Table.

Brief summary of each “omic” manuscript, including type of omic technology utilized, study population, and major findings. Ox-phos: oxidative phosphorylation. PsA: pseudomonas aeruginosa. 2DE: 2D gel electrophoresis. DIGE: 2D difference gel electrophoresis. CE: capillary electrophoresis. MS: mass spectrometry. MALDI: matrix-assisted laser desorption/ionization. A1AT: alpha-1 antitrypsin. SDS PAGE: SDS-polyacrylamide gel electrophoresis. GC: gas chromatography. LC: liquid chromatography. Ribo-seq: ribosomal profiling technique

Author	Omic Technology	Methods/ Models	Major Findings
Frank [53]	Genomics-DNA microarray	887 critically ill patients with septic shock	5 SNPs were associated with SA-AKI: BCL2, SERPINA, SIK3 genes.
Vilander [54]	Genomics-SNP genotyping	837 septic patients, 627 with septic shock	SNPs in SERPINA4,5 but not BCL2 nor SIK3, associated with SA-AKI after controlling for confounders.
Tran [47]	Transcriptomics- Gene expression microarray	Global and tubule-specific PGC-1a knockout mice exposed to endotoxemia	Ox-phos genes were selectively suppressed during SA-AKI, and PGC1a was proportionally suppressed. PGC1a KO mice suffered persistent kidney injury after sepsis.
Basu [57]	Transcriptomics- Gene expression microarray	179 critically ill children with septic shock	Elevated expression of 21 genes predicted SA-AKI. The genes mainly related to immune signaling and function.
Ferreyra [56]	Transcriptomics- Gene expression microarray	Mice exposed to intranasal staph enterotoxin B	Global gene-expression changes found a host-wide Interferon- response.
Ge [59]	Transcriptomics- Gene expression microarray	Whole-blood derived miRNAs from septic patients with/ without AKI	2 miRNAs that regulate AKT, NOX5 expression (involved in oxidative stress, mitochondrial dysfunction) significantly overexpressed in SA-AKI.
Hultstrom [39]	Transcriptomics- Gene expression microarrays	Microarray studies of renal gene expression after AKI in 6 different models	5254 differentially expressed genes. 2/3 found in only 1 model. 4 genes in all 6 models. Pathway analysis showed MYC to be a central connection in AKI.
Holly [66]	Urine Proteomics- DIGE, MS	Rat CLP sepsis	Meprin-1-alpha, a brush-border enzyme, was changed in rats with septic AKI, and an inhibitor of this enzyme prevented acute renal failure in aged mice.
Gong [65]	Serum proteomics- 2DE, MS	20 patients with severe sepsis receiving CVVH	10 proteins differentially expressed in pts getting CVVH, 7 proteins decreased in serum, 3 increased.
Thongboonkerd [63]	Plasma proteomics- 2DE, MS	Intraperitoneal injection of feces into pigs	27 unique proteins whose levels changed in sepsis, related to inflammation, oxidative/nitrosative stress, and cytoskeleton.
Metzger [67]	Urine Proteomics- CE-MS	Critically ill patients	6 proteins associated with AKI--albumin, A1AT, b2- microglobulin upregulated; collagen, fibrinogen downregulated.
Maddens [69]	Urine, plasma, tissue proteomics- gel free technique	Mice after uterine ligation and E Coli inoculation	Urinary chitinase3-like proteins and acidic mammalian chitinase were only detected in septic mice with AKI.
Wu [60]	Tissue Proteomics- DIGE, MS	Mouse CLP sepsis	Phosphorylated myosin regulatory light chain 12B was upregulated in septic AKI, which is important for cytoskeletal integrity.
Carrick [68]	Urinary proteomics- MALDI-MS	95 septic patients	39 urinary peptides were markers of AKI; proteins included b-2-microglobulin, collagen, fibrinogen,A1AT.
Matejovic [62]	Tissue proteomics- 2DE, MS	Continuous infusion of PsA in pigs and biopsies of renal cortical tissue.	21 proteins were differentially regulated in septic AKI, specifically Na/H exchange regulatory cofactor 3.
Hashida [64]	Proteomics from hemofilter adsorbates- SDS PAGE, MS	20 critically ill patients with AKI requiring CRRT.	3 proteins, including carbonic anhydrase 1 and leucine-rich alpha-glycoprotein, were in all septic patients with AKI but not in non-septic patients.
Hinkelbein [61]	Tissue proteomics- DIGE, MS	Rat CLP sepsis	Myosin and cytochrome C oxidase proteins upregulated; major urinary protein 5 downregulated in SA-AKI. These proteins correlate with mitochondrial energy production and electron transport.
Waltz [70]	Tissue (whole kidney) metabolomics- LC/MS	Mice CLP sepsis	Sepsis resulted in increased glucose and glycolytic intermediates, decreased TCA cycle intermediates, increased renal osmolytes (pinitol, urea, taurine), and metabolites associated with inflammation; decreased antioxidants (ascorbate, a-tocopherol, erogthioneine).
Li [72]	Tissue and serum metabolomics-NMR	Mice after intraperitoneal injection of LPS	Decreased antioxidants/regulatory osmolytes (betaine, taurine), membrane repair metabolites (choline, phosphocholine, ethanolamine). Decreased glucose, lactate, alanine, citrate and a-oxoglutarate, increased ketone bodies, creatine, creatinine, and ATP breakdown products (adenosine, inosine), marker of energy deficiency. Oxidative stress, energy metabolism pathways most significantly affected.
Rodrigues [73]	Urine metabolomics-NMR	Rat CLP sepsis	Elevated urinary creatine, allantoin, and dimethylglycine in CLP compared to sham mice.
Izquierdo-Garcia [71]	Tissue, plasma, and urine metabolomics- NMR	Pigs infused with E Coli	Metabolic differences between sepsis and controls--Tissue: increased lactate, nicotinuric acid; decreased value, aspartate, glucose, threonine. Serum: increased lactate, pyruvate, alanine, glutamine; decreased glucose, betaine. Urine: increased ascorbic acid, isovaleroglycine, aminoadipic acid, N-acetylglutamine, N-acetylaspartate, and decreased myoinositol, phenylacetylglycine. Altogether signified alterations of cellular energy pathways, specifically fatty acid metabolism.
Hato [74]	Unbiased transcriptomics, tissue metabolomics- DIGE, MS; GC/MS, LC/MS	Endotoxin preconditioning in CLP mouse model	There are benefits of preconditioning from molecules involved in antibacterial defense, redox balance, and tissue healing, specifically increased itaconate in proximal RTECs, that protect the kidney.
Hato [38]	Transcriptomics (RNAseq), proteomics (nascent), metabolomics (GC/MS, LC/MS) Ribo-seq translatomics	Mice injected with LPS. Transcriptomics performed on S1 and S2/S3 kidney segments after laser and manual microdissection.	Activation of Eif2ak2/Eif2a axis is the key mediator of translation initiation block in late-phase sepsis in RTECs. Reversal of this axis mitigated kidney injury and this global translational shutdown is likely an important contributor to SA-AKI.