Kidney Damage Biomarkers and Incident Chronic Kidney Disease During Blood Pressure Reduction: A Case-Control Study

  • 0San Francisco Veterans Affairs Medical Center and University of California, San Francisco, San Francisco, California (W.R.Z., M.G.S.).

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Summary

This summary is machine-generated.

Intensive blood pressure lowering did not worsen kidney injury markers in patients who developed chronic kidney disease (CKD). Instead, biomarker levels decreased, suggesting benign changes rather than intrinsic kidney damage.

Area Of Science

  • Nephrology
  • Cardiovascular Medicine
  • Biomarker Research

Background

  • The relationship between intensive systolic blood pressure (SBP) lowering and intrinsic kidney injury in chronic kidney disease (CKD) incidence remains unclear.
  • The Systolic Blood Pressure Intervention Trial (SPRINT) provides an opportunity to investigate this association.

Purpose Of The Study

  • To compare kidney damage biomarker changes in participants who developed incident CKD versus controls.
  • To compare biomarker changes between intensive (<120 mm Hg) and standard (<140 mm Hg) SBP management groups within the SPRINT trial.

Main Methods

  • A nested case-control study was conducted within the SPRINT trial.
  • 9 urinary biomarkers of kidney damage were measured at baseline and 1 year in 162 incident CKD cases and 162 matched controls.
  • Linear mixed-effects models were used to analyze biomarker changes over 1 year.

Main Results

  • Higher baseline levels of urinary albumin, kidney injury molecule-1, and monocyte chemoattractant protein-1 were associated with increased odds of incident CKD.
  • Incident CKD cases in the intensive SBP group showed greater decreases in albumin-creatinine ratio (ACR), interleukin-18, YKL-40, and uromodulin compared to controls.
  • Compared to the standard group, the intensive group's CKD cases had greater decreases in ACR, β2-microglobulin, α1-microglobulin, YKL-40, and uromodulin.

Conclusions

  • Incident CKD associated with intensive SBP lowering may involve benign changes in renal blood flow, not intrinsic kidney injury.
  • Observed decreases in kidney damage biomarkers do not support the hypothesis of increased intrinsic kidney injury with intensive SBP lowering.

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