Biomarkers of Kidney Tubule Health, CKD Progression, and Acute Kidney Injury in SPRINT (Systolic Blood Pressure Intervention Trial) Participants

SPRINT compared the effect of intensive versus standard systolic blood pressure targets on cardiovascular morbidity and mortality. In this ancillary study, we evaluated the use of exploratory factor analysis (EFA) to combine biomarkers of kidney tubule health in urine and plasma and then study their...

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Vydáno v:American journal of kidney diseases Ročník 78; číslo 3; s. 361
Hlavní autoři: Bullen, Alexander L, Katz, Ronit, Jotwani, Vasantha, Garimella, Pranav S, Lee, Alexandra K, Estrella, Michelle M, Shlipak, Michael G, Ix, Joachim H
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 01.09.2021
ISSN:1523-6838, 1523-6838
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Abstract SPRINT compared the effect of intensive versus standard systolic blood pressure targets on cardiovascular morbidity and mortality. In this ancillary study, we evaluated the use of exploratory factor analysis (EFA) to combine biomarkers of kidney tubule health in urine and plasma and then study their role in longitudinal eGFR change and risk of acute kidney injury (AKI). Observational cohort nested in a clinical trial. 2,351 SPRINT participants with eGFR < 60 ml/min/1.73m at baseline. Levels of neutrophil gelatinase-associated lipocalin (NGAL), interleukin-18 (IL-18), chitinase-3-like protein (YKL-40), kidney injury molecule-1 (KIM-1), monocyte chemoattractant protein-1 (MCP-1), alpha-1 microglobulin (α1m) and beta-2 microglobulin (β2m), uromodulin (UMOD), fibroblast growth factor-23 (FGF23), and intact parathyroid hormone (PTH). Longitudinal changes in eGFR and risk of AKI. We performed EFA to capture different tubule pathophysiologic processes. We used linear mixed effects models to evaluate the association of each factor with longitudinal changes in eGFR. We evaluated the association of the tubular factors scores with AKI using Cox proportional hazards regression. From ten biomarkers, EFA generated four factors reflecting tubule injury/repair (NGAL, IL-18 and YKL-40), tubule injury/fibrosis (KIM-1 and MCP-1), tubule reabsorption (α1m and β2m), and tubule reserve/mineral metabolism (UMOD, FGF23, and PTH). Each SD higher tubule reserve/mineral metabolism factor scores were associated with a 0.58% (0.39%, 0.67%) faster eGFR decline independent of baseline eGFR and albuminuria. Both the tubule injury/repair (HR per SD higher 1.18 [1.10, 1.37]) and tubule injury/fibrosis factors (HR 1.23 [1.02, 1.48]) were independently associated with future risk of AKI. The factors require validation in other settings. EFA allows parsimonious subgrouping of biomarkers into factors which are differentially associated with progressive eGFR decline and AKI. These subgroups may provide insights into the pathological processes driving adverse kidney outcomes.
AbstractList SPRINT compared the effect of intensive versus standard systolic blood pressure targets on cardiovascular morbidity and mortality. In this ancillary study, we evaluated the use of exploratory factor analysis (EFA) to combine biomarkers of kidney tubule health in urine and plasma and then study their role in longitudinal eGFR change and risk of acute kidney injury (AKI). Observational cohort nested in a clinical trial. 2,351 SPRINT participants with eGFR < 60 ml/min/1.73m at baseline. Levels of neutrophil gelatinase-associated lipocalin (NGAL), interleukin-18 (IL-18), chitinase-3-like protein (YKL-40), kidney injury molecule-1 (KIM-1), monocyte chemoattractant protein-1 (MCP-1), alpha-1 microglobulin (α1m) and beta-2 microglobulin (β2m), uromodulin (UMOD), fibroblast growth factor-23 (FGF23), and intact parathyroid hormone (PTH). Longitudinal changes in eGFR and risk of AKI. We performed EFA to capture different tubule pathophysiologic processes. We used linear mixed effects models to evaluate the association of each factor with longitudinal changes in eGFR. We evaluated the association of the tubular factors scores with AKI using Cox proportional hazards regression. From ten biomarkers, EFA generated four factors reflecting tubule injury/repair (NGAL, IL-18 and YKL-40), tubule injury/fibrosis (KIM-1 and MCP-1), tubule reabsorption (α1m and β2m), and tubule reserve/mineral metabolism (UMOD, FGF23, and PTH). Each SD higher tubule reserve/mineral metabolism factor scores were associated with a 0.58% (0.39%, 0.67%) faster eGFR decline independent of baseline eGFR and albuminuria. Both the tubule injury/repair (HR per SD higher 1.18 [1.10, 1.37]) and tubule injury/fibrosis factors (HR 1.23 [1.02, 1.48]) were independently associated with future risk of AKI. The factors require validation in other settings. EFA allows parsimonious subgrouping of biomarkers into factors which are differentially associated with progressive eGFR decline and AKI. These subgroups may provide insights into the pathological processes driving adverse kidney outcomes.
