Cardiovascular complications after renal transplantation

Abstract

According to Lindholm [1] between the second and fifth year after renal transplantation, 41.4% of graft loss is accounted for by rejection and no less than 49.2% by death with a functioning graft, while other causes account for a further 9.4%. Thus, reduction of cardiovascular death will be a very efficient measure to preserve grafts. According to the EDTA Registry [2], the frequency of death from cardiovascular causes increases markedly with age in patients with a functioning graft who had suffered from standard primary renal disease. The recent summary on cardiovascular disease in renal patients by the National Kidney Foundation (Table 1) states that clinical coronary artery disease and left ventricular hypertrophy by echocardiography are definitely more frequent in recipients with renal grafts, although substantially less so than in patients on hemodialysis or peritoneal dialysis [3]. The survival advantage conferred by transplantation is well illustrated by the studies of Port et al. [4] and Bonal et al. [5]. The relative mortality of graft recipients beyond the first month after transplantation was substantially lower, particularly in diabetic patients [4] and high risk elderly patients [5], than in hemodialysed patients on the transplant waiting list. In the study of the Catalunya registry, cardiovascular comorbidity was also substantially lower in transplanted patients (Figure 1) and this was paralleled by substantially better actuarial 5-year survival (0.86 after transplantation versus 0.77 on hemodialysis). Using multivariate analysis Cosio [6] found that apart from age, diabetes and smoking, length of time on dialysis was an independent predictor of post-transplantation death. In contrast, duration of pretransplantation dialysis treatment was not an independent predictor in the study of Arend [7], but there is little doubt that much of the pathology causing cardiac death after transplantation has been acquired in the pretransplantation period of endstage renal failure. This is indicated by several studies [8, 9] which document that cardiovascular abnormalities at the time of transplantation are independent and potent predictors of subsequent death with functioning graft. In the study of MacGregor [8] left ventricular mass index (LVM) was significantly higher in those patients who subsequently died (median 167 versus 134 g/m², p 0.03) as were end-systolic (4.3 versus 3.4 cm, p 0.01) and end-diastolic (5.8 versus 5.2 cm. p <0.01) diameters and systolic dysfunction (fractional shortening 27 versus 33, p <0.01). Further studies are required to asses to what extent echocardiographic studies exaggerate the frequency of left ventricular hypertrophy (LVH) by artefactual overestimation of LVM when hypervolemia and cardiac dilatation are present. It has been claimed that in graft recipients LVH is more prominent in patients with the DD genotype of the ACE gene polymorphism [10]. In a prospective Canadian cohort study in which patients were followed with echocardiography, successful renal transplantation led to significant reversal of systolic dysfunction, concentric LVH and LV dilatation [11]. Of note, de novo ischemic heart disease developed only in one of 102 patients, in contrast to a recent follow-up study in which 23% of patients with a functioning graft for 15 years developed de novo coronary heart disease [12]. Apparently partial reversal of LVH [11] is incomplete. Cardiac pathology and risk of cardiac death are not normalized in this population and the remarkable rate of de novo development of coronary disease may play a role [12, 13].