Renal transplantation in the modern immunosuppressive era in Spain: four-year results from a multicenter database focus on post-transplant cardiovascular disease

Abstract

To evaluate cardiovascular disease (CVD) after renal transplantation we established a CVD database (no-intervention) including all patients transplanted among 2000-2002 in 14 hospitals from Spain (Renal Forum Group) (n=2600). They were prospective followed annually thereafter and we present herein the most important results concerning survival figures and CVD at four years. Mean recipient age was 49.7+/-13.7 years: 16% retransplanted and 12.5% hyperimmunized. Tacrolimus, mycophenolate mofetil, and steroids was used in 63%. Acute rejection (AR) rate at 1 year was 14.8%. Graft and patient survival at 48 months were 85.6% (death censored) and 91.7% respectively. The first cause of graft loss was vascular in the first year, death with function during the 2-3 years, and chronic allograft nephropathy at the 4th year. Donor age, time on dialysis, acute tubular necrosis (ATN), AR, SCr at 6 months, the use of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers in the first year, and systolic blood pressure at 24 months were independent risk factors for graft loss at 4th year. The first cause of death was CVD (predominantly ischemic heart disease (IHD) in the first year). Recipient age, ATN, and SCr at 6 months were independent predictors of mortality. Despite worsening of donor age, comorbidity, and advanced age of recipients, survival figures at four years are considered good in our Spanish non-selected population. Cardiovascular mortality is the most important cause of death and graft loss particularly, IHD in the first year. Therefore, to decrease post-transplant mortality a careful cardiovascular evaluation and treatment in the waiting list and a close follow-up of patients after transplantation is mandatory.

Posttransplantation Proteinuria

“…At 6 months, 15% of patients were on RAAS inhibitors, but this increased to 45% by the end of the study (52). In a multivariate analysis, the use of RAAS inhibitors at 12 months was associated with 64% higher risk for graft loss at 4 years (hazard ratio 1.64; 95% CI 1.01 to 2.65; P ϭ 0.042) (52). This risk was adjusted for important confounding variables such as donor age, acute rejection, serum creatinine, and BP (52).…”

“…In a multivariate analysis, the use of RAAS inhibitors at 12 months was associated with 64% higher risk for graft loss at 4 years (hazard ratio 1.64; 95% CI 1.01 to 2.65; P ϭ 0.042) (52). This risk was adjusted for important confounding variables such as donor age, acute rejection, serum creatinine, and BP (52). It is certainly possible that this finding was due to selection bias, with high-risk patients with proteinuria being preferentially started on RAAS blockade.…”

“…A prospective cohort study from Spain followed 2600 kidney transplant recipients for 4 years (52). Baseline proteinuria, assessed at 6 months after transplantation, averaged 0.4 Ϯ 0.7 g/d, with 13% having Ͼ1 g/d (52). At 6 months, 15% of patients were on RAAS inhibitors, but this increased to 45% by the end of the study (52).…”

“…Baseline proteinuria, assessed at 6 months after transplantation, averaged 0.4 Ϯ 0.7 g/d, with 13% having Ͼ1 g/d (52). At 6 months, 15% of patients were on RAAS inhibitors, but this increased to 45% by the end of the study (52). In a multivariate analysis, the use of RAAS inhibitors at 12 months was associated with 64% higher risk for graft loss at 4 years (hazard ratio 1.64; 95% CI 1.01 to 2.65; P ϭ 0.042) (52).…”

Adiponectin, leptin, nitric oxide, and C-reactive protein levels in kidney transplant recipients: comparison with the hemodialysis and chronic renal failure

“…[24][25][26][27] In KTR, the most common cause of late allograft loss and leading cause of KTR deaths is CVD. 28 There are still unanswered points about how and why KTR keep on suffering from CVD despite the restoration of glomerular dysfunction. The interaction between adiponectin, leptin, and NO seems to affect inflammation and endothelial dysfunction which play important role in the pathophysiology of atherosclerosis and need to be well understood since they can predict CVD or may help to develop new treatment strategies.…”