Abstract
Background and Aims: Albuminuria is defined as the presence of albumin in urine over 30 mg/g (albumin to creatinine ratio (ACR)). There is evidence of association between albuminuria and cardiovascular risk even in the normoalbuminuria condition (<30 mg/g ACR). However, molecular changes linked to early development of albuminuria are underexplored and normoalbuminuric subjects are usually considered at no risk in clinical practice. By stratifying the normoalbuminuria condition, we aimed to identify early alterations in urine which may aid in assessing individual cardiovascular risk while revealing pathophysiological processes behind albuminuria development.
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