Early renal, vascular damage seen in individuals with normoalbuminuria
Molecular evidence confirms early renal and vascular damage within the normoalbuminura condition, a recent study has shown.
The authors sought to identify early molecular alterations behind albuminuria development in hypertensive patients under renin–angiotensin system (RAS) suppression, who were classified as either control (albumin to creatinine ratio [ACR], <10 mg/g) or high-normal (ACR, 10–30 mg/g).
Untargeted and targeted mass spectrometry were utilized to quantify and confirm urinary protein alterations. The authors also examined coordinated protein responses with biological significance in albuminuria development. Finally, they carried out immunohistochemistry assays in human kidney and arterial tissue to in situ evaluate the associated damage.
Overall, 2,663 identified proteins indicated inflammation, immune response, ion transport, and lipids metabolism (p≤0.01). A1AT, VTDB, and KNG1 differed in high-normal individuals (p<0.05) and correlated with ACR as well as high-normal condition (odds ratio, 20.76, 6.00, and 7.04, respectively; p<0.001).
After 12 months, protein variations persisted and intensified among progression to moderately increased albuminuria. At tissue level, differential protein expression presented in kidney from those with moderately increased albuminuria and atherosclerotic aortas for the three proteins, which confirmed their capacity to indicate subclinical organ damage.
“A continuous association between albuminuria and cardiorenal risk exists further below moderately increased albuminuria ranges,” the authors said. “If only based in ACR >30 mg/g, a significant percentage of individuals may be out of the scope for therapeutic management.”