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Mechanism of podocyte damage in the development of sickle cell nephropathy

Several factors including genetic ones such as APOL1 risk variants (G1 and G2) and HMOX1 GT repeats have been shown to influence the development of sickle cell nephropathy (SCN). We have previously shown that APOL1 high risk genotypes are associated with SCN in our steady-state sickle cell disease (SCD) paediatric population from the Democratic Republic of Congo (DRC) (unpublished data). However, data on associations between these genetic determinants and kidney disease among SCD patients living in Belgium are lacking. In the current project, we will investigate the association between markers of SCN and some genetic determinants among steady-state SCD paediatric patients living in Belgium compared with paediatric population living in Africa (DRC). We will further enumerate the basic mechanism of kidney injury induced by these variants using podocytes cell lines generated from urine of patients carrying these high-risk genetic determinants in order to promote therapeutic measures. Moreover, we will unravel the nephroprotective mechanism of hydroxyurea, an approved drug use for reducing vaso-occlusive crisis in SCD population, among sickle cell nephropathic patients.

Date:1 Nov 2019 →  Today
Keywords:Sickle cell disease, Sickle cell nephropathy, Apolipoprotein L1
Disciplines:Genetics, Urology and nephrology not elsewhere classified, Hematology not elsewhere classified
Project type:PhD project