title: Spironolactone further reduces urinary albumin excretion and plasma B-type natriuretic peptide levels in hypertensive type II diabetes treated with angiotensin-converting enzyme inhibitor.
abstract: 1. Over the course of treatment with angiotensin-converting enzyme inhibitor (ACEI), plasma levels of aldosterone have been shown to increase and this increase would blunt the effectiveness of the ACEI (aldosterone escape phenomenon). 2. In the present study, we assessed a potential renal benefit of additional aldosterone blockade with spironolactone in hypertensive diabetic patients treated with ACEI showing the phase of aldosterone escape. 3. The present clinical study was a randomized prospective study to assess difference between the clinical effects of spironolactone and furosemide. Thirty hypertensive type II diabetics (DM2) with a urinary alubumin:creatinine ratio (ACR) above 30 mg/g creatinine (showing albuminuria) and plasma B-type natriuretic peptide (BNP) levels above 100 pg/mL (showing mild heart failure) were treated with an ACEI (imidapril 5 mg/day) for 1 year and then randomly divided into two groups, one group receiving additional spironolactone (25 mg/day) treatment and the other receiving furosemide (20 mg/day) treatment. Blood pressure, ACR and plasma BNP levels were monitored in both groups. 4. Treatment with the ACEI reduced ACR initially but, in 1 year, ACR tended to increase. Additional spironolactone treatment progressively reduced ACR, whereas furosemide treatment did not show any effect. Plasma BNP levels were reduced by ACEI and were further reduced by additional spironolactone treatment, but not furosemide treatment. Blood pressure levels in both groups were comparable. 5. In conclusion, additional therapy with spironolactone in ACEI treatment exerts a renoprotective, as well as cardioprotective, effect in hypertensive diabetes.
authors.affiliation: Division of Nephrology, Endocrinology and Hypertension, Tohoku University Hospital, Sendai, Japan. ogawa-s@mail.tains.tohoku.ac.jp
authors.forename: Susumu
authors.initials: S
authors.lastname: Ogawa
authors.forename: Kazuhisa
authors.initials: K
authors.lastname: Takeuchi
authors.forename: Takefumi
authors.initials: T
authors.lastname: Mori
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Nako
authors.forename: Sadayoshi
authors.initials: S
authors.lastname: Ito
mesh_terms: D000419:Albuminuria / Q000097:blood / Q000188:drug therapy* / Q000652:urine; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D003404:Creatinine / Q000652:urine; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy* / Q000652:urine; D004232:Diuretics / Q000627:therapeutic use; D005665:Furosemide / Q000627:therapeutic use; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000188:drug therapy* / Q000652:urine; D048289:Imidazolidines / Q000627:therapeutic use*; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use*; D020097:Natriuretic Peptide, Brain / Q000097:blood*; D013148:Spironolactone / Q000627:therapeutic use*; D016896:Treatment Outcome
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D004232:Diuretics; D048289:Imidazolidines; D000451:Mineralocorticoid Receptor Antagonists; D020097:Natriuretic Peptide, Brain; D013148:Spironolactone; D005665:Furosemide; D003404:Creatinine; C065166:imidapril