Emerging data on finerenone have drawn significant interest from nephrologists and cardiologists for its clinical potential in patient management. Its nonsteroidal structure, greater receptor selectivity, and reduced risk of hyperkalemia make it a distinctive choice for clinicians. Mineralocorticoid receptors (MRs) are expressed in the collecting ducts, endothelial and vascular smooth muscle cells of the interlobar arteries, as well as in podocytes, mesangial cells, and renal fibroblasts. These receptors are also present in cardiovascular and inflammatory cells. MR activation contributes to ischemia-reperfusion injury (IRI) and mediates calcineurin inhibitor (CNI) toxicity, proteinuria, and fibrosis in both the cardiovascular system and kidneys. Blocking MR activation with finerenone may exert therapeutic effects in renal allografts by mitigating IRI, preventing CNI toxicity, reducing proteinuria and renal fibrosis, and lowering the risk of renal and cardiovascular events. Preclinical and clinical studies in the general population with diabetes have demonstrated that finerenone effectively reduces proteinuria and improves renal and cardiovascular outcomes. However, clinical evidence in kidney transplant recipients remains extremely limited, and the efficacy and safety of finerenone in this population are yet to be established. To date, no clinical trials specifically investigating finerenone in kidney transplantation have been published, with only the EFFEKTOR trial currently underway. This review discusses the mechanistic rationale, extrapolates evidence from nontransplant populations, identifies key knowledge gaps, and proposes future research directions to evaluate the safety and efficacy of finerenone in kidney transplant recipients.

Introduction: Aluminium exposure and toxicity are uncommon in humans. However it may occur in patients on long term haemodialysis (HD) due to water exposure during treatment. We retrospectively assessed the extent of aluminium exposure in our HD and peritoneal dialysis (PD) patients from 2002 to 2008. Materials and Methods: The study population included 43 HD patients and 77 PD patients whose blood samples were collected at four monthly intervals. In addition, HD patients were also interviewed on lifestyle factors (aluminium cookware, diet, aluminium-containing medications and tap water consumption) that may impact on serum aluminium levels. Reverse osmosis (RO) water aluminium levels were also collected during this timeframe. : More patients on HD had readings above the accepted range (>0.01mg/L) than peritoneal dialysis (36.9% vs. 23.8%). The mean aluminium values for HD and PD patients were 63.35 ± 34.69μg/L and 38.34 ± 17.02μg/L respectively (p<0.05). Use of aluminium cookware was identified as a risk factor for high aluminium readings in HD patients. The trend of serum aluminium correlated with that of RO water aluminium during the studied period. There was no evidence of clinical toxicity in our patients during follow up. Conclusion The study showed that HD patients are at a higher risk of aluminium toxicity compared to PD patients. Treated RO water aluminium should be analysed on a regular basis to prevent aluminium toxicity in HD patients. Lifestyle factors may have an impact on aluminium levels in patients with renal disease.
Complications ; Dialysis ; Heavy Metal Toxicity ; Risk Factors