Massimo Taccone-Gallucci

Cardiovascular disease is a leading cause of morbidity and mortality in end-stage renal disease (ESRD) patients on maintenance hemodialysis (HD). Neither traditional nor emerging risk factors for cardiovascular disease can explain completely this excess of morbidity and mortality and the role and timing of primary prevention strategies in this population has not been clarified. The aim of this study was to assess if an aggressive pharmacological preventive treatment may reduce the myocardial ischemic burden and then improve the cardiovascular outcome In ESRD patients. Forty-three asymptomatic ESRD patients on maintenance HD were evaluated. Asymptomatic patients with neither history nor clinical evidence of cardiovascular disease were considered. A total of 31 ESRD patients were enrolled into the study and were submitted to Tc-99m SESTAMIBI myocardial gated- single-photon emission computed tomography (SPECT) stress test. All patients then received an aggressive medical regimen with statins, antiplatelet drugs, ACE inhibitors (ACE-I) and/or Angiotensin II Receptor Blockers (ARB) and other hypotensive, glucose-lowering medications, sevelamer, calcium carbonate and calcitriol if required. A significant reduction of coronary functional reserve was found in more than 50% of otherwise asymptomatic HD patients and may often be reverted by prolonged aggressive medical therapy. After a four-year follow-up under aggressive medical therapy no significant difference was observed neither in the incidence of conventional and emerging cardiovascular risk factors nor in cardiovascular outcome of patients with or without silent myocardial ischemia (SMI). As cardiovascular disease (CVD) is by far the first cause of death in ESRD, an aggressive medical management may be highly advisable for the primary prevention of major adverse cardiac events in all HD patients despite the stress test evidence of inducible myocardial ischemia .

Cardiovascular disease (CVD) is the main cause of death among haemodialysis (HD) patients. Emerging cardiovascular risk factors such as oxidative stress and chronic inflammation are involved in these patients together with traditional risk factors. Here we investigate the effects of a short-term folate treatment on some markers of chronic inflammation in two groups of HD patients with and without vascular occlusive disease (VOD). Homocysteine (HCy), C-reactive protein (CRP), Folate, fibrinogen and alpha1 acid glycoprotein (alpha1AGP) were dosed before and after a 3-month course of high-dose folate (25 mg intravenous calcium laevofolinate pentahydride once weekly) and again after a one-month washout in 15 HD patients with established VOD (group A) and in 15 comparable HD patients with no diagnosis of VOD (group B). Baseline HCy and CRP were significantly elevated in patients of both groups A and B compared to normal values. Folate treatment significantly reduced HCy in patients of both groups A and B and alpha1AGP only in patients of group A, while the other markers were not modified. After the one-month washout a significant raise of CRP could be observed in patients of group A; again, the other markers were not modified. Our results suggest that significant reduction of serum HCy can be achieved in both patients with or without VOD after administration of high-dose folic acid. Hence, folic acid supply is useful in the treatment of hyperhomocysteinemia in HD patients, although it is not sufficient to modify their chronic inflammatory status.