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APOL1 Nephrotoxicity: What Does Ion Transport Have to Do With It?
Opeyemi A Olabisi1, John F Heneghan2
1Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, MA; Harvard Medical School, Boston, MA.
Seminars in Nephrology
|November 8, 2017
Summary
Apolipoprotein L1 (APOL1) protects against certain parasites but specific gene changes increase kidney disease risk. Abnormal ion efflux may explain APOL1-related kidney damage.
Area of Science:
- Nephrology
- Parasitology
- Molecular Biology
Background:
- Apolipoprotein L1 (APOL1) is a human serum protein conferring resistance to Trypanosoma brucei brucei.
- Certain Trypanosoma subspecies have evolved resistance to APOL1-mediated lysis.
- APOL1 gene variants (G1, G2) linked to kidney disease risk are associated with restored trypanolytic activity.
Purpose of the Study:
- To explore the potential role of ion dysregulation in APOL1-associated nephropathy.
- To connect the lytic mechanism of APOL1 against trypanosomes to its pathogenic effects in the kidney.
Main Methods:
- Review of existing literature on APOL1 function, trypanosome resistance, and kidney disease.
- Discussion of experimental findings implicating potassium efflux in APOL1-induced cell death.
Main Results:
- APOL1 forms pores in parasite membranes, causing depolarization.
- APOL1 nephropathy pathogenesis remains unclear.
- Aberrant intracellular potassium efflux is observed in APOL1-treated kidney cells.
Conclusions:
- Abnormal cation efflux, particularly potassium, is a plausible mechanism in APOL1 nephropathy.
- Further research is needed to elucidate the precise role of ion transport in APOL1-related kidney diseases.
Keywords:
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