Microalbuminuria breakthrough under chronic renin–angiotensin–aldosterone system suppression

Cerezo, César; Ruilope, Luís M.; Segura, Julián; García-Donaire, José Antonio; Cruz, Juan; Banegas, José R.; Waeber, Bernard; Rabelink, Ton J.; Messerli, Franz H.

doi:10.1097/hjh.0b013e32834d9e0f

Cited by 39 publications

(28 citation statements)

References 25 publications

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“…This enhanced risk was associated in many patients with the risk attributable to the presence of diabetes. This situation of risk can also be observed during chronic renin-angiotensin system blockade, as we previously described (36). The development of new-onset albuminuria during longterm administration of an ACE inhibitor or angiotensin receptor blocker is accompanied by an increased number of CVD events (36).…”

Section: Discussionmentioning

confidence: 78%

Association Between High and Very High Albuminuria and Nighttime Blood Pressure: Influence of Diabetes and Chronic Kidney Disease

et al. 2016

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OBJECTIVENighttime blood pressure (BP) and albuminuria are two important and independent predictors of cardiovascular morbidity and mortality. Here, we examined the quantitative differences in nighttime systolic BP (SBP) across albuminuria levels in patients with and without diabetes and chronic kidney disease. RESEARCH DESIGN AND METHODSA total of 16,546 patients from the Spanish Ambulatory Blood Pressure Monitoring Registry cohort (mean age 59.6 years, 54.9% men) were analyzed. Patients were classified according to estimated glomerular filtration rate (eGFR), as ‡60 or <60 mL/min/1.73 m 2 (low eGFR), and urine albumin-to-creatinine ratio, as normoalbuminuria (<30 mg/g), high albuminuria (30-300 mg/g), or very high albuminuria (>300 mg/g). Office and 24-h BP were determined with standardized methods and conditions. RESULTSHigh albuminuria was associated with a statistically significant and clinically substantial higher nighttime SBP (6.8 mmHg higher than with normoalbuminuria, P < 0.001). This association was particularly striking at very high albuminuria among patients with diabetes and low eGFR (16.5 mmHg, P < 0.001). Generalized linear models showed that after full adjustment for demographic, lifestyles, and clinical characteristics, nighttime SBP was 4.8 mmHg higher in patients with high albuminuria than in those with normoalbuminuria (P < 0.001), and patients with very high albuminuria had a 6.1 mmHg greater nighttime SBP than those with high albuminuria (P < 0.001). These differences were 3.8 and 3.1 mmHg, respectively, among patients without diabetes, and 6.5 and 8 mmHg among patients with diabetes (P < 0.001). CONCLUSIONSAlbuminuria in hypertensive patients is accompanied by quantitatively striking higher nighttime SBP, particularly in those with diabetes with very high albuminuria and low eGFR.

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Section: Discussionmentioning

confidence: 78%

Association Between High and Very High Albuminuria and Nighttime Blood Pressure: Influence of Diabetes and Chronic Kidney Disease

et al. 2016

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“…Patient selection and classification was previously described in an initial paper describing development of high albuminuria in patients during chronic RAS suppression [10].…”

Section: Patientsmentioning

confidence: 99%

“…Our group [10], among others, has described the development of de novo proteinuria during long-term antihypertensive therapy and particularly during chronic RAS suppression. In addition, a recent study conducted by our group has shown that well-controlled hypertensive patients who develop albuminuria under chronic RAS suppression, which besides are in an early stage of chronic kidney disease (CKD) development, present an increased oxidative damage.…”

Section: Introductionmentioning

confidence: 99%

Prediction of development and maintenance of high albuminuria during chronic renin–angiotensin suppression by plasma proteomics

Baldán-Martín

Cuesta

Alvarez-Llamas

et al. 2015

International Journal of Cardiology

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“…13 Briefly, 1143 patients were followed up for a minimum period of 3 years with visits to the Hypertension Unit, Hospital Universitario 12 de Octubre, Madrid, at least every 6 months. After that, the patients continued with their annual revisions.…”

Section: Patient Recruitmentmentioning

confidence: 99%

Plasma Molecular Signatures in Hypertensive Patients With Renin–Angiotensin System Suppression

et al. 2016

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A lbuminuria is a risk factor strongly associated with cardiovascular and renal complications particularly when diabetes mellitus and hypertension are present. However, in the absence of these 2 processes, albuminuria can be equally relevant as a predictor.1 These facts reflect the enormous relevance of albuminuria to monitor cardiovascular disease, the first cause of death in the general population.2 Different factors promote the development of albuminuria 3 and lead finally to an increased albumin leakage through the glomerular barrier. [4][5][6][7] Renin-angiotensin system (RAS) suppression is considered the therapy of choice to prevent the development of new-onset albuminuria in naïf patients 8,9 and to diminish the amount of excreted albuminuria. 10 The positive effect depends on a reduction in blood pressure, 11 as well as a modification of intraglomerular hemodynamics and permeability.12 Recent studies conducted by our group have shown that despite an apparently adequate RAS suppression, a relevant percentage of hypertensive patients develop de novo albuminuria pointing to a progression of cardiovascular disease probably facilitated by an inappropriate therapeutic response to angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. 13Moreover, we have also found an increased systemic oxidative damage in hypertensive patients who develop albuminuria under chronic RAS suppression suggesting that oxidative stress is one of the mechanisms underlying the development of albuminuria 14 in this situation. These considerations highlight the need to continue searching for potential mechanisms and indicators of the development and progression of albuminuria in hypertensive patients under RAS suppression, considering that it will contribute Abstract-Albuminuria is a risk factor strongly associated with cardiovascular disease, the first cause of death in the general population. It is well established that renin-angiotensin system suppressors prevent the development of new-onset albuminuria in naïf hypertensive patients and diminish its excretion, but we cannot forget the percentage of hypertensive patients who develop de novo albuminuria. Here, we applied multiple proteomic strategy with the purpose to elucidate specific molecular pathways involved in the pathogenesis and provide predictors and chronic organ damage indicators. Briefly, 1143 patients were followed up for a minimum period of 3 years. One hundred and twenty-nine hypertensive patients chronically renin-angiotensin system suppressed were recruited, classified in 3 different groups depending on their albuminuria levels (normoalbuminuria, de novo albuminuria, and sustained albuminuria), and investigated by multiple proteomic strategies. Our strategy allowed us to perform one of the deepest plasma proteomic analysis to date, which has shown 2 proteomic signatures: (1) with predictive value of de novo albuminuria and (2) sustained albuminuria indicator proteins. These proteins are involved in inflammation, immune as well as in the proteasome...

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Microalbuminuria breakthrough under chronic renin–angiotensin–aldosterone system suppression

Abstract: These data indicate that a reappraisal of renin-angiotensin-aldosterone system (RAAS) suppression is required when microalbuminuria appears in patients under chronic RAAS suppression.

Cited by 39 publications

References 25 publications

Association Between High and Very High Albuminuria and Nighttime Blood Pressure: Influence of Diabetes and Chronic Kidney Disease

Association Between High and Very High Albuminuria and Nighttime Blood Pressure: Influence of Diabetes and Chronic Kidney Disease

Prediction of development and maintenance of high albuminuria during chronic renin–angiotensin suppression by plasma proteomics

Plasma Molecular Signatures in Hypertensive Patients With Renin–Angiotensin System Suppression

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