Identification of prognostic biomarkers for antibiotic associated nephrotoxicity in cystic fibrosis
•Repeated use of antibiotics to treat pulmonary exacerbations may lead to kidney injury.•We lack early urinary biomarkers to recognize kidney injury.•Using a kidney-on-a-chip and a CF cohort, we identify new urinary biomarkers of kidney injury.•Urinary soluble Fas, a marker of apoptosis, was associa...
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| Veröffentlicht in: | Journal of cystic fibrosis 2024-03, Vol.23 (2), p.293-299 |
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| creator | Hart, Andrew Cesar, Francine Zelnick, Leila R O'Connor, Nick Bailey, Zoie Lo, Jordan Van Ness, Kirk Stanaway, Ian B. Bammler, Theo K. MacDonald, James W. Thau, Matthew R. Himmelfarb, Jonathan Goss, Christopher H. Aitken, Moira Kelly, Edward J. Bhatraju, Pavan K. |
| description | •Repeated use of antibiotics to treat pulmonary exacerbations may lead to kidney injury.•We lack early urinary biomarkers to recognize kidney injury.•Using a kidney-on-a-chip and a CF cohort, we identify new urinary biomarkers of kidney injury.•Urinary soluble Fas, a marker of apoptosis, was associated with chronic kidney disease in CF.
Our objective was to discover novel urinary biomarkers of antibiotic-associated nephrotoxicity using an ex-vivo human microphysiological system (MPS) and to translate these findings to a prospectively enrolled cystic fibrosis (CF) population receiving aminoglycosides and/or polymyxin E (colistin) for a pulmonary exacerbation.
We populated the MPS with primary human kidney proximal tubule epithelial cells (PTECs) from three donors and modeled nephrotoxin injury through exposure to 50 µg/mL polymyxin E for 72 h. We analyzed gene transcriptional responses by RNAseq and tested MPS effluents. We translated candidate biomarkers to a CF cohort via analysis of urine collected prior to, during and two weeks after antibiotics and patients were followed for a median of 3 years after antibiotic use.
Polymyxin E treatment resulted in a statistically significant increase in the pro-apoptotic Fas gene relative to control in RNAseq of MPS: fold-change = 1.63, FDR q-value = 7.29 × 10−5. Effluent analysis demonstrated an acute rise of soluble Fas (sFas) concentrations that correlated with cellular injury. In 16 patients with CF, urinary sFas concentrations were significantly elevated during antibiotic treatment, regardless of development of AKI. Over a median of three years of follow up, we identified seven cases of incident chronic kidney disease (CKD). Urinary sFas concentrations during antibiotic treatment were significantly associated with subsequent development of incident CKD (unadjusted relative risk = 2.02 per doubling of urinary sFas, 95 % CI = 1.40, 2.90, p |
| doi_str_mv | 10.1016/j.jcf.2023.10.021 |
| format | Article |
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Our objective was to discover novel urinary biomarkers of antibiotic-associated nephrotoxicity using an ex-vivo human microphysiological system (MPS) and to translate these findings to a prospectively enrolled cystic fibrosis (CF) population receiving aminoglycosides and/or polymyxin E (colistin) for a pulmonary exacerbation.
We populated the MPS with primary human kidney proximal tubule epithelial cells (PTECs) from three donors and modeled nephrotoxin injury through exposure to 50 µg/mL polymyxin E for 72 h. We analyzed gene transcriptional responses by RNAseq and tested MPS effluents. We translated candidate biomarkers to a CF cohort via analysis of urine collected prior to, during and two weeks after antibiotics and patients were followed for a median of 3 years after antibiotic use.
Polymyxin E treatment resulted in a statistically significant increase in the pro-apoptotic Fas gene relative to control in RNAseq of MPS: fold-change = 1.63, FDR q-value = 7.29 × 10−5. Effluent analysis demonstrated an acute rise of soluble Fas (sFas) concentrations that correlated with cellular injury. In 16 patients with CF, urinary sFas concentrations were significantly elevated during antibiotic treatment, regardless of development of AKI. Over a median of three years of follow up, we identified seven cases of incident chronic kidney disease (CKD). Urinary sFas concentrations during antibiotic treatment were significantly associated with subsequent development of incident CKD (unadjusted relative risk = 2.02 per doubling of urinary sFas, 95 % CI = 1.40, 2.90, p < 0.001).
Using an ex-vivo MPS, we identified a novel biomarker of proximal tubule epithelial cell injury, sFas, and translated these findings to a clinical cohort of patients with CF.
