PARP inhibitors and the Kidney

Poly (ADP-ribose) polymerases (PARPs) are crucial in repairing DNA after a damaging event. However, several studies indicate that more extensive disruption causes overactivity of PARP and can ultimately lead to cellular necrosis particularly the setting ischemia- related or sepsis-related acute kidney injury (AKI). Though anti-cancer effects inhibitors (PARPis) well known, especially cases Breast Cancer gene mutations, there exists potential for use these drugs treating ischemic AKI. beneficial PARPis attenuating AKI has been shown animal models, testing yet be done humans. Studies have also found interact with proximal tubular transporter channels cause physiologic increase serum creatinine, however long- term on function, proteinuria hematuria unclear. The patients chronic disease (CKD) malignancy may result amplification adverse such as anemia thrombocytopenia. Safe dosing agents advanced CKD end stage (ESKD) is determined populations were excluded from clinical trials. This manuscript reviews current data opens door further research this arena.