Key result
Acute cerebral hemorrhage is linked to elevated plasma renin activity that parallels clinical severity.
Why the study?
The changes in plasma renin activity levels following acute cerebrovascular disease attacks and their clinical significance were not well understood.
Observational (n=45)
Plasma renin activity increases following acute cerebrovascular events, correlating with clinical prognosis and survival rather than acting as a causative factor.
Answers are grounded in this paper and cite their sources.
Elevated renin after cerebral hemorrhage may reflect severity rather than drive events; leaves open whether renin modulation affects cerebrovascular outcomes.
Serial estimations of plasma renin activity (PRA) were carried out on patients with cerebrovascular diseases (CVD) to investigate the changes of PRA levels following the attack.Samples were collected at 24 hrs after the acute attack, and every week thereafter at 6:00A.M. from following patients in the supine position: 4 patients with cerebrovascular hemorrhage, 5 with cerebral thrombosis, 6 with traumatic sub-arachnoid hemorrhage, and 4 cases with recurrent stroke. As the control, PRA in the age-matched normal subjects was measured under the same condition. PRA was determined by radioimmunoassay using RENIN RIAKIT. Levels more than 1.98ng/ml/h (mean+2S.D. of normal persons 42 to 79 years old) are considered to be high PRA.Patients with cerebral hemorrhage had markedly elevated PRA at 24 hrs after the attack (3.6±1.1ng/ml/h) and increased further to reach the maximal value of 6.6±0.7ng/ml/h. While those with traumatic subarachnoid hemorrhage showed normal PRA levels (1.5±0.5ng/ml/h) at 24 hrs, which increased later reaching the peak of 2.7±0.3ng/ml/h. PRA in thrombosis was normal at 24hrs and slowly elevated. The peak value (3.7±0.5ng/ml/h) was obtained during 1 to 4 weeks after the attack. In survival cases of these patients, elevated PRA levels gradually decreased, whereas in fatal cases, PRA levels remained elevated. No correlation was found between the PRA levels and the blood pressure. The same results were obtained in 4 patients with recurrent CVD attack. PRA levels of these patients were increase after the second attack of CVD, although PRA levels before the attack were within normal range.These findings suggest that the elevated levels of PRA found in patients with CVD may not be a causative factor for CVD but may be the results of CVD.The present studies demonstrate that plasma levels of renin activity change in parallel with the clinical situation of the disease, and that the elevated levels of PRA indicate the existence of vascular disturbance but also the decrease of cerebral blood flow. Therefore, measurement of PRA levels seems to be a prognostic value of CVD.
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Reiko OTSUKI (1982) conducted an observational in Acute cerebrovascular diseases (n=45). Acute cerebrovascular disease vs. Healthy controls was evaluated on Plasma renin activity at 24 hours post-attack in cerebral hemorrhage patients. Acute cerebrovascular disease, particularly cerebral hemorrhage, caused markedly elevated plasma renin activity at 24 hours that paralleled clinical severity, indicating it is a result rather than a cause of the disease.
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