RESULTS: Patients with PTDM were older (P=0.002) and had a higher prevalence of family history of DM (61% vs. 9%, P<0.001) and a higher rate of HCV seropositivity (72% vs. 37%, P=0.002; odds ratio = 1.94; 95% confidence interval = 1.26-2.98). The prevalence of pancreatic autoantibodies (anti-glutamic acid decarboxylase, islet cell antibody) was similar between patients with and without PTDM. In logistic regression analysis (r = 0.61, P<0.001), age, family history, and HCV infection were independent variables for predicting development of PTDM. CONCLUSION: HCV infection was associated with the development of PTDM, in addition to family history and increased age. The rate of autoantibodies against pancreatic cells was not increased in patients with HCV, which suggested that nonimmunologic mechanisms were likely to have a role in the pathogenesis of PTDM.

The effect of angiotensin converting enzyme gene polymorphism on chronic allograft dysfunction in living donor renal transplant recipients.

BACKGROUND: Chronic allograft dysfunction (CAD), the major cause of the failure of kidney allografts, may be caused by immunological and non-immunological haemodynamic factors. Renin-angiotensin system has been implicated in the development of intraglomerular hypertension and has a central role on progression in chronic renal disease. Polymorphism in 16th intron of the ACE gene has been reported to predict the circulating angiotensin II levels. The aim of this study was to investigate the effect of the both recipient and donor angiotensin converting enzyme (ACE) genotype on the development of CAD in renal allograft recipients. PATIENTS AND METHODS: A total of 143 renal transplant recipients (95 male, 48 female, mean age 32 +/- 10 yr) were included. In order to exclude the effect of cold ischaemia, only patients transplanted from living donors were selected. Factors analysed in the development of CAD were donor and recipient age, past history of acute rejection, presence of hypertension and hypercholesterolaemia, serum uric acid level and ACE gene polymorphism. RESULTS: Forty of the patients (28%) had CAD. Homozygous deletion type ACE gene polymorphism was detected in 59 renal transplant recipients (42%) and in 31 donors of the patients (37%). On comparing patients with and without CAD, donor age, rate of acute rejection and hypertension and serum uric acid levels were significantly higher in CAD (+) groups. Neither recipient nor donor ACE genotype was associated with time to CAD. Cox regression analysis revealed donor age (p < 0.001), presence of hypertension (p=0.002) and serum uric acid levels (p=0.009), but neither donor nor recipient ACE genotype as independent factors for predicting development of CAD. CONCLUSION: Donor age, presence of hypertension and serum uric acid levels was independent factors. Donor and recipient ACE genotype seemed to have no influence on the development of CAD in living donor transplanted patients.