Objective. To determine the safety and efficacy of prednisone in patients with symptomatic heart failure (HF) and hyperuricemia.

This study raises more questions than what it seeks to answer (as good research should), and what it does not say is more interesting than what it does. So you need an editorial to say all that (click on the link to the editorial at the bottom of the PUSH-PATH3 abstract).
The research question is straight forward enough: Is it safe to use glucocorticosteroid to treat gouty attacks in renally impaired patients suffering from classes 3 or 4 (severe) congestive heart failure?
The answer resulting from this elegant study is: YES, it is both safe and effective.
Why would you want to use steroid in this situation? Because the usual alternatives for treating acute Gout are potentially far more hazardous: NSAIDs can worsen kidney failure, and Colchicine can accumulate in renal impairment to cause toxicities like marrow suppression. Of course there’s Pegloticase and Canakinumab too, the latter at SGD20000 per pop.
Why are you concerned about steroid in this context? It can worsen heart failure and pulmonary oedema by retaining sodium and causing hypokaelaemia. It may also worsen heart failure through inhibition of TNF, like Infliximab may and therefore contraindicated in classes 3 & 4 CCF.
Surprisingly, none of the nasties happened. Instead, not only did it resolve the Gout attack (as expected), serum uric acid dropped by a whopping 3mg% (unexpected as it is not known to be a uricosuric agent), the renal impairment and heart failure improved too, with serum Creatinine lowering and diuresis ensuing.
Naturally, all these left us speculating “why”:
1) The heart failure obviously improved due to diuresis, which occurred as the renal impairment improved. But could it be that inhibition of TNF or other mediators of inflammation actually improved cardiac function directly?
2) The Gout attack resolved due to the steroid calming the inflammasome. But why was there such a dramatic urate lowering? Obviously the ensuing diuresis excreted the uric acid along with it. Or does steroid have a direct uricosuric or xanthine oxidase inhibitory effect as well?
3) The kidneys improved, resulting in a diuresis, lowering serum uric acid and resolving the heart failure. But how? It is known that uric acid is highly nephrotoxic. Perhaps the steroid limited the collateral inflammatory damage from the uric acid.
It’s a shame such good, simple and clinically important studies don’t get done much anymore. Big Pharma will rather vilify steroids to promote their costly targeted therapies and patented drugs. Inflammation is the real enemy, the rampaging bull in the fine china store. For all inflammatory diseases, we need to act decisively and aggressively, taking the bull by the horns as it were, by treating the inflammation to full remission, with whatever it takes (including “nasty” steroids).

Urate lowering therapies in the treatment of gout: a systematic review and meta-analysis

OBJECTIVE: In patients with gout, serum uric acid (sUA) concentrations should be lowered at least…

In a country like the USA where cost is no issue, and far more effective urate lowering therapies (ULT) like Benzbromarone are not made available due to exaggerated hepatotoxicity concerns, and even Lesinurad has to be co-prescribed with an XOI; then yes, Febuxostat is the best there is.
But for the overwhelming majority of Gout sufferers who are under-excretors, uricouric agents like Benzbromarone easily halves serum uric acid, and it is very safe with regular monitoring and obsessive hydration.
Only in those who fail to achieve target (and I’m now very stringent about SUA <5mg% especially for those with sonographically/DECT detected tophi), that I add on (not replace with) an XOI (Allopurinol or Febuxostat).

Arhalofenate lowered uric acid and also prevented flares in a phase IIb trial

We all love 2-(or more)-in-1, and along comes Arhalofenate which is both uricosuric (inhibits URAT1) and anti IL1. Too bad its efficacy in trial dose is underwhelming in both roles.

Objective Gout, caused by hyperuricaemia, is a multifactorial disease. Although genome-wide association studies (GWASs) of gout have been reported, they included self-reported gout cases in which clinical information was insufficient.…

For treatment of Gout, augmenting urate excretion is the way to go for 95% of patients.
This Genome Wide Association Study (GWAS) to sieve out key operative genes in Gout patients, not only yielded ABCG2 and URAT1 which are major urate transporters in gut and kidneys (not surprising), but also other genes involved with lipid and glucose metabolism.
This is very interesting as it demonstrates a genetic link among the diseases of the Metabolic Syndrome. The message to me is that I need to treat every single one of these diseases to target to prevent cardiovascular complications.