Introduction: It is well known that the deposition of uricacid crystals exert direct toxic effect on the renal parenchymaand vasculature. Both experimental and someclinical studies suggest the possibility that an increased uricacid level can lead to kidney disease even without depositionof uric acid crystals. However, other studies yieldedconflicting results, especially regarding the role of uric acidin the progression of established kidney disease.Aim: To evaluate retrospectively the relationship betweenasymptomatic hyperuricemia and renal function decline innon-gouty hypertensive patients.Methods: We enrolled 97 hypertensive subjects, 48 withchronic kidney diseases (CKD) and 49 without CKD. Fiftysevenof them had normal (N) serum uric acid (SUA) level(SUA\7 mg/dl in men and\6 mg/dl in women) and 40had hyperuricemia (U). Patients with hyperuricemia hadhigher systolic blood pressures and lower estimated glomerularfiltration rate (eGFR) than N. At the end of followupperiod (mean: 16 months), eGFR reduction was similarin the two groups (N: -3.6 ± 12.3; U: -3 ± 13.4 ml/min/1.73 m2).186Results: Two-way ANOVA showed that this result was notinfluenced by renal dysfunction, diabetes, macroproteinuria,gender or smoking habit. The percentage of subjectswith a value of eGFR reduction above the median was notsignificantly different in the two groups (N: 24.6 %; U:27.5 %). The absence of a significant difference betweenthe two groups, regarding the eGFR decline was confirmedby the multiple logistic regression analysis, where thevariables associated with a greater eGFR reduction wereonly the proteinuria and the smoking habit.Conclusions: Our findings do not support the hypothesis ofa significant effect of asymptomatic hyperuricemia on therenal function decline in subjects with arterialhypertension.
|Numero di pagine||1|
|Stato di pubblicazione||Published - 2013|