2013•Brazilian Journal of NephrologyOpen access

Spironolactone reduces blood pressure and albuminuria of obese hypertensive patients with Metabolic Syndrome

Danielle Guedes Andrade Ezequiel, Rogério Baumgratz de Paula, Júlio César Moraes Lovisi, Thaís Chehuen Bicalho, Sergio Franca de Souza Filho, Sarah de Paula Iennaco de Rezende, Mônica Barros Costa

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Abstract

INTRODUCTION: In recent years, a role for aldosterone in pathophysiology of metabolic syndrome and hypertension in this syndrome has been suggested. However, the treatment with antagonists of mineralocorticoid receptor in these individuals has not properly addressed. OBJECTIVE: To evaluate the effects of mineralocorticoid receptor blockade on blood pressure, inflammatory, metabolic and renal parameters in non-diabetic hypertensive individuals with the metabolic syndrome. METHODS: Twenty nine patients with metabolic syndrome were enrolled in a prospective protocol that consisted of 2 periods: baseline (2 weeks) in which demographic data were obtained and antihypertensive medicines were withdrawn, and treatment period when the individuals were treated with spironolactone 25-50 mg once-a-day, for 16 weeks. In both periods, inflammatory, metabolic and renal parameters were assessed and the 24-hour ambulatory blood pressure monitorization was performed. RESULTS: After spironolactone treatment, 24 hour systolic and diastolic blood pressure decreased from 143.5 ± 15.17 mmHg to 133.2 ± 17.34 mmHg (p = 0.025) and from 85.2 ± 11.10 mmHg to 79.3 ± 11.78 mmHg (p = 0.026), respectively. HDL-cholesterol increased from 44.0 ± 8.67 mg/dl to 49.0 ± 6.75mg/dl (p = 0.000) and C-reactive protein decreased significantly from 6.3 ± 7.54 mg/l to 4.6 ± 6.3 mg/l (p = 0.009). Fasting plasma glucose, insulin, HOMA-IR and triglycerides did not change significantly after mineralocorticoid receptor blockade. Estimated glomerular filtration rate did not change whereas the logarithm of albuminuria decreased significantly from 2.5 ± 0.92 to 2.0 ± 0.9 (p = 0.028). CONCLUSION: In hypertensive subjects with MS the administration of spironolactone in monotherapy was effective for hypertension control, decreased urinary albumin excretion and increased HDL-cholester ol plasma.

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INTRODUCTION: In recent years, a role for aldosterone in pathophysiology of metabolic syndrome and hypertension in this syndrome has been suggested. However, the treatment with antagonists of mineralocorticoid receptor in these individuals has not properly addressed. OBJECTIVE: To evaluate the effects of mineralocorticoid receptor blockade on blood pressure, inflammatory, metabolic and renal parameters in non-diabetic hypertensive individuals with the metabolic syndrome. METHODS: Twenty nine patients with metabolic syndrome were enrolled in a prospective protocol that consisted of 2 periods: baseline (2 weeks) in which demographic data were obtained and antihypertensive medicines were withdrawn, and treatment period when the individuals were treated with spironolactone 25-50 mg once-a-day, for 16 weeks. In both periods, inflammatory, metabolic and renal parameters were assessed and the 24-hour ambulatory blood pressure monitorization was performed. RESULTS: After spironolactone treatment, 24 hour systolic and diastolic blood pressure decreased from 143.5 ± 15.17 mmHg to 133.2 ± 17.34 mmHg (p = 0.025) and from 85.2 ± 11.10 mmHg to 79.3 ± 11.78 mmHg (p = 0.026), respectively. HDL-cholesterol increased from 44.0 ± 8.67 mg/dl to 49.0 ± 6.75mg/dl (p = 0.000) and C-reactive protein decreased significantly from 6.3 ± 7.54 mg/l to 4.6 ± 6.3 mg/l (p = 0.009). Fasting plasma glucose, insulin, HOMA-IR and triglycerides did not change significantly after mineralocorticoid receptor blockade. Estimated glomerular filtration rate did not change whereas the logarithm of albuminuria decreased significantly from 2.5 ± 0.92 to 2.0 ± 0.9 (p = 0.028). CONCLUSION: In hypertensive subjects with MS the administration of spironolactone in monotherapy was effective for hypertension control, decreased urinary albumin excretion and increased HDL-cholester ol plasma.

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Available abstract

INTRODUCTION: In recent years, a role for aldosterone in pathophysiology of metabolic syndrome and hypertension in this syndrome has been suggested. However, the treatment with antagonists of mineralocorticoid receptor in these individuals has not properly addressed. OBJECTIVE: To evaluate the effects of mineralocorticoid receptor blockade on blood pressure, inflammatory, metabolic and renal parameters in non-diabetic hypertensive individuals with the metabolic syndrome. METHODS: Twenty nine patients with metabolic syndrome were enrolled in a prospective protocol that consisted of 2 periods: baseline (2 weeks) in which demographic data were obtained and antihypertensive medicines were withdrawn, and treatment period when the individuals were treated with spironolactone 25-50 mg once-a-day, for 16 weeks. In both periods, inflammatory, metabolic and renal parameters were assessed and the 24-hour ambulatory blood pressure monitorization was performed. RESULTS: After spironolactone treatment, 24 hour systolic and diastolic blood pressure decreased from 143.5 ± 15.17 mmHg to 133.2 ± 17.34 mmHg (p = 0.025) and from 85.2 ± 11.10 mmHg to 79.3 ± 11.78 mmHg (p = 0.026), respectively. HDL-cholesterol increased from 44.0 ± 8.67 mg/dl to 49.0 ± 6.75mg/dl (p = 0.000) and C-reactive protein decreased significantly from 6.3 ± 7.54 mg/l to 4.6 ± 6.3 mg/l (p = 0.009). Fasting plasma glucose, insulin, HOMA-IR and triglycerides did not change significantly after mineralocorticoid receptor blockade. Estimated glomerular filtration rate did not change whereas the logarithm of albuminuria decreased significantly from 2.5 ± 0.92 to 2.0 ± 0.9 (p = 0.028). CONCLUSION: In hypertensive subjects with MS the administration of spironolactone in monotherapy was effective for hypertension control, decreased urinary albumin excretion and increased HDL-cholester ol plasma.

Key concepts: Spironolactone, Medicine, Mineralocorticoid receptor, Blood pressure, Internal medicine, Endocrinology, Metabolic syndrome, Albuminuria

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