According to studies, patients with diabetes who have non-albuminuric chronic kidney disease (CKD) lose renal function at a slower rate than those who have normal renal function. It showed the presence of protective variables, the identification of which may lead to the identification of intervention targets. For a study, researchers sought to find protective clinical characteristics and nonclinical biomarkers that contribute to the link between non-albuminuric CKD and a low risk of CKD progression.

Among people with diabetes and CKD involved in the Chronic Renal Insufficiency Cohort (CRIC) Study in the United States, they looked for significant relationships between numerous clinical variables and 33 nonclinical biomarkers with normoalbuminuria and a low incidence of CKD progression. In linear regression, factors that were substantially linked with both normoalbuminuria and a low rate of CKD advancement were evaluated to quantify their potential contributions to the connection between non-albuminuric CKD and the rate of CKD progression.

SBP, HbA1c, eGFR, and 6 biomarkers [-trace protein (BTP), kidney injury molecule (KIM-1), fibrinogen, fractalkine, brain natriuretic peptide (BNP), and high-sensitivity troponin-T (hsTnT)] were all linked to normoalbuminuria and a slow rate of eGFR reduction. For normoalbuminuria, the univariate -coefficient was 0.93 [95% (CI): 0.82, 1.05]. When all linked covariates and biomarkers were taken into account, the regression coefficient fell to 0.54. (95% CI: 0.40, 0.67). Lower levels of SBP, HbA1c, BTP, KIM-1, hsTnT, BNP, fibrinogen, and fractalkine were shown to be associated with non-albuminuric CKD and a low rate of eGFR.

Lower SBP levels and biomarkers with pro-inflammatory and vascular modifying properties may account for up to 40% of the connection between non-albuminuric CKD and a low rate of CKD development. Further research into these biomarkers might lead to therapeutic approaches.