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. 2022 Sep 22;7(18):e161783. doi: 10.1172/jci.insight.161783

Figure 4. The Cpt2–Acsl4+Acsl5+Acsm5– signature is a feature of established CKD.

Figure 4

(A) Representative photomicrograph of neutral lipid accumulation in PTCs evaluated by Oil Red O staining in kidney allografts from 3 KTRs with chronic injury of various severity. Original magnification, ×40. Creat, creatinine; PU, urine protein-to-creatinine ratio. (B) Expression of Cpt2, Acsl4, Acsl5, and Acsm5 transcripts by expression profiling by array in the tubulointerstitial compartment of 24 healthy kidneys donors and 10 kidneys with diabetic kidney disease. Data are from public repositories (NCBI GEO accession GSE30122). Bars represent mean ± SD. P values were computed with a Student’s t test. (C) Expression of Cpt2, Acsl4, Acsl5, and Acsm5 transcripts by RNA-Seq in whole kidneys of 12- and 24-week-old UmodC147W/+ mice and wild-type mice (5 to 10 mice per condition). Data are from public repositories (GEO accession GSE102566). Bars represent mean ± SD. P values were computed with a Student’s t test. FPKM, fold-change per kilobase million. (D) Intrarenal expression of CPT2, ACSL4, ACSL5, and ACSM5 transcript levels as a function of the renal function (eGFR) of 201 healthy kidney donors and individuals with CKD. Data are from public repositories (Nephroseq). R is the Pearson’s correlation coefficient, and the P values were computed with a Student’s t test.