Risk Factors and Prognosis for Proteinuria in Renal Transplant Recipients

Abstract

Introduction Proteinuria in renal transplant recipients has been recognized as a risk factor of progression of chronic allograft nephropathy and for cardiovascular disease, the main causes of transplant failure. Patients and methods We analyzed the risk factors for persistent proteinuria (>0.5 g/day) among 337 kidney allograft recipients with a minimum follow-up of 6 months, among a series of 375 transplants performed during a decade, as well as their association with allograft and patient survivals. Patients with proteinuria greater than 0.5 g/d were treated with angiotensin-converting enzyme inhibitors (ACEI) and/or angiotensin-receptor blockers. Results After a mean follow-up of 53.35 ± 52.63 months, 68 patients (20.17%) had persistent proteinuria greater than 0.5 g/d. Female patients ( P = .012), body mass index (BMI) >25 ( P = .008), pretransplant HLA sensitization ( P = .039), and delayed graft function (DGF; P = .001) were associated with proteinuria. Induction treatment with antithymocyte globulin ( P = .030) and treatment with tacrolimus instead of cyclosporine ( P = .046) were associated with an increased risk of proteinuria. Multivariate analysis confirmed the independent value of DGF (RR = 2.23; 95% confidence interval [CI] 1.22 to 4.07; P = .009) and BMI >25 (RR = 1.968; 95% CI 1.05 to 3.68; P = .035) to predict postransplant proteinuria. The mean values of serum creatinine ( P = .000) and systolic blood pressure ( P < .05) were persistently higher from the early stages after transplantation in the proteinuric group. Graft survival at 5 years was 69% among patients who developed proteinuria and 93% in those without proteinuria ( P = .000), with no differences in patient survival ( P = .062). Conclusion Proteinuria in renal transplant recipients was related to immunological and nonimmunological factors, some of which, such as hypertension and obesity could be modifiable. Proteinuria in renal transplant recipients predicted a worse allograft survival despite of intensive treatment of hypertension including ACEI/angiotensin-receptor blockers.