Acute kidney injury: Effect of hemodialysis membrane on Hgf and recovery of renal function

ObjectivesAcute kidney injury (AKI) is associated with a high mortality and morbidity rate. In this study we investigated whether dialysis membranes influence the recovery of renal function, through the regulation of hepatocyte growth factor (HGF).Design and methods21 patients were enrolled and assigned to hemodialysis (HD) with cellulose (CE, N = 11) versus polymethylacrylate (PMMA, N = 10) membranes in alternating order.HGF and IL-1 were measured in serum and in peripheral blood mononuclear cells (PBMC) supernatants collected immediately before the first HD session (T0), at 15 minutes (T15), at 240 minutes (T240) and after the last HD, when renal recovery occurred. Eight healthy volunteers were the controls (CON).ResultsTime to renal function recovery was lower in CE than in PMMA patients. Serum HGF in HD patients was significantly higher than in CON. HGF levels were higher in CE than in PMMA patients at T15 (13.4 ± 2.7 vs 8.9 ± 3.0 ng/mL, P = 0.004) and T240.At recovery, HGF levels decreased. IL-1 serum levels showed a similar trend (at T15 CE: 20.5 ± 2.9 vs PMMA: 16.9 ± 3.2 pg/mL, P = 0.005). HGF release significantly increased in the course of HD, resulting in higher levels in CE than that in PMMA patients.Considering all the patients, basal HGF release negatively correlated with time to renal recovery (r2 = 0.42, P < 0.01).ConclusionsHere we demonstrated that dialysis membranes influence the cytokine profile in AKI patients, HGF release being higher in patients treated with the CE membrane, in comparison to PMMA. Our results suggest that treatment with CE might improve clinical outcomes, possibly through increased release of HGF.

► Acute kidney injury (AKI) is a common and severe condition;
► HGF is up-regulated in the course of hemodialysis (HD) in patients with AKI;
► Different dialytic membranes influence clinical outcomes and HGF production in AKI;
► HD-related HGF induction could promote renal recovery after AKI.