Impact of mineralocorticoid receptor antagonist in renal transplant patients: a systematic review and meta-analysis of randomized controlled trials

BACKGROUND: Mineralocorticoid receptor (MR) antagonism can stop the occurrence of acute kidney injury induced by ischemia/reperfusion (IR) in pig and rodent and pig models. However, there are controversies regarding MR antagonist use in renal transplant patients to attenuate IR injury. We aim to perform this study to build evidence regarding benefits of MR antagonist use in renal transplant patients. METHODS: We searched four authentic databases during August 2019. We included randomized controlled trials (RCTs) which compared MR antagonists versus control in renal transplant patients. Data were extracted from eligible studies and pooled in a meta-analysis model using RevMan software. Our primary outcome was serum creatinine. Our secondary outcomes were serum potassium, serum aldosterone, urinary heat shock protein 72 (Hsp72), and 8-hydroxy-2-deoxyguanosine (8-OHdG). RESULTS: Four RCTs with 167 patients were included in our analysis. We found that MR antagonists were significantly superior to control group in decreasing serum creatinine after removal of heterogeneity (MD = - 0.23, 95% CI [- 0.44, - 0.02], p = 0.04). Control group was superior to MR antagonists in serum potassium and aldosterone respectively, (MD = 0.28, 95% CI [0.17, 0.38], p < 0.00001), (MD = 33.08, 95% CI [28.61, 37.54], p < 00001). MR antagonists were significantly associated with reduction in Urinary Hsp72, and Urinary 8-OHdG respectively (MD = - 3.08, 95% CI [- 5.45, - 0.71], p = 0.01), (MD = - 0.24, 95% CI [- 0.40, -0.09], p = 0.002). CONCLUSION: Although an improvement in serum creatinine and urinary Hsp72 and 8-OHdG, as an expression of renoprotection induced by MR antagonists, was observed in kidney transplanted recipients, the different designs of the 4 studies limit the meaningful of this conclusion. Thus, more powered RCTs are warranted.