Evolution of left ventricular mass in renal transplant recipients: the influence of glucose homeostasis and oxidative stress.

Background: Left ventricular hypertrophy, considered an independent factor for cardiovascular mortality, is frequent among renal transplant recipients (RTR), in whom we investigated changes in left ventricular mass (LVM) after grafting and associations with possible causal factors, especially glucose metabolism and oxidative stress.

Methods: We performed a prospective study of 37 RTR without prior diabetes mellitus who were evaluated at three times after transplantation (medians of 0.6, 16 and 28 months) by means of the LVM index (LVMI, echocardiographic measure of LVM related to body surface area, g/m(2)), oral glucose tolerance test and determinations of malondialdehyde and total glutathione (GSH), as well as glomerular filtration rate (GFR) estimate by the Modification of Diet in Renal Disease formula. We calculated the overall increment (DeltaLVMI) and percent change of LVMI. Patients were diagnosed to be prediabetic (PD) or new-onset diabetes after transplant (NODAT) according to ADA criteria.

Results: The mean LVMI decreased significantly over time among whole group baseline = 108.34 ± 27.71 g/m(2) versus middle: 100.03 ± 27.53 g/m(2) versus final: 90.62 ± 24.06 g/m(2) (P = .000). However, 13.5% of subjects showed an increased LVMI and 59.5%, a decrease less than 20%. Patients with NODAT at the end of the study showed a positive DeltaLVMI, which was negative in nondiabetics (0.24 ± 16.14 versus -19.86 ± 12.61 g/m(2), P = .018). Compared with DeltaLVMI(-) recipients, patients with DeltaLVMI(+) showed a greater proportion of PD and NODAT at baseline (60% and 40% versus 18.8% and 12.5%, P = .017), and significantly higher all-time fasting glycemia, lower estimated GFR, and greater increments of malondialdehyde and GSH over time. Those with a <20% LVMI decrease experienced progressive GFR impairment over time, as opposed to those with an LVMI decrease > 20%, who showed greater and improving GFR over the whole study.

Conclusions: LVMI does not always improve in RTR; the evolution of ventricular mass after renal transplantation is influenced by glucose metabolism disorders, oxidative stress, and graft function.