The Systolic Blood Pressure Intervention Trial (SPRINT) compared the effect of intensive versus standard systolic blood pressure targets on cardiovascular morbidity and mortality. In this ancillary study, we evaluated the use of exploratory factor analysis (EFA) to combine biomarkers of kidney tubule health in urine and plasma and then study their role in longitudinal estimated glomerular filtration rate (eGFR) change and risk of acute kidney injury (AKI).RATIONALE & OBJECTIVEThe Systolic Blood Pressure Intervention Trial (SPRINT) compared the effect of intensive versus standard systolic blood pressure targets on cardiovascular morbidity and mortality. In this ancillary study, we evaluated the use of exploratory factor analysis (EFA) to combine biomarkers of kidney tubule health in urine and plasma and then study their role in longitudinal estimated glomerular filtration rate (eGFR) change and risk of acute kidney injury (AKI).Observational cohort nested in a clinical trial.STUDY DESIGNObservational cohort nested in a clinical trial.2,351 SPRINT participants with eGFR < 60 mL/min/1.73 m2 at baseline.SETTING & PARTICIPANTS2,351 SPRINT participants with eGFR < 60 mL/min/1.73 m2 at baseline.Levels of neutrophil gelatinase-associated lipocalin (NGAL), interleukin 18 (IL-18), chitinase-3-like protein (YKL-40), kidney injury molecule 1 (KIM-1), monocyte chemoattractant protein 1 (MCP-1), α1-microglobulin (A1M) and β2-microglobulin (B2M), uromodulin (UMOD), fibroblast growth factor 23 (FGF-23), and intact parathyroid hormone (PTH).EXPOSURELevels of neutrophil gelatinase-associated lipocalin (NGAL), interleukin 18 (IL-18), chitinase-3-like protein (YKL-40), kidney injury molecule 1 (KIM-1), monocyte chemoattractant protein 1 (MCP-1), α1-microglobulin (A1M) and β2-microglobulin (B2M), uromodulin (UMOD), fibroblast growth factor 23 (FGF-23), and intact parathyroid hormone (PTH).Longitudinal changes in eGFR and risk of AKI.OUTCOMELongitudinal changes in eGFR and risk of AKI.We performed EFA to capture different tubule pathophysiologic processes. We used linear mixed effects models to evaluate the association of each factor with longitudinal changes in eGFR. We evaluated the association of the tubular factors scores with AKI using Cox proportional hazards regression.ANALYTICAL APPROACHWe performed EFA to capture different tubule pathophysiologic processes. We used linear mixed effects models to evaluate the association of each factor with longitudinal changes in eGFR. We evaluated the association of the tubular factors scores with AKI using Cox proportional hazards regression.From 10 biomarkers, EFA generated 4 factors reflecting tubule injury/repair (NGAL, IL-18, and YKL-40), tubule injury/fibrosis (KIM-1 and MCP-1), tubule reabsorption (A1M and B2M), and tubule reserve/mineral metabolism (UMOD, FGF-23, and PTH). Each 1-SD higher tubule reserve/mineral metabolism factor score was associated with a 0.58% (95% CI, 0.39%-0.67%) faster eGFR decline independent of baseline eGFR and albuminuria. Both the tubule injury/repair and tubule injury/fibrosis factors were independently associated with future risk of AKI (per 1 SD higher, HRs of 1.18 [95% CI, 1.10-1.37] and 1.23 [95% CI, 1.02-1.48], respectively).RESULTSFrom 10 biomarkers, EFA generated 4 factors reflecting tubule injury/repair (NGAL, IL-18, and YKL-40), tubule injury/fibrosis (KIM-1 and MCP-1), tubule reabsorption (A1M and B2M), and tubule reserve/mineral metabolism (UMOD, FGF-23, and PTH). Each 1-SD higher tubule reserve/mineral metabolism factor score was associated with a 0.58% (95% CI, 0.39%-0.67%) faster eGFR decline independent of baseline eGFR and albuminuria. Both the tubule injury/repair and tubule injury/fibrosis factors were independently associated with future risk of AKI (per 1 SD higher, HRs of 1.18 [95% CI, 1.10-1.37] and 1.23 [95% CI, 1.02-1.48], respectively).The factors require validation in other settings.LIMITATIONSThe factors require validation in other settings.EFA allows parsimonious subgrouping of biomarkers into factors that are differentially associated with progressive eGFR decline and AKI. These subgroups may provide insights into the pathological processes driving adverse kidney outcomes.CONCLUSIONSEFA allows parsimonious subgrouping of biomarkers into factors that are differentially associated with progressive eGFR decline and AKI. These subgroups may provide insights into the pathological processes driving adverse kidney outcomes.
