Patrick D. Dummer

TL;DR: It is found that expression of the risk-variant APOL1 alleles interferes with endosomal trafficking and blocks autophagic flux, which ultimately leads to inflammatory-mediated podocyte death and glomerular scarring.

TL;DR: Two models for APOL1 trypanolytic activity are discussed: one involving lysosome permeabilization and another involving colloid-osmotic swelling of the cell body, as well as their relevance to human pathophysiology, which suggests that both mechanisms may be operative.

TL;DR: An additional mechanism by which anti-proteinuric therapies are beneficial in the treatment of glomerular diseases may be a reduction in injury to the podocyte by albumin, which is strongly associated with progression of chronic kidney disease.

TL;DR: Findings provide a mechanism by which APOL1 variants damage podocytes and suggest novel therapeutic strategies for CKD, and the secondary structure of AP OL1 risk variant RNA acts as a scaffold for protein kinase R, suggesting potential therapeutic strategies.

TL;DR: An update on the biological functions for circulating (trypanosome resistance) and intracellular (emerging role for autophagy) APOL1 is provided and a multimer model for AP OL1 in kidney cells is introduced that reconciles the gain-of-function variants with the recessive inheritance pattern of APOL2 renal risk alleles.