Biochemical interaction of pyrvinium in gentamicin-induced acute kidney injury by modulating calcium dyshomeostasis and mitochondrial dysfunction

Acute kidney injury (AKI) has a poor clinical prognosis and increases the risk of chronic kidney failure (CKD). It is a common complication of organ failure in hospitalised patients (10-15% of all hospitalizations) and in intensive care unit (ICU) patients, with an incidence of up to 50%. Concerning ICU, AKI has a mortality rate ranging from 27% to 35%, rising to 60%-65% when dialysis is needed, with roughly 5%-20% of survivors requiring dialysis on discharge. AKI is believed to cause over 7 million deaths per year worldwide. Currently, there is no treatment for AKI or its progression to CKD. When activated by AKI, numerous pathways have been suggested as possible contributors to CKD progression. Wnt/beta-catenin is a crucial regulator of kidney development that increases following the injury. Despite the overwhelming evidence that Wnt/beta-catenin promotes AKI, tubulointerstitial fibrosis, a hallmark of CKD progression, is also promoted by this pathway. The therapeutic potential of Wnt/ beta-catenin in the treatment of AKI and the progression from AKI to CKD is being studied. This hypothesis aims to determine whether the Wnt/beta-catenin inhibitor pyrvinium has a beneficial effect on the renal dysfunction and damage caused by Gentamicin.

Automated summary

Acute kidney injury (AKI) has a poor clinical prognosis and increases the risk of chronic kidney failure (CKD). There is currently no treatment for AKI or its progression to CKD, but research is ongoing on the potential therapeutic use of Wnt/beta-catenin inhibitors in preventing renal dysfunction.