Addressing the pathophysiology of venous thrombosis and chronic kidney disease in sickle cell trait using a mouse model.

ABSTRACT:

Abstract

Sickle cell trait (SCT) is present in participants who possess a single copy of the βS-globin gene mutation. Although most affected individuals are asymptomatic, SCT is a well-established risk factor for venous thrombosis and renal complications, including chronic and end-stage kidney disease. After prolonged hypoxia, SCT red blood cells (RBCs) can undergo sickling, and hypoxia-mediated RBC sickling can be enhanced by cellular dehydration, hyperosmolarity, and/or acidosis. Some or all of these conditions may be encountered in the nidus of venous thrombi and in the medulla of the kidney. We sought to determine whether Townes sickle trait (AS) mice develop kidney dysfunction and manifest enhanced venous thrombosis. We demonstrated that the harsh environment within the inner

SUBMITTER: Trebak F 

PROVIDER: S-EPMC12159902 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature