Tykarski A, Głuszek J, Banaszak F
Kliniki Nadciśnienia Tetniczego I.K. AM, Poznaniu.
Pol Arch Med Wewn. 1993 Mar;89(3):223-9.
Serum uric acid and oxypurines (hypoxanthine and xanthine) renal excretion of uric acid and oxypurines as well as plasma adenosine deaminase activity and AMP deaminase activity were studied in 18 patients with essential hypertension and in 17 healthy subjects. The aim of the study was to evaluate uric acid production rate in essential hypertension. Serum uric acid was significantly higher (7.04 +/- 2.03 mg% = 370.5 +/- 106 mumol/l; p < 0.01) in essential hypertension in comparison with control group (5.2 +/- 1.0 mg% = 275.0 +/- 51.9 mumol/l) and plasma oxypurines were increased insignificantly. Impairment of fractional excretion of uric acid (p < 0.05) was found in patients with essential hypertension. Plasma adenosine deaminase activity and plasma AMP deaminase activity did not differ in the studied groups. Increased production of uric acid does not contribute the incidence of hyperuricemia in essential hypertension. The results suggest that tubular defect of oxypurines excretion similar to that of uric acid exists in patients with essential hypertension.
对18例原发性高血压患者和17名健康受试者的血清尿酸和氧嘌呤（次黄嘌呤和黄嘌呤）、尿酸和氧嘌呤的肾脏排泄以及血浆腺苷脱氨酶活性和AMP脱氨酶活性进行了研究。本研究的目的是评估原发性高血压患者的尿酸生成率。与对照组（5.2±1.0mg% = 275.0±51.9μmol/L）相比，原发性高血压患者的血清尿酸显著更高（7.04±2.03mg% = 370.5±106μmol/L；p<0.01），血浆氧嘌呤略有升高。原发性高血压患者的尿酸排泄分数受损（p<0.05）。所研究的两组中血浆腺苷脱氨酶活性和血浆AMP脱氨酶活性无差异。尿酸生成增加并非原发性高血压患者高尿酸血症发生的原因。结果表明，原发性高血压患者存在与尿酸类似的氧嘌呤排泄肾小管缺陷。
