RESUMO
Chronic allograft nephropathy [CAN] is a devasting long-term complication of kidney transplantation that is responsible for a significant proportion of graft loss. Activin A, a member of the transforming growth factor-beta [TGF- beta] superfamily of proteins, has a pro-fibrotic activity. The biologic effects of activin A are countered by follistatin, which is a high affinity extracellular binding protein for activin A. To study serum activin A and follistatin levels in the post-renal transplant patients and their correlation to renal hemodynamics, graft function and survival. The study included 20 post-renal transplant patients [Group I] and 20 age and sex matched healthy subjects [Group II] as controls. Serum activin A and serum follistatin were measured by enzyme linked immunosorbent assay [ELISA]. Serum C-reactive protein [S.CRP] was measured by turbidimetry. Serum and urinary alkaline phosphatase [S.ALP, U.ALP] were measured by spectrophotometry. Renal henwdynamics were evaluated by duplex Doppler ultrasonography; resistive and pulsatility indices [RI, PI] were calculated. Ten patients were categorized as chronic allograft nephropathy [CAN; group Ia]. The other ten patients had a stable renal function [non-CAN; group Ib]. There was a statistically significant increase in serum activin A [S.activin A], S.ALP, S.CRP, RI and PI and a statistically significant decrease in U.ALP and follistarin/activin ratio in patients with CAN than healthy controls, versus a statistically significant difference only in S. activin A and follistatin/activin ratio between non-CAN and controls. There was no statistically significant differences in S. follistatin between the studied groups. In post-renal transplant patients, S.activin A showed a statistically significant positive correlation with S. creatinine, S.CRP, RI and PI versus a statistically significant negative correlation with creatinine clearance, U.ALP and follistatin/Activin ratio. U.ALP showed a statistically significant positive correlation with creatinine clearance versus a statistically significant negative correlation with S. creatinine, S. activin A, S.CRP, RI and PI. Enhanced activin A activity together with normal follistatin level and the decrease in follistatin/activin ratio in post-renal transplant patients, showed that there is a dysregulation of activin-follistatin axis with the increase of the unbound biologically active activin A with deterioration of renal function. Also, there is an increased activity of ongoing inflammation accompanied by impaired renal function among renal allograft recipients that led to enhanced renal fibrosis and a degree of tubular dysfunction