Asymptomatic hyperuricaemia jeopardizes renal function reserve in healthy subjects: Early renovascular compromise is more robust in males

Abstract

IntroductionWhether asymptomatic hyperurcaemia (AH) necessitates treatment is controversial. Increased serum uric acid (sUA) promotes degradation of the vasodilator nitric oxide and may thus impair the renal vasodilator response. Thus, impaired renal function reserve (RFR) may be an early pathogenetic mechanism of ensuing renal disease in AH. Aim of the workTo study the effect of AH on the RFR in healthy subjects. Subjects and methodsClinical history, physical examination and laboratory investigations included fasting serum urea, creatinine, UA, glucose, glycated haemoglobin, electrolytes and proteinuria were measured in 66 healthy subjects. Abdominal ultrasonography was done. Average renal resistive index (RRI) in the 3 interlobar arteries bilaterally was measured at baseline (RRIPre) and 4-hours after ingestion of 1 g/kg protein meal, to yield RRIPost. RFR% was calculated as 100 × (RRIPre − RRIPost)/RRIPre. ResultsThe median age (IQR) of the patients was 46.5 (40–51.8 years); they were 38 males and 28 females with a sUA of 6.6 (5.5–8.1 mg/dl). Median RRIPre and RRIPost were 0.72 (0.62–0.76) and 0.59 (0.53–0.66), respectively. Median RFR was 14.3 (7.2–21.8%). There was a significant correlation between sUA and RRIPre (r = 0.3, p = 0.01) and was more robust in males (r = 0.5, p = 0.001). sUA ≥ 7.6 mg/dL was predictive of RRI > 0.7. RFR was significantly higher in subjects in the lowest sUA tertile (p = 0.004). ConclusionsIn AH, spectral Doppler may provide early evidence of renovascular dysfunction. Marginal sUA increases within normal range are associated with increased RRI and decreased RFR, particularly in males; possibly indicating early renovascular compromise.