Recent evidence indicates that prednisone
can potentiate renal responsiveness to diuretics in heart failure
(HF). However, the optimal dose of prednisone
is not known.
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.
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.
Only low-dose prednisone
significantly enhanced urine output. However, high-dose prednisone
induced a more potent renal sodium excretion than low-dose prednisone