Subclinical Kidney Damage in Hypertensive Patients:A Renal Window Opened on the CardiovascularSystem. Focus on Microalbuminuria

Giuseppe Mule', Giulio Geraci, Giovanni Cerasola, Santina Cottone, Onofrio Cacciatore, Epifanio Di Natale, Antonella Castiglia, Claudia Cusumano, Dario Altieri

Research output: Chapter in Book/Report/Conference proceedingChapter

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The kidney is one of the major target organs of hypertension.Kidney damage represents a frequent event in the course of hypertensionand arterial hypertension is one of the leading causes of end-stagerenal disease (ESRD).ESRD has long been recognized as a strong predictor of cardiovascular(CV) morbidity and mortality. However, over the past 20 years a large andconsistent body of evidence has been produced suggesting that CV riskprogressively increases as the estimated glomerular filtration rate (eGFR)declines and is already significantly elevated even in the earliest stages ofrenal damage. Data was supported by the very large collaborative metaanalysisof the Chronic Kidney Disease Prognosis Consortium, whichprovided undisputable evidence that there is an inverse associationbetween eGFR and CV risk. It is important to remember that in evaluatingCV disease using renal parameters, GFR should be assessed simultaneouslywith albuminuria.Indeed, data from the same meta-analysis indicate that also increasedurinary albumin levels or proteinuria carry an increased risk of all-causeand CV mortality. Thus, lower eGFR and higher urinary albumin valuesare not only predictors of progressive kidney failure, but also ofall-cause and CV mortality, independent of each other and of traditionalCV risk factors.Although subjects with ESRD are at the highest risk of CV diseases,there will likely be more events in subjects with mil-to-moderate renaldysfunction, because of its much higher prevalence.These findings are even more noteworthy when one considers that amild reduction in renal function is very common in hypertensive patients.The current European Society of Hypertension (ESH)/European Societyof Cardiology (ESC) guidelines for the management of arterial hypertensionrecommend to sought in every patient signs of subclinical(or asymptomatic) renal damage. This was defined by the detection ofeGFR between 30 mL/min/1.73 m2 and 60 mL/min/1.73 m2 or the presenceof microalbuminuria (MAU), that is an amount of albumin in theurine of 30–300 mg/day or an albumin/creatinine ratio, preferentially onmorning spot urine, of 30–300 mg/g.There is clear evidence that urinary albumin excretion levels, evenbelow the cut-off values used to define MAU, are associated with anincreased risk of CV events. The relationships of MAU with a variety ofrisk factors, such as blood pressure, diabetes and metabolic syndrome andwith several indices of subclinical organ damage, may contribute, at leastin part, to explain the enhanced CV risk conferred by MAU. Nonetheless,several studies showed that the association between MAU and CV diseaseremains when all these risk factors are taken into account in multivariateanalyses. Therefore, the exact pathophysiological mechanisms explainingthe association between MAU and CV risk remain to be elucidated. Thesimple search for MAU and in general of subclinical renal involvement inhypertensive patients may enable the clinician to better assess absoluteCV risk, and its identification may induce physicians to encouragepatients to make healthy lifestyle changes and perhaps would prompt tomore aggressive modification of standard CV risk factors.
Original languageEnglish
Title of host publicationHypertension: from basic research to clinical practice
Number of pages30
Publication statusPublished - 2017

Publication series


All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)

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    Mule', G., Geraci, G., Cerasola, G., Cottone, S., Cacciatore, O., Di Natale, E., Castiglia, A., Cusumano, C., & Altieri, D. (2017). Subclinical Kidney Damage in Hypertensive Patients:A Renal Window Opened on the CardiovascularSystem. Focus on Microalbuminuria. In Hypertension: from basic research to clinical practice (pp. 279-308). (ADVANCES IN INTERNAL MEDICINE).