Interaction of Aldosterone and Extracellular Volume in the Pathogenesis of Obesity-Associated Kidney Disease: A Narrative Review

Bomback, Andrew S.; Klemmer, Philip J.

doi:10.1159/000209744

Cited by 43 publications

(26 citation statements)

References 120 publications

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“…It is possible that this combination was enough to make these patients exquisitely sensitive to slight volume changes [27]. Regardless of the mechanism, this study suggests that patients receiving aldosterone antagonism should have their serum creatinine and potassium followed in a manner similar to that used in those who are initiating therapy with RAS blockade, i.e., serum creatinine should be checked within 1–2 weeks after the initiation of therapy.…”

Section: Discussionmentioning

confidence: 99%

Predictors of Hyperkalemia Risk following Hypertension Control with Aldosterone Blockade

2009

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Background: Aldosterone antagonists have proven efficacy for management of resistant hypertension and proteinuria reduction; however, they are not widely used due to risk of hyperkalemia. This study assesses the risk factors for hyperkalemia in patients with chronic kidney disease (CKD) and resistant hypertension whose blood pressure (BP) is reduced to a guideline goal. Methods: This is a two-center study conducted in university-based hypertension clinics directed by clinical hypertension specialists. Forty-six patients with resistant hypertension and stages 2 or 3 CKD (mean estimated glomerular filtration rate (eGFR) 56.5 ± 16.2 ml/min/1.73 m²) were evaluated for safety and efficacy of aldosterone blockade added to preexisting BP-lowering regimens. All patients were on three mechanistically complementary antihypertensive agents including a diuretic and a renin-angiotensin system blocker. Patients were evaluated after a median of 45 treatment days. The primary endpoint was change in systolic BP. Secondary endpoints included change in serum potassium, creatinine, eGFR, diastolic BP and tolerability. Results: The mean age of the patients studied was 64.9 ± 10.7 years, all were obese and 86% had type 2 diabetes, with 82% being African-American. Addition of aldosterone antagonism yielded a further mean reduction in systolic BP of 14.7 ± 5.1 mm Hg (p = 0.001). Females with BMI >30 and those with a baseline systolic BP >160 mm Hg were more likely to have a greater BP reduction to aldosterone antagonism. In total, 39% of the patients had a >30% decrease in eGFR when the BP goal was achieved. The mean increase in serum potassium was 0.4 mEq/l above baseline (p = 0.001), with 17.3% manifesting hyperkalemia, i.e. serum potassium >5.5 mEq/l. Predictors of hyperkalemia included a baseline eGFR of ≤45 ml/min/1.73 m² in whom serum potassium was >4.5 mEq/l on appropriately dosed diuretics. Contributing risks in this subgroup included a systolic BP reduction of >15 mm Hg associated with an eGFR fall of >30%. Conclusion: Aldosterone antagonism is effective and safe for achieving a BP goal among people with diabetic nephropathy when added to a triple antihypertensive regimen that includes a blocker of the renin-angiotensin system and an appropriately selected and dosed diuretic. Caution is advised when using aldosterone blockade for BP control in people with advanced stage 3 nephropathy with a serum potassium of >4.5 mEq/l for safety reasons.

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Section: Discussionmentioning

confidence: 99%

Predictors of Hyperkalemia Risk following Hypertension Control with Aldosterone Blockade

2009

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“…However, CKD [22,23] and ESRD [24] are notable states of relative hyperaldosteronism despite ECV expansion -that is, aldosterone levels are not sufficiently suppressed for the degree of ECV expansion ( fig. 2 ) -leading to proinflammatory MR activation [22,23,25,26] . In experimental studies, some of the adverse tissue effects of inappropriate MR activation occur at non-epithelial MR receptors, develop rapidly, are non-genomic, and have the potential to be attenuated by the use of MRAs.…”

Section: Introductionmentioning

confidence: 99%

Mineralocorticoid Receptor Antagonists in End-Stage Renal Disease: Efficacy and Safety

Bomback¹

2016

Blood Purif

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Mineralocorticoid receptor antagonists (MRAs) that block aldosterone's effects on both epithelial and non-epithelial receptors have become a mainstay of therapy for chronic heart failure. Given that cardiovascular events remain the leading cause of death for patients with end-stage renal disease (ESRD), the question of whether these MRAs can be employed in dialysis patients arises. This review summarizes the rationale for blocking aldosterone in patients with chronic and end-stage kidney disease and surveys the data on both the efficacy and safety of using MRAs in the ESRD population. A small but growing body of literature suggests that use of MRAs by ESRD patients is associated with lower blood pressure, reduced left ventricular (LV) mass, and improved LV ejection fraction. Recently, a large randomized trial found an overall 3-year mortality rate of 6.4% in ESRD patients on spironolactone 25 mg daily vs. 19.7% in ESRD patients on no MRA therapy (p = 0.002), without a significantly increased risk of hyperkalemia.

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“…It has been suggested that CTRP1 may be a mineralocorticoidreleasing factor [7]. CTRP1 stimulates aldosterone production through the induction of CYP11B2 gene expression [1].…”

Section: Introductionmentioning

confidence: 99%

“…CTRP1 stimulates aldosterone production through the induction of CYP11B2 gene expression [1]. Obesity and metabolic syndrome are frequently associated with elevated levels of aldosterone [7] and it is well known that obesity is the leading cause of hypertension [8,9]. Elevated aldosterone levels and expanded extracellular volume are key components of obesity-induced renal disease via aldosterone's non-epithelial effects on the kidney [7].…”

Section: Introductionmentioning

confidence: 99%

CTRP1: A Molecular Link between Obesity and Hypertension

Chalupová¹,

Halupova²

2016

J Mol Biomark Diagn

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Interaction of Aldosterone and Extracellular Volume in the Pathogenesis of Obesity-Associated Kidney Disease: A Narrative Review

Cited by 43 publications

References 120 publications

Predictors of Hyperkalemia Risk following Hypertension Control with Aldosterone Blockade

Predictors of Hyperkalemia Risk following Hypertension Control with Aldosterone Blockade

Mineralocorticoid Receptor Antagonists in End-Stage Renal Disease: Efficacy and Safety

CTRP1: A Molecular Link between Obesity and Hypertension

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