APOL1 and Kidney Health: How a Gene Variant Affects Kidney Function
Author Information
Author(s): Kumar Vinod, Kaur Prabhjot, Ayasolla Kameshwar, Jha Alok, Wiqas Amen, Vashistha Himanshu, Saleem Moin A., Popik Waldemar, Malhotra Ashwani, Gebeshuber Christoph A., Skorecki Karl, Singhal Pravin C.
Primary Institution: Department of Medicine and Feinstein Institute for Medical Research, Zucker School of Medicine, Hempstead, NY, USA
Hypothesis
Patients carrying APOL1 risk alleles (G1 and G2) have a higher risk of developing Focal Segmental Glomerulosclerosis (FSGS); we hypothesized that escalated levels of miR193a contribute to kidney injury by activating renin–angiotensin system (RAS) in the APOL1 milieus.
Conclusion
The study found that APOL1 risk alleles increase miR193a levels, leading to higher renin expression and activation of the renin-angiotensin system, which contributes to kidney injury.
Supporting Evidence
- APOL1 risk alleles enhance the expression of miR193a and induce podocyte injury.
- G0/DPDs displayed attenuated renin but enhanced expression of VDR and WT1.
- G1/DPDs and G2/DPDs exhibited enhanced expression of renin but decreased expression of VDR and WT1.
- miR193a regulates the activation of RAS and podocyte molecular markers through modulation of VDR and WT1.
Takeaway
Some people have a gene that makes their kidneys more likely to get sick. This study looked at how a tiny molecule in the body can make that worse.
Methodology
The study involved evaluating differentiated podocytes expressing different APOL1 variants and measuring levels of renin, Vitamin D receptor, and other molecular markers.
Limitations
The study was not designed to validate a causal role of RAS in the development and progression of APOL1G1/G2 mediated podocyte injury or the development of FSGS.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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