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Diabetic kidney disease (DKD) is a major cause of morbidity and mortality in individuals with type 2 diabetes mellitus (T2DM). The aim of this study was to investigate whether albumin structural alterations correlate with DKD severity and evaluate whether native and reduced albumin concentrations could complement the diagnosis of DKD. To this end, one hundred and seventeen T2DM patients without (n = 42) and with (n = 75) DKD (DKD I-III upon KDIGO classification) were evaluated; the total albumin concentration (tHA) was quantified by a bromocresol green assay, while structural alterations were profiled via liquid chromatography–high-resolution mass spectrometry (LC-HRMS). The concentrations of native albumin (eHA, effective albumin) and reduced albumin (rHA) were subsequently assessed. The HRMS analyses revealed a reduced relative amount of native albumin in DKD patients along with an increased abundance of altered forms, especially those bearing oxidative modifications. Accordingly, both eHA and rHA values varied during the stages of progressive renal failure, and these alterations were dose-dependently correlated with renal dysfunction. A ROC curve analysis revealed a significantly greater sensitivity and specificity of eHA and rHA than of tHA for diagnosing DKD. Importantly, according to the multivariate logistic regression analysis, the eHA was identified as an independent predictor of DKD. [ABSTRACT FROM AUTHOR]

Background: Hypertension and chronic kidney disease (CKD) are closely interlinked pathophysiologic states, such that high blood pressure (BP) is an independent risk factor for disease progression in both adult and pediatric patients with kidney disorders and progressive decline in kidney function can conversely lead to worsening BP control. Summary: Hypertension in CKD is not only associated with GFR loss, but increases cardiovascular risk, which is the leading source of mortality and morbidity in this population. Given this complex relationship between hypertension, CKD, and CVD, an optimal management of BP in CKD is mandatory to break an established vicious pathophysiological cycle that leads to adverse outcomes. Key Messages: New promising molecules for the treatment of CKD, with interesting mechanisms, particularly regarding their pathophysiological interactions with arterial hypertension, are available or under development and in the very next future they may change the way we treat high BP in CKD patients. [ABSTRACT FROM AUTHOR]