title: The effects of nesiritide on renal function and diuretic responsiveness in acutely decompensated heart failure patients with renal dysfunction.
abstract: BACKGROUND
  Strategies to preserve renal function and enhance diuretic responsiveness during therapy for heart failure (HF) are needed. We hypothesized that brain natriuretic peptide (nesiritide) added to standard HF therapy would preserve renal function and enhance diuretic responsiveness.
  
  
  METHODS
  Patients with HF with underlying renal dysfunction who were admitted with volume overload were randomized to standard therapy with nesiritide (2 mug/kg bolus; 0.01 mug/kg/min for 48 hours) or without nesiritide. Patients requiring intravenous vasodilator or inotropic therapy for rapid symptom relief were ineligible. In all patients, diuretics were administered according to a standardized dosing algorithm.
  
  
  RESULTS
  Patients (n = 72) had a mean creatinine level of 1.75 +/- 0.59 mg/dL. Patients receiving nesiritide had a lesser increase in creatinine (P = .048) and blood urea nitrogen (P = .02), but a greater reduction in blood pressure (P < .01). Nesiritide did not enhance diuretic responsiveness (P = .57) but increased 3'5' cyclic guanosine monophosphate and decreased endothelin more (P < .05 for both). There were no differences in the change in atrial natriuretic peptide, N-terminal pro-brain natriuretic peptide, plasma renin activity, angiotensin II, and aldosterone between groups.
  
  
  CONCLUSIONS
  When used as adjuvant "renal protective" therapy in patients with HF with renal dysfunction, the recommended dose of nesiritide reduced blood pressure, did not seem to worsen renal function, and suppressed endothelin but did not enhance diuretic responsiveness or prevent activation of the renin-angiotensin-aldosterone system.
authors.affiliation: Mayo Clinic College of Medicine, Division of Cardiovascular Diseases, Rochester, Minneosta 55905.
authors.forename: Theophilus E
authors.initials: TE
authors.lastname: Owan
authors.forename: Horng H
authors.initials: HH
authors.lastname: Chen
authors.forename: Robert P
authors.initials: RP
authors.lastname: Frantz
authors.forename: Barry L
authors.initials: BL
authors.lastname: Karon
authors.forename: Wayne L
authors.initials: WL
authors.lastname: Miller
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Rodeheffer
authors.forename: David O
authors.initials: DO
authors.lastname: Hodge
authors.forename: John C
authors.initials: JC
authors.lastname: Burnett
authors.forename: Margaret M
authors.initials: MM
authors.lastname: Redfield
mesh_terms: D000368:Aged; D000465:Algorithms; D001806:Blood Urea Nitrogen; D003404:Creatinine / Q000097:blood; D006152:Cyclic GMP / Q000097:blood; D004231:Diuresis / Q000187:drug effects*; D004334:Drug Administration Schedule; D004359:Drug Therapy, Combination; D004727:Endothelium / Q000187:drug effects; D005260:Female; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D007668:Kidney / Q000187:drug effects* / Q000503:physiopathology; D008297:Male; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use; D045283:Natriuretic Agents / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D020097:Natriuretic Peptide, Brain / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D051436:Renal Insufficiency, Chronic / Q000097:blood / Q000503:physiopathology*; D013148:Spironolactone / Q000627:therapeutic use; D013318:Stroke Volume; D013997:Time Factors
chemical_list: D000451:Mineralocorticoid Receptor Antagonists; D045283:Natriuretic Agents; D020097:Natriuretic Peptide, Brain; D013148:Spironolactone; D003404:Creatinine; D006152:Cyclic GMP