
Mechanisms associated with early nephron-specific kidney injury biomarkers in young adults vary according to the blood pressure (BP) status, reports a study.
A total of 1,055 adults were included in the cross-sectional analysis. Kidney biomarkers were as follows: estimated glomerular filtration rate (eGFR), urinary albumin-to-creatinine ratio (uACR), alpha-1 microglobulin (uA1M), neutrophil gelatinase-associated lipocalin (uNGAL), uromodulin (uUMOD), and CKD273 classifier.
The authors analysed the markers of oxidative stress (gamma-glutamyl transferase [GGT]; malondialdehyde [MDA]), inflammation (interleukin 6 [IL-6], C-reactive protein [CRP], and fibrinogen), and endothelial function (soluble intercellular adhesion molecule-1, soluble vascular cell adhesion molecule-1 [sVCAM-1], von Willebrand factor antigen [vWFag], monocyte chemoattractant protein-1 [MCP-1], plasminogen activator inhibitor -1 activity [PAI-1act], urinary nitrate-to-nitrite ratio).
Individuals with hypertension (mean age 24.8 years, 73.2 percent men, 39 percent Black) had higher GGT, CRP, IL-6, MCP-1, and PAI-1act levels (p≤0.024 for all) than normotensive participants.
In the hypertensive group, eGFR negatively correlated and uNGAL positively correlated with IL-6, while uA1M showed a positive association with PAI-1act (p≤0.047 for all). In the same group, UMOD positively correlated with fibrinogen and CKD273 classifier negatively correlated with MCP-1 (p≤0.021 for all).
On the other hand, eGFR was positively associated with MDA and negatively with GGT in the normotension group. Additionally, CKD273 classifier positively correlated with GGT, sVCAM-1, and vWFag, whereas uACR showed a negative association with CRP (p≤0.033 for all).
“Hypertension and kidney disease share common pathophysiological pathways involved in endothelial dysfunction including increased oxidative stress and chronic inflammation,” the authors said.