open access

Vol 8, No 6 (2004)
Prace oryginalne
Published online: 2004-12-14
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Mechanism of hyperuricemia in severe primary hypertension

Andrzej Tykarski, Paweł Łopatka, Anna Posadzy-Małaczyńska, Jerzy Głuszek
Nadciśnienie tętnicze 2004;8(6):411-423.

open access

Vol 8, No 6 (2004)
Prace oryginalne
Published online: 2004-12-14

Abstract

Background Studies concerning mechanisms of relationship between high blood pressure and high uric acid level were focused on mild to moderate forms of hypertension. Most reserarchers are of opinion that hyperuricemia in hypertensive patients is caused by impaired clearance of uric acid. This problem has not been investigated in severe forms of hypertension. The aim of the study was to find out the reason of freaquent incidence of hypeuricemia in patients with severe and treatment resistant forms of hypertension by means of evaluation of uric acid production and excretion.
Material and methods Sixty patients with primary hypertension aged 36 to 61 years (mean age 46.7 ± 6.2 years) including 30 patients with mild hypertension (group HT-M) and 30 patients with severe hypertension (group HT-S) were studied. Control group consisted of 30 normotensive subjects (group NT).
We measured serum uric acid (Pua) and oxypurines (Pox) concentration, activity of enzymes adenosine deaminase and AMP deaminase in red blood cells and evaluated clearance (Cua) and fractional excretion (FEua) of uric acid.
Results Mean Pua was 6.04 ± 1,5 mg/dl in hypertensives and 4.46 ± 1.1 mg/dl in normotensives (p < 0.0001). It was higher (p < 0.01) in HT-S group (6.57 ± 1.5 mg/dl) than in HT-M group (5.51 ± 1.3 mg/dl), while Cua was significantly (p < 0.05) lower in HT-S group (7.75 ± 1.2 ml/min) than in HT-M group (8.66 ± 1.9 ml/min). Similar differences in FEua were found.
Pox was significantly (p < 0.001) higher in hypertensives (9.07 ± 2.5 mg/dl) in comparison with control group (6.95 ± ± 2.9 mg/dl) and in HT-S group (9.55 ± 1.6 mg/dl) in comparison with HT-M group (7.59 ± 2.4 mg/dl). Pua to Pox ratio was significantly decreased (p < 0.05) in group HT-S (0.64 ± 0.17) comparing with group HT-M (0.78 ± 0.2).
Adenine and AMP deaminases activity was highest in severe hypertension (6.27 ± 1.3 c.u. and 5.75 ± 1.3 c.u. respectively) in comparison with mild hypertension (4.83 ± 1.2 c.u. i 4.84 ± 1.0 c.u. respectively) and with control subjects (4.39 ± 1.2 c.u. i 4.96 ± 1.2 c.u. respectively).
Conclusions 1. Plasma uric acid level and prevalance of hyperuricemia is higher in severe hypertension than in mild hypertension. 2. Renal excretion of uric acid is more impaired in severe forms of hypertension. 3. Results of Pua/Pox ratio and red blood cells activity of adenine and AMP deaminases suggests that also uric acid production (i.e. purine nucleotides degradation and conversion of oxypurines to uric acid) is increased in severe hypertension.

Abstract

Background Studies concerning mechanisms of relationship between high blood pressure and high uric acid level were focused on mild to moderate forms of hypertension. Most reserarchers are of opinion that hyperuricemia in hypertensive patients is caused by impaired clearance of uric acid. This problem has not been investigated in severe forms of hypertension. The aim of the study was to find out the reason of freaquent incidence of hypeuricemia in patients with severe and treatment resistant forms of hypertension by means of evaluation of uric acid production and excretion.
Material and methods Sixty patients with primary hypertension aged 36 to 61 years (mean age 46.7 ± 6.2 years) including 30 patients with mild hypertension (group HT-M) and 30 patients with severe hypertension (group HT-S) were studied. Control group consisted of 30 normotensive subjects (group NT).
We measured serum uric acid (Pua) and oxypurines (Pox) concentration, activity of enzymes adenosine deaminase and AMP deaminase in red blood cells and evaluated clearance (Cua) and fractional excretion (FEua) of uric acid.
Results Mean Pua was 6.04 ± 1,5 mg/dl in hypertensives and 4.46 ± 1.1 mg/dl in normotensives (p < 0.0001). It was higher (p < 0.01) in HT-S group (6.57 ± 1.5 mg/dl) than in HT-M group (5.51 ± 1.3 mg/dl), while Cua was significantly (p < 0.05) lower in HT-S group (7.75 ± 1.2 ml/min) than in HT-M group (8.66 ± 1.9 ml/min). Similar differences in FEua were found.
Pox was significantly (p < 0.001) higher in hypertensives (9.07 ± 2.5 mg/dl) in comparison with control group (6.95 ± ± 2.9 mg/dl) and in HT-S group (9.55 ± 1.6 mg/dl) in comparison with HT-M group (7.59 ± 2.4 mg/dl). Pua to Pox ratio was significantly decreased (p < 0.05) in group HT-S (0.64 ± 0.17) comparing with group HT-M (0.78 ± 0.2).
Adenine and AMP deaminases activity was highest in severe hypertension (6.27 ± 1.3 c.u. and 5.75 ± 1.3 c.u. respectively) in comparison with mild hypertension (4.83 ± 1.2 c.u. i 4.84 ± 1.0 c.u. respectively) and with control subjects (4.39 ± 1.2 c.u. i 4.96 ± 1.2 c.u. respectively).
Conclusions 1. Plasma uric acid level and prevalance of hyperuricemia is higher in severe hypertension than in mild hypertension. 2. Renal excretion of uric acid is more impaired in severe forms of hypertension. 3. Results of Pua/Pox ratio and red blood cells activity of adenine and AMP deaminases suggests that also uric acid production (i.e. purine nucleotides degradation and conversion of oxypurines to uric acid) is increased in severe hypertension.
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Keywords

hyperuricemia; uric acid; severe hypertension

About this article
Title

Mechanism of hyperuricemia in severe primary hypertension

Journal

Arterial Hypertension

Issue

Vol 8, No 6 (2004)

Pages

411-423

Published online

2004-12-14

Bibliographic record

Nadciśnienie tętnicze 2004;8(6):411-423.

Keywords

hyperuricemia
uric acid
severe hypertension

Authors

Andrzej Tykarski
Paweł Łopatka
Anna Posadzy-Małaczyńska
Jerzy Głuszek

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