Effects of Glucocorticoid Immunosuppression on Serum Cystatin C Concentrations in Renal Transplant Patients

Abstract

Cystatin C is a nonglycosylated basic protein (13.36 kDa) and can be found in a variety of biologic fluids (1). Cystatin C serum concentration is not influenced by gender, inflammation, or lean tissue mass and is regarded to be mainly determined by glomerular filtration rate (GFR) (2)(3)(4)(5). Cystatin C has been described as meeting many of the characteristics of an ideal GFR marker (e.g., endogenously produced at a constant rate, freely filtered in the glomerulus, neither reabsorbed nor secreted in the renal tubule, not extrarenally eliminated) and has been reported to be at least as accurate as the commonly used serum creatinine to detect impaired renal function in various patient groups, including renal transplant patients (6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24). Despite this, Bokenkamp et al. (25) reported that cystatin C is higher in children with renal transplants than in children with other renal pathologies but comparable GFRs, suggesting an underestimation of GFRs by cystatin C in renal transplant patients. This finding suggested immunosuppression as a major influencing factor because all patients had received prednisolone and cyclosporin A medication. Interestingly, neither prednisolone nor cyclosporin A was believed to change cystatin C concentrations because no dose-dependent increase of cystatin C was found. In contrast, an in vitro study by Bjarnadottir et al. (26) described a dose-dependent increase of cystatin C production in HeLa cells exposed to dexamethasone. To further clarify these findings, we conducted a nested case-control study in a cohort of renal transplant patients who were prospectively monitored during a 1-year period (20). The present study aimed to elucidate the influence of glucorticoid immunosuppression on cystatin C concentrations in serum from renal transplant patients.