title: Effect of Corticosteroid on Renal Water and Sodium Excretion in Symptomatic Heart Failure: Prednisone for Renal Function Improvement Evaluation Study.
abstract: BACKGROUND
  Recent evidence indicates that prednisone can potentiate renal responsiveness to diuretics in heart failure (HF). However, the optimal dose of prednisone is not known.
  
  
  METHODS
  Thirty-eight patients with symptomatic HF were randomized to receive standard HF care alone (n = 10) or with low-dose (15 mg/d, n = 8), medium-dose (30 mg/d, n = 10), or high-dose prednisone (60 mg/d, n = 10), for 10 days. During this time, we recorded the 24-hour urinary output and the 24-hour urinary sodium excretion, at baseline, on day 5 and day 10. We also monitored the change in the concentration of serum creatinine, angiotensin II, aldosterone, high-sensitive C-reactive protein, tumor necrosis factor-α, interleukin 1β, and interleukin 6.
  
  
  RESULTS
  Low-dose prednisone significantly enhanced urine output. However, the effects of medium- and high-dose prednisone on urine output were less obvious. As for renal sodium excretion, high-dose prednisone induced a more potent natriuresis than low-dose prednisone. Despite the potent diuresis and natriuresis induced by prednisone, serum creatinine, angiotensin II, and aldosterone levels were not elevated. These favorable effects were not associated with an inflammatory suppression by glucocorticoids.
  
  
  CONCLUSIONS
  Only low-dose prednisone significantly enhanced urine output. However, high-dose prednisone induced a more potent renal sodium excretion than low-dose prednisone.
authors.affiliation: *Heart Center, The First Hospital of Hebei Medical University, Hebei Medical University, Shijiazhuang, China; and †Department of Pharmacology, Hebei Medical University, Shijiazhuang, China.
authors.forename: Chao
authors.initials: C
authors.lastname: Liu
authors.forename: Qingzhen
authors.initials: Q
authors.lastname: Zhao
authors.forename: Yuzhi
authors.initials: Y
authors.lastname: Zhen
authors.forename: Jianlong
authors.initials: J
authors.lastname: Zhai
authors.forename: Gang
authors.initials: G
authors.lastname: Liu
authors.forename: Mingqi
authors.initials: M
authors.lastname: Zheng
authors.forename: Guoping
authors.initials: G
authors.lastname: Ma
authors.forename: Le
authors.initials: L
authors.lastname: Wang
authors.forename: Li
authors.initials: L
authors.lastname: Tian
authors.forename: Lishuang
authors.initials: L
authors.lastname: Ji
authors.forename: Lizhuo
authors.initials: L
authors.lastname: Li
authors.forename: Linan
authors.initials: L
authors.lastname: Duan
authors.forename: Kunshen
authors.initials: K
authors.lastname: Liu
mesh_terms: D015415:Biomarkers / Q000097:blood / Q000652:urine; D016207:Cytokines / Q000097:blood; D004231:Diuresis / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D005260:Female; D005938:Glucocorticoids / Q000008:administration & dosage / Q000627:therapeutic use*; D006333:Heart Failure / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology / Q000652:urine; D006801:Humans; D007668:Kidney / Q000187:drug effects* / Q000503:physiopathology; D007677:Kidney Function Tests; D008297:Male; D008875:Middle Aged; D011241:Prednisone / Q000008:administration & dosage / Q000627:therapeutic use*; D012964:Sodium / Q000652:urine*; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D016207:Cytokines; D005938:Glucocorticoids; D012964:Sodium; D011241:Prednisone