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. Author manuscript; available in PMC: 2023 Jul 1.
Published in final edited form as: Kidney Int. 2021 Dec 18;102(1):136–148. doi: 10.1016/j.kint.2021.10.041

Figure 1 -. Analysis schematic:

Figure 1 -

APOL1 risk variants were genotyped for Black participants with FSGS from the NEPTUNE cohort. There were 16 high-risk (“HR,” 2 risk variants) and 14 low-risk (“LR,” 0 or 1 risk variant) participants. Three glomerular transcriptomic analyses were used to illuminate mRNA expression differences as a function of risk genotype and APOL1 expression. (1) differential expression to identify genes with varying expression between the HR and LR FSGS group. (2) transcriptome-wide correlation of single genes with APOL1 to identify similarities and differences between genes coexpressed with APOL1 specifically in HR versus LR state. (3) differential co-expression to go beyond solely APOL1 correlations and identify groups of genes whose co-expression differs with each other in the HR and LR APOL1 state. The latter two analyses empowered identification of potential molecular perturbations between groups that are not reflected through differential expression.