Exploring the Relationship Between Angiogenesis Inhibition of sFLT-1 and Sickle Cell Nephropathy.

Abstract

Background: Sickle cell anaemia (SCA) is a chronic haemoglobinopathy associated with multi-organ complications, among which nephropathy remains a significant cause of morbidity and mortality. Early detection of sickle cell nephropathy (SCN) is crucial, yet conventional markers such as serum creatinine and estimated glomerular filtration rate (eGFR) often fail to detect early renal impairment. Emerging biomarkers like soluble fms-like tyrosine kinase-1 (sFLT-1) have shown potential in identifying early endothelial and glomerular injury in SCA. This study explores the role of angiogenesis inhibition via sFLT-1 in the pathogenesis of renal injury in SCD, aiming to identify correlations between elevated sFLT-1 levels, proteinuria, and declining renal function. Methodology: A cross-sectional analytical study was conducted involving confirmed SCD patients and age- and sex-matched controls. Serum sFLT-1 levels were measured using enzyme-linked immunosorbent assay (ELISA). At the same time, renal function was assessed through estimated glomerular filtration rate (eGFR), serum creatinine, and urinary microalbumin and microalbumin: creatinine ratio quantification. Statistical analyses included correlation studies and group comparisons to determine the association between sFLT-1 concentrations and renal impairment indicators. Results: SCD patients demonstrated significantly elevated sFLT-1 levels compared to controls (p < 0.001). Higher sFLT-1 levels were strongly associated with increased albuminuria and reduced eGFR, indicating early renal damage. These findings suggest that elevated sFLT-1 contributes to glomerular endothelial dysfunction, possibly via inhibition of vascular endothelial growth factor (VEGF)-mediated repair mechanisms. Conclusion: The study reveals a significant relationship between angiogenesis inhibition by sFLT-1 and renal dysfunction in individuals with SCD. sFLT-1 may serve as a promising early biomarker for SCD nephropathy and a potential therapeutic target to preserve renal function in this vulnerable population. Furthermulticentred and longitudinal studies are recommended to establish causality and explore interventional strategies.