Is selenium deficiency an important risk factor for chronic graft nephropathy? A pilot study

Lipid peroxidation by free radicals is a key step in the development of atherosclerosis. Chronic graft nephropathy (CGN) is a common cause of allograft failure and shares many histologic features with atherosclerosis. Although hyperlipidemia is a common finding in renal transplant recipients, not all patients develop CGN. We hypothesized that the degree of damage sustained is related to recipient antioxidant status and that only those who are antioxidant deficient succumb to free radical attack and develop CGN. We aimed to determine the antioxidant profiles of patients with biopsy-proven CGN and to compare their profiles to transplant patients with good renal function.

Plasma selenium and vitamin A and E concentrations were measured in 10 patients with CGN and 10 contemporaneous, sex-matched patients with normal renal graft function, who received the same immunosuppressive therapy.

Patients with CGN had significantly lower plasma selenium concentrations compared with those with normal renal allograft function (P<0.05). There were no significant differences in plasma vitamin A or E concentrations between the two groups. There was no difference in the prevalence of any of the immunologic or nonimmunologic risk factors: human leukocyte antigen mismatches, panel-reactive antibody status, number of rejection episodes, cold ischemic time, hyperlipidemia, hypertension, diabetes, and cytomegalovirus infection between the two groups.

Patients with CGN have evidence of selenium deficiency, suggesting that impaired antioxidant status may contribute to the development of CGN.