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Semin Nephrol. 2017 Nov;37(6):546-551. doi: 10.1016/j.semnephrol.2017.07.008.

APOL1 Nephrotoxicity: What Does Ion Transport Have to Do With It?

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Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, MA; Harvard Medical School, Boston, MA. Electronic address:
Harvard Medical School, Boston, MA; Division of Nephrology, Vascular Biology Research Center, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA; Surgical Immunotherapy at Roger Williams Medical Center, Providence, RI.


Apolipoprotein L1 (APOL1) protein is the human serum factor that protect human beings against Trypanosoma brucei brucei, the cause of trypanosomiasis. Subspecies of T b brucei that cause human sleeping sickness-T b gambiense and T b rhodesiense evolved molecular mechanisms that enabled them to evade killing by APOL1. Sequence changes (termed G1 and G2) in the APOL1 gene that restored its ability to kill T b rhodesiense also increase the risk of developing glomerular diseases and accelerate progression to end-stage kidney disease. To lyse trypanosome parasites, APOL1 forms pores in the trypanosome endolysosomal and mitochondrial membranes, resulting in rapid membrane depolarization. However, the molecular mechanism underlying APOL1 nephropathy is unknown. Recent experimental evidence has shown that aberrant efflux of intracellular potassium is an early event in APOL1-induced death of human embryonic kidney cells. Here, we discuss the possibility that abnormal efflux of cellular potassium or other cations may be relevant to the pathogenesis of APOL1 nephropathy.


African American; Apolipoprotein L1; end-stage kidney disease; focal segmental glomerulosclerosis

[Available on 2018-11-01]
[Indexed for MEDLINE]

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