This study was undertaken to evaluate the relation between the urinary excretion of guanidinoacetic acid (GAA) and other substances in hypertensive patients (6 with borderline hypertension and 29 with hypertension) and 12 normal controls. In 10 of the hypertensive patients, GAA was measured before and after 4 weeks of treatment with calcium entry blocker. In hypertensive patients the rate of GAA urinary excretion was 43.5 ± 17–4 μg/min, which was much lower than in the controls (77.2 ± 35.9 μg/min) (p < 0.01). There was no significant difference among these groups in creatinine clearance (CCr), serum creatinine (Cr), β2-microglobulin (BMG) or in the urinary excretion of BMG, N-acetyl-D-glucosaminidase (NAG) or radiosensitive microalbumin (mAlb). The urinary excretion rate of GAA was positively correlated with CCr (r = 0.62; p < 0.01), and negatively correlatd with mean blood pressure (r = -0.49; p < 0.01). Finally, the GAA excretion was significantly correlated with urinary NAG (r = 0.24; p < 0.05) and serum BMG (r = -0.31; p < 0.05), but not with urinary mAlb (r = 0.12; p > 0.05). Ten hypertensive patients followed for 4 weeks attained their ultimate mean blood pressure reduction after treatment (from 119.3 ± 8.0 to 101.7 ± 13.5 mm Hg; p < 0.001), but the GAA/Cr ratio in the urinary excretion was significantly elevated (from 0.054 ± 0.016 to 0.070 ± 0.02; p < 0.01). These findings show that in hypertension the urinary excretion rate of GAA may be a more sensitive indicator of renal damage than BMG, NGA, or mAlb and it can be elevated by successful antihypertensive therapy.

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