Prednisone in Uric Acid Lowering in Symptomatic Heart Failure Patients with Hyperuricemia — The PUSH-PATH3 Study

DISCUSSION

Prednisone resulted in a striking SUA reduction, as well as a significant improvement in renal function in the symptomatic HF patients with hyperuricemia. These favorable effects induced by prednisone were accompanied by a dramatic increase in urine output and an improvement in clinical status. We used prednisone as an add-on therapy. Therefore, our data did not support the use of glucocorticoids (GC) in lieu of diuretics.

Uric acid is the final product of purine degradation with xanthine oxidase, an enzyme implicated as a mechanistic participant in oxidant stress. About 70% of the uric acid is excreted through the kidneys and 30% through the gastrointestinal tract11. Hyperuricemia results from either over-production or reduced excretion of uric acid, or both. In decompensated HF, glomerular filtration and tubular excretion of UA are impaired as a result of venous congestion3,12. The level of SCr reduction was well correlated with the level of SUA, indicating renal function improvement contributed much to SUA lowering in HF. Additionally, gout is a common comorbidity in patients with HF5. However, drug options are restricted. HF therapy and pharmacological agents used for gout exclude nonsteroidal antiinflammatory drugs because of their nephrotoxicity. Therefore, a drug that can lower UA and treat gouty arthritis as well as induce potent diuresis will be ideal in this setting.

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It is noteworthy that renal-protective effects induced by prednisone were accompanied by a potent diuresis in symptomatic patients with systolic HF. Coupled with the newly emerging evidence that oral prednisolone and naproxen are equally effective in the initial treatment of gouty arthritis13, prednisone might be the drug of choice for HF patients with hyperuricemia or gouty arthritis.

The role of GC in HF has changed. Using corticosteroids to treat HF was first reported in the 1950s7. With the advent of a potent diuretic such as furosemide, intractable cardiac edema became less intractable and GC vanished from the treatment of HF7,8. However, data show that GC can successfully overcome diuretic resistance in the patients who fail to respond to loop or combined diuretic therapy7,14. We demonstrated that GC could improve renal responsiveness to atrial natriuretic peptide by upregulating natriuretic peptide receptor-A expression in the inner medullary collecting duct cells both in vivo and in vitro, and produce a potent diuretic action in decompensated HF15. Moreover, there is evidence demonstrating that GC can dilate renal vasculature and increase renal plasma flow and glomerular filtration rate, a process that involves multiple pathways such as increased renal prostaglandin, nitric oxide, and dopamine production7,8.

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