[Display omitted]</description><identifier>ISSN: 1569-1993</identifier><identifier>ISSN: 1873-5010</identifier><identifier>EISSN: 1873-5010</identifier><identifier>DOI: 10.1016/j.jcf.2023.10.021</identifier><identifier>PMID: 37949747</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Acute Kidney Injury - chemically induced ; Acute Kidney Injury - diagnosis ; Adult ; Aminoglycosides - adverse effects ; Anti-Bacterial Agents - adverse effects ; Biomarkers - urine ; Chronic kidney injury ; Cystic Fibrosis - drug therapy ; fas Receptor ; Female ; Humans ; Kidney Tubules, Proximal - drug effects ; Kidney Tubules, Proximal - metabolism ; Male ; Nephrotoxicity ; Prognosis ; Prospective Studies ; Urinary biomarkers</subject><ispartof>Journal of cystic fibrosis, 2024-03, Vol.23 (2), p.293-299</ispartof><rights>2023 European Cystic Fibrosis Society</rights><rights>Copyright © 2023 European Cystic Fibrosis Society. Published by Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c348t-31ea4902189d9daf6c7a0628d5332658ff02a21e2aab919cd1dfd103a9b57e6a3</cites><orcidid>0000-0002-6192-8916 ; 0000-0002-7328-7626 ; 0000-0002-8461-5111 ; 0000-0002-5198-1246 ; 0000-0002-6164-7065</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jcf.2023.10.021$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37949747$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hart, Andrew</creatorcontrib><creatorcontrib>Cesar, Francine</creatorcontrib><creatorcontrib>Zelnick, Leila R</creatorcontrib><creatorcontrib>O'Connor, Nick</creatorcontrib><creatorcontrib>Bailey, Zoie</creatorcontrib><creatorcontrib>Lo, Jordan</creatorcontrib><creatorcontrib>Van Ness, Kirk</creatorcontrib><creatorcontrib>Stanaway, Ian B.</creatorcontrib><creatorcontrib>Bammler, Theo K.</creatorcontrib><creatorcontrib>MacDonald, James W.</creatorcontrib><creatorcontrib>Thau, Matthew R.</creatorcontrib><creatorcontrib>Himmelfarb, Jonathan</creatorcontrib><creatorcontrib>Goss, Christopher H.</creatorcontrib><creatorcontrib>Aitken, Moira</creatorcontrib><creatorcontrib>Kelly, Edward J.</creatorcontrib><creatorcontrib>Bhatraju, Pavan K.</creatorcontrib><title>Identification of prognostic biomarkers for antibiotic associated nephrotoxicity in cystic fibrosis</title><title>Journal of cystic fibrosis</title><addtitle>J Cyst Fibros</addtitle><description>•Repeated use of antibiotics to treat pulmonary exacerbations may lead to kidney injury.•We lack early urinary biomarkers to recognize kidney injury.•Using a kidney-on-a-chip and a CF cohort, we identify new urinary biomarkers of kidney injury.•Urinary soluble Fas, a marker of apoptosis, was associated with chronic kidney disease in CF.
Our objective was to discover novel urinary biomarkers of antibiotic-associated nephrotoxicity using an ex-vivo human microphysiological system (MPS) and to translate these findings to a prospectively enrolled cystic fibrosis (CF) population receiving aminoglycosides and/or polymyxin E (colistin) for a pulmonary exacerbation.
We populated the MPS with primary human kidney proximal tubule epithelial cells (PTECs) from three donors and modeled nephrotoxin injury through exposure to 50 µg/mL polymyxin E for 72 h. We analyzed gene transcriptional responses by RNAseq and tested MPS effluents. We translated candidate biomarkers to a CF cohort via analysis of urine collected prior to, during and two weeks after antibiotics and patients were followed for a median of 3 years after antibiotic use.
Polymyxin E treatment resulted in a statistically significant increase in the pro-apoptotic Fas gene relative to control in RNAseq of MPS: fold-change = 1.63, FDR q-value = 7.29 × 10−5. Effluent analysis demonstrated an acute rise of soluble Fas (sFas) concentrations that correlated with cellular injury. In 16 patients with CF, urinary sFas concentrations were significantly elevated during antibiotic treatment, regardless of development of AKI. Over a median of three years of follow up, we identified seven cases of incident chronic kidney disease (CKD). Urinary sFas concentrations during antibiotic treatment were significantly associated with subsequent development of incident CKD (unadjusted relative risk = 2.02 per doubling of urinary sFas, 95 % CI = 1.40, 2.90, p < 0.001).
Using an ex-vivo MPS, we identified a novel biomarker of proximal tubule epithelial cell injury, sFas, and translated these findings to a clinical cohort of patients with CF.