Author Bullen, Alexander L
Garimella, Pranav S
Katz, Ronit
Estrella, Michelle M
Lee, Alexandra K
Ix, Joachim H
Shlipak, Michael G
Jotwani, Vasantha
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  givenname: Alexander L
  surname: Bullen
  fullname: Bullen, Alexander L
  organization: Nephrology Section, Veterans Affairs San Diego Healthcare System, La Jolla, CA; Division of Nephrology and Hypertension, Department of Medicine, University of California San Diego, San Diego, CA
– sequence: 2
  givenname: Ronit
  surname: Katz
  fullname: Katz, Ronit
  organization: Department of Obstetrics & Gynecology, University of Washington, Seattle, Washington, USA
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  givenname: Vasantha
  surname: Jotwani
  fullname: Jotwani, Vasantha
  organization: Kidney Health Research Collaborative, Department of Medicine, University of California, San Francisco, CA; Department of Medicine, San Francisco VA Medical Center, San Francisco, CA
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  givenname: Pranav S
  surname: Garimella
  fullname: Garimella, Pranav S
  organization: Division of Nephrology and Hypertension, Department of Medicine, University of California San Diego, San Diego, CA
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  givenname: Alexandra K
  surname: Lee
  fullname: Lee, Alexandra K
  organization: Kidney Health Research Collaborative, Department of Medicine, University of California, San Francisco, CA
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  givenname: Michelle M
  surname: Estrella
  fullname: Estrella, Michelle M
  organization: Kidney Health Research Collaborative, Department of Medicine, University of California, San Francisco, CA; Department of Medicine, San Francisco VA Medical Center, San Francisco, CA
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  givenname: Michael G
  surname: Shlipak
  fullname: Shlipak, Michael G
  organization: Kidney Health Research Collaborative, Department of Medicine, University of California, San Francisco, CA; Department of Medicine, San Francisco VA Medical Center, San Francisco, CA; Department of Epidemiology and Biostatistics, University of California, San Francisco, CA
– sequence: 8
  givenname: Joachim H
  surname: Ix
  fullname: Ix, Joachim H
  email: joix@ucsd.edu
  organization: Nephrology Section, Veterans Affairs San Diego Healthcare System, La Jolla, CA; Division of Nephrology and Hypertension, Department of Medicine, University of California San Diego, San Diego, CA; Division of Preventive Medicine, Department of Family Medicine and Public Health, University of California San Diego, San Diego, CA. Electronic address: joix@ucsd.edu
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33857535$$D View this record in MEDLINE/PubMed
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Snippet SPRINT compared the effect of intensive versus standard systolic blood pressure targets on cardiovascular morbidity and mortality. In this ancillary study, we...
The Systolic Blood Pressure Intervention Trial (SPRINT) compared the effect of intensive versus standard systolic blood pressure targets on cardiovascular...
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Title Biomarkers of Kidney Tubule Health, CKD Progression, and Acute Kidney Injury in SPRINT (Systolic Blood Pressure Intervention Trial) Participants
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