Studies on Renal Uric Acid Metabolism in Patients with Primary Aldosteronism Comparisons with Normotensive Subjects or Essential Hypertensives

It is recognized that hyperuricemia induces gouty attacks, and is also one of the risk factors for cardiovascular, and renal diseases. It is reported that the incidence of hyperuricemia among essential hypertensives is very high, and that it is caused by a decrease in renal excretion of uric acid. However, the detailed mechanism of renal uric acid metabolism in primary aldosteronism, of secondary hypertension, is not clarified yet. Therefore, this study was conducted to elucidate renal uric acid metabolism in 16 patients with primary aldosteronism (PA) as compared with 25 normotensive subjects (NT) and 34 essential hypertensives (low renin hypertensives (LRH), 11 cases, and normal renin hypertensives (NRH), 23 cases). All subjects were hospitalized and received a regular diet (Na; 120 mEq, K; 75 mEq, daily) for more than two weeks, after which renal clearance tests were performed, and serum uric acid (SUA) levels, fractional excretions of uric acid (FEUA), sodium (FENa), and inorganic phosphorus (FEp) were determined. Furthermore, the effects of adrenalectomy on SUA, FEUA, FENa, and FEp were evaluated in 8 cases of PA. SUA was lower in PA than in LRH, NRH or NT, and the decrease of SUA was more obvious in male subjects. FEUA, an index of renal excretion of uric acid, correlated negatively with SUA and positively with both FENa, an index of renal excretion of sodium, and FEp, an index of excretion of sodium at the renal proximal tubules, in each 4 groups. FEUA and FEp were significantly higher in PA than in LRH, NRH or NT. A significant increase in SUA, and significant decreases in FEUA and FEP were observed after the surgical extraction of the adrenal adenoma in PA compared to levels before the surgery. These results suggest that uric acid transport may be closely related to sodium transport in the renal tubules, particularly at the proximal site, and the lower SUA in PA might result from the suppression of reabsorption and/or an enhancement of secretion of uric acid in the renal proximal tubules, being related to the escape phenomenon