[Display omitted]</description><subject>Acute Kidney Injury - chemically induced</subject><subject>Acute Kidney Injury - diagnosis</subject><subject>Adult</subject><subject>Aminoglycosides - adverse effects</subject><subject>Anti-Bacterial Agents - adverse effects</subject><subject>Biomarkers - urine</subject><subject>Chronic kidney injury</subject><subject>Cystic Fibrosis - drug therapy</subject><subject>fas Receptor</subject><subject>Female</subject><subject>Humans</subject><subject>Kidney Tubules, Proximal - drug effects</subject><subject>Kidney Tubules, Proximal - metabolism</subject><subject>Male</subject><subject>Nephrotoxicity</subject><subject>Prognosis</subject><subject>Prospective Studies</subject><subject>Urinary biomarkers</subject><issn>1569-1993</issn><issn>1873-5010</issn><issn>1873-5010</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9ULtOAzEQtBCIhMAH0KAraS74kXtYVCjiEQmJBmrLZ69hQ3IOtoPI3-OQQEnj9e7OjHaGkHNGx4yy-mo-nhs35pSL3I8pZwdkyNpGlBVl9DD_q1qWTEoxICcxzillDW3aYzIQjZzIZtIMiZlZ6BM6NDqh7wvvilXwr72PCU3RoV_q8A4hFs6HQmdkHm03OkZvUCewRQ-rt-CT_0KDaVNgX5jND9thF3zEeEqOnF5EONvXEXm5u32ePpSPT_ez6c1jacSkTaVgoCcyu2illVa72jSa1ry1lRC8rlrnKNecAde6k0way6yzjAotu6qBWosRudzpZgcfa4hJLTEaWCx0D34dFW9bycXPMyJsBzX5whjAqVXAbHWjGFXbbNVc5WzVNtvtKF-VORd7-XW3BPvH-A0zA653AMgmPxGCigahN2AxgEnKevxH_huc-4w2</recordid><startdate>202403</startdate><enddate>202403</enddate><creator>Hart, Andrew</creator><creator>Cesar, Francine</creator><creator>Zelnick, Leila R</creator><creator>O'Connor, Nick</creator><creator>Bailey, Zoie</creator><creator>Lo, Jordan</creator><creator>Van Ness, Kirk</creator><creator>Stanaway, Ian B.</creator><creator>Bammler, Theo K.</creator><creator>MacDonald, James W.</creator><creator>Thau, Matthew R.</creator><creator>Himmelfarb, Jonathan</creator><creator>Goss, Christopher H.</creator><creator>Aitken, Moira</creator><creator>Kelly, Edward J.</creator><creator>Bhatraju, Pavan K.</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-6192-8916</orcidid><orcidid>https://orcid.org/0000-0002-7328-7626</orcidid><orcidid>https://orcid.org/0000-0002-8461-5111</orcidid><orcidid>https://orcid.org/0000-0002-5198-1246</orcidid><orcidid>https://orcid.org/0000-0002-6164-7065</orcidid></search><sort><creationdate>202403</creationdate><title>Identification of prognostic biomarkers for antibiotic associated nephrotoxicity in cystic fibrosis</title><author>Hart, Andrew ; 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Our objective was to discover novel urinary biomarkers of antibiotic-associated nephrotoxicity using an ex-vivo human microphysiological system (MPS) and to translate these findings to a prospectively enrolled cystic fibrosis (CF) population receiving aminoglycosides and/or polymyxin E (colistin) for a pulmonary exacerbation.
We populated the MPS with primary human kidney proximal tubule epithelial cells (PTECs) from three donors and modeled nephrotoxin injury through exposure to 50 µg/mL polymyxin E for 72 h. We analyzed gene transcriptional responses by RNAseq and tested MPS effluents. We translated candidate biomarkers to a CF cohort via analysis of urine collected prior to, during and two weeks after antibiotics and patients were followed for a median of 3 years after antibiotic use.
Polymyxin E treatment resulted in a statistically significant increase in the pro-apoptotic Fas gene relative to control in RNAseq of MPS: fold-change = 1.63, FDR q-value = 7.29 × 10−5. Effluent analysis demonstrated an acute rise of soluble Fas (sFas) concentrations that correlated with cellular injury. In 16 patients with CF, urinary sFas concentrations were significantly elevated during antibiotic treatment, regardless of development of AKI. Over a median of three years of follow up, we identified seven cases of incident chronic kidney disease (CKD). Urinary sFas concentrations during antibiotic treatment were significantly associated with subsequent development of incident CKD (unadjusted relative risk = 2.02 per doubling of urinary sFas, 95 % CI = 1.40, 2.90, p < 0.001).
Using an ex-vivo MPS, we identified a novel biomarker of proximal tubule epithelial cell injury, sFas, and translated these findings to a clinical cohort of patients with CF.
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| fulltext | fulltext |
| identifier | ISSN: 1569-1993 |
| ispartof | Journal of cystic fibrosis, 2024-03, Vol.23 (2), p.293-299 |
| issn | 1569-1993 1873-5010 1873-5010 |
| language | eng |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Acute Kidney Injury - chemically induced Acute Kidney Injury - diagnosis Adult Aminoglycosides - adverse effects Anti-Bacterial Agents - adverse effects Biomarkers - urine Chronic kidney injury Cystic Fibrosis - drug therapy fas Receptor Female Humans Kidney Tubules, Proximal - drug effects Kidney Tubules, Proximal - metabolism Male Nephrotoxicity Prognosis Prospective Studies Urinary biomarkers |
| title | Identification of prognostic biomarkers for antibiotic associated nephrotoxicity in cystic fibrosis |
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