Background: Studies have shown that people with nonalbuminuric chronic kidney disease (NACKD) have a slow rate of CKD progression. This suggests the presence of protective factors, the identification of which may open up targets for intervention. Methods: We tested for significant associations of several clinical factors and 34 nonclinical biomarkers with (1) normoalbuminuria and (2) a low rate of CKD progression among participants with diabetes and CKD enrolled in the Chronic Renal Insufficiency Cohort (CRIC) Study in the United States. Factors significantly associated with both normoalbuminuria and a low rate of CKD progression were used in mediation analysis to assess the direct effects of normoalbuminuria on low rate of CKD progression and its indirect effect mediated through the clinical factors and nonclinical biomarkers. Results: Systolic blood pressure (SBP), HbA1c, and six biomarkers (kidney injury molecule (KIM-1); neutrophil gelatinase-associated lipocalin; fibrinogen; fractalkine; brain natriuretic peptide (BNP) and high-sensitivity troponin-T) were associated with both normoalbuminuria and a low rate of eGFR decline. Mediation analysis showed that 30.5% (95% CI: 15.1%, 45.0%) of the association between NACKD and a low rate of CKD progression was mediated by these clinical and nonclinical biomarkers. Of these, the independently significant mediators were lower levels of KIM-1 (proportion mediated effect [PME]: 8.1% [2.4, 14.1]); SBP (PME: 6.7% [0.9, 12.9%]); and BNP (PME: 4.6% [1.5, 8.4]). Conclusion: Lower levels of SBP and biomarkers that have pro-inflammatory and vascular modulating features mediated a considerable proportion of the association between NACKD and low rate of CKD progression. Further investigation of these mediators may lead to therapeutic interventions.