“Biomarking” the transition from genetic risk to kidney disease

Etty Kruzel-Davila; Karl Skorecki

doi:10.1016/j.kint.2018.03.005

“Biomarking” the transition from genetic risk to kidney disease

Etty Kruzel-Davila, Karl Skorecki

Research output: Contribution to journal › Comment/debate

3 Scopus citations

Abstract

Only some individuals carrying the high-risk APOL1 genotype go on to develop kidney disease phenotypes. In this issue of Kidney International, Nadkarni and colleagues report the associations of several biomarkers with renal outcomes in individuals with high-risk APOL1 genotypes. In the era of precision medicine, these findings should translate into improved longitudinal risk assessment for this high-risk population and might also provide additional insights regarding sites and mechanisms of APOL1 nephropathy.

Original language	English
Pages (from-to)	1270-1272
Number of pages	3
Journal	Kidney International
Volume	93
Issue number	6
DOIs	https://doi.org/10.1016/j.kint.2018.03.005
State	Published - Jun 2018
Externally published	Yes

Bibliographical note

Publisher Copyright:
© 2018 International Society of Nephrology

Funding

The authors wish to acknowledge research support from the Israel Science Foundation (grant 182/15 to KS), the Ernest and Bonnie Beutler Fund, and the Harvey and Gloria Kaylie Foundation to Rambam Health Care Campus.

Funders	Funder number
Ernest and Bonnie Beutler Fund
Harvey and Gloria Kaylie Foundation
Israel Science Foundation	182/15

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10.1016/j.kint.2018.03.005

Cite this

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title = "“Biomarking” the transition from genetic risk to kidney disease",

abstract = "Only some individuals carrying the high-risk APOL1 genotype go on to develop kidney disease phenotypes. In this issue of Kidney International, Nadkarni and colleagues report the associations of several biomarkers with renal outcomes in individuals with high-risk APOL1 genotypes. In the era of precision medicine, these findings should translate into improved longitudinal risk assessment for this high-risk population and might also provide additional insights regarding sites and mechanisms of APOL1 nephropathy.",

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“Biomarking” the transition from genetic risk to kidney disease

Abstract

Bibliographical note

Funding

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