In the setting of intensive systolic blood pressure (SBP) lowering, incident chronic kidney disease (CKD) was accompanied by decreases in levels of kidney damage biomarkers and may reflect benign changes in renal blood flow rather than intrinsic injury. This according to a recent case-control study that compared changes in kidney damage biomarkers between incident CKD case participants and matched control participants was well as between case participants in the intensive (<120 mm Hg) vs the standard (<140 mm Hg) SBP management groups of SPRINT (Systolic Blood Pressure Intervention Trial). Case participants (n = 162) were adults with developed incident CKD during trial follow-up (128 in the intensive and 34 in the standard group), and control participants (n = 162) without incident CKD. 9 urinary biomarkers of kidney damage were measured at 1 baseline and at 1 year. Researchers found:

• Higher concentrations of urinary albumin, kidney injury molecule-1, and monocyte chemoattractant protein-1 at baseline were significantly associated with greater odds of incident CKD.
• After 1 year of BP intervention, incident CKD case participants in the intensive group had significantly greater decreases in albumin-creatinine ratio (ACR), interleukin-18, anti-chitinase-3-like protein 1 (YKL-40), and uromodulin than the matched control participants.
• Those in the intensive group had significantly greater decreases in ACR, β₂-microglobulin, α₁-microglobulin, YKL-40, and uromodulin.