Harnessing the Full Potential of Multi-Omic Analyses to Advance the Study and Treatment of Chronic Kidney Disease

Abstract

Chronic kidney disease (CKD) was the 12th leading cause of death globally in 2017 with the prevalence of CKD estimated at ~9%. Early detection and intervention for CKD may improve patient outcomes, but standard testing approaches even in developed countries do not facilitate identification of patients at high risk of developing CKD, nor those progressing to end-stage kidney disease (ESKD). Recent advances in CKD research are moving towards a more personalised approach for CKD. Heritability for CKD ranges from 30% to 75%, yet identified genetic risk factors account for only a small proportion of the inherited contribution to CKD. More in depth analysis of genomic sequencing data in large cohorts is revealing new genetic risk factors for common diagnoses of CKD and providing novel diagnoses for rare forms of CKD. Multi-omic approaches are now being harnessed to improve our understanding of CKD and explain some of the so-called ‘missing heritability’. The most common omic analyses employed for CKD are genomics, epigenomics, transcriptomics, metabolomics, proteomics and phenomics. While each of these omics have been reviewed individually, considering integrated multi-omic analysis offers considerable scope to improve our understanding and treatment of CKD. This narrative review summarises current understanding of multi-omic research alongside recent experimental and analytical approaches, discusses current challenges and future perspectives, and offers new insights for CKD.

Harnessing Genomic Analysis to Explore the Role of Telomeres in the Pathogenesis and Progression of Diabetic Kidney Disease

“…As well as the genetic variation responsible for the modulation of telomere regulation during disease, epigenetic medications affecting telomere regulation have been uncovered, with this topic recently reviewed by Dogan and Forsyth [ 155 ]. Epigenetics broadly refers to the study of gene expression changes that are not the result of genetic mutation but instead due to alterations in factors such as DNA methylation, histone modifications, and non-coding RNA (ncRNA) [ 156 ].…”