How renal response differs in gout and healthy patients?

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How renal response differs in gout and healthy patients?

Gout is characterized by sudden, severe attacks of pain, redness and tenderness in joints, often the joint at the base of the big toe. Men are more likely to get gout and women become susceptible to gout after menopause. Gout is triggered with excess uric acid in blood which causes pain and inflammation.

To determine whether a change in serum uric acid (sUA) levels results in the corresponding change in the fractional excretion of uric acid (FEUA) and also to check the renal response in different patients who are suffering from gout versus healthy subjects, a study was conducted.

The fractional excretion of uric acid was calculated from previous studies and four new phase I studies in healthy patients with gout before and after treatment to lower or raise sUA. Patients were given xanthine oxidase to inhibit or lower sUA as well as infusion of uric acid and provision of high-purine diet to raise sUA. Graphs were plotted of FEUA versus sUA before and after treatment. Percent change in FEUA per mg/dL change in sUA for the phase I studies were calculated separately in healthy subjects and those with gout. The results were compared using Student's t test.

After comparing previous data and new phase I clinical data, results were evaluated that changing sUA by a non-renal mechanism leads to a change in FEUA. The magnitude of change is greater in subjects with higher baseline of FEUA that with gout. The healthy patients excreted more urate than patients with gout at physiological urate filtered load. Difference was disappeared when the urate-filtered load is decreased to ~5000 mg/24 hours.

After evaluation, it was concluded that there are consistent observations in patients with less saturated urate reabsorption system in patients with gout versus healthy subjects which resulted in elevated retention of uric acid. But, further investigation is still needed which could lead to the discovery of mechanisms responsible for the etiology of hyperuricemia/ gout.

Joint Bone Spine
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