Malignant Phase Hypertension Research Articles

The Case for Treating Severe Hypertension; Two Reversible Complications of Malignant Phase Hypertension; Renin-Secreting Tumours Another Reversible Cause of Secondary Aldosteronism in Hypertension

The Case for Treating Severe Hypertension; Two Reversible Complications of Malignant Phase Hypertension; Renin-Secreting Tumours Another Reversible Cause of Secondary Aldosteronism in Hypertension

Malignant hypertension: effect of therapy on renin and aldosterone.

Plasma renin activity (PRA) and aldosterone secretion rate (ASR) were measured in 22 patients in balance on a 100 mEq sodium diet during the malignant phase of hypertension and at intervals during long-term follow-up on pharmacological therapy. Three patients had normal PRA and ASR during malignant hypertension. Eighty-six per cent of patients had an increased ASR, but only in 36% was PRA concomitantly increased during malignant hypertension (one patient developed elevated PRA in the postmalignant period). PRA fell to normal in 87% of patients after antihypertensive therapy. ASR fell to normal on drug therapy in six patients, and in all of these there was a period during the postmalignant phase in which ASR was increased while PRA was normal or suppressed. In addition to this group with reversible hyperaldosteronism, all but two of the remaining patients with elevated ASR had periods during which ASR was increased at the same time that PRA was normal or suppressed. These data raise the possibility that either a nonrenin aldosterone-stimulating hormone is secreted in malignant hypertension or that excessive stimulation of the adrenal by angiotensin can lead to persistent hyperfunction of aldosterone-secreting cells with a quantitatively deranged feedback control. One patient had an aldosterone-secreting adenoma and had manifestations of the hyperaldosteronism antedating the development of malignant hypertension.

Malignant Hypertension: Effect of Therapy on Renin and Aldosterone

Plasma renin activity (PRA) and aldosterone secretion rate (ASR) were measured in 22 patients in balance on a 100 mEq sodium diet during the malignant phase of hypertension and at intervals during long-term follow-up on pharmacological therapy. Three patients had normal PRA and ASR during malignant hypertension. Eighty-six per cent of patients had an increased ASR, but only in 36% was PRA concomitantly increased during malignant hypertension (one patient developed elevated PRA in the postmalignant period). PRA fell to normal in 87% of patients after antihypertensive therapy. ASR fell to normal on drug therapy in six patients, and in all of these there was a period during the postmalignant phase in which ASR was increased while PRA was normal or suppressed. In addition to this group with reversible hyperaldosteronism, all but two of the remaining patients with elevated ASR had periods during which ASR was increased at the same time that PRA was normal or suppressed. These data raise the possibility that either a nonrenin aldosterone-stimulating hormone is secreted in malignant hypertension or that excessive stimulation of the adrenal by angiotensin can lead to persistent hyperfunction of aldosterone-secreting cells with a quantitatively deranged feedback control. One patient had an aldosterone-secreting adenoma and had manifestations of the hyperaldosteronism antedating the development of malignant hypertension.

Microangipathic hemolytic anemia and the development of the malignant phase of hypertension.

Evidence of microangiopathic hemolytic anemia (MHA) was found in 14 of 22 patients with malignant phase hypertension, and in one of these, a patient with proliferative glomerulonephritis, MHA and m...

Microangiopathic Hemolytic Anemia and the Development of the Malignant Phase of Hypertension

Evidence of microangiopathic hemolytic anemia (MHA) was found in 14 of 22 patients with malignant phase hypertension, and in one of these, a patient with proliferative glomerulonephritis, MHA and malignant hypertension developed together during a three-month period of observation. Among 61 rats subjected to unilateral nephrectomy, injected with DOCA, and given 1% saline to drink, 42 developed evidence of MHA. Eighty-four per cent of these also had fibrinoid necrosis and/or plasmatic vasculosis in the remaining kidney at autopsy. Blood pressure rose to 150 mm Hg or more in 72% of these DOCA-injected animals. In 29 control rats subjected to unilateral nephrectomy only, blood pressure rose to 150 mm Hg or more in 21%, MHA developed in 14%, and fibrinoid lesions were found in none. The significance of these observations is discussed in relation to the possibility that MHA is either a consequence of malignant hypertension or a contributory factor in its pathogenesis.

MICROANGIOPATHIC HÆMOLYTIC ANÆMIA AND THE PATHOGENESIS OF MALIGNANT HYPERTENSION

The relation between severe hypertension and microangiopathic hæmolytic anæmia (M.H.A.) was explored in detail in nine patients with both conditions. Blood-films were also examined in eighty-seven cases of hypertension. Of twenty-four patients with malignant-phase hypertension, sixteen had evidence of M.H.A.: of the remaining patients none had evidence of M.H.A. A hypothesis is suggested for the relation between M.H.A. and malignant hypertension in which the following are the important steps: high arterial pressure or primary vascular disease increases the permeability of small blood-vessels to fibrinogen; fibrin is deposited in the wall and lumen of vessels, and persists either because the deposition of new fibrin is increased or because fibrinolysis is impaired; fibrin deposits fragment red blood-cells, leading to hæmolysis and further deposition of fibrin.

Hypertensive Vascular Disease Induced by Heterologous Renin

Chronic treatment with crude hog, or rat, renin administered subcutaneously to uninephrectomized rats elicits hypertension, renal and vascular lesions, hypertrophy of the zona glomerulosa of the adrenals, and renin depletion in the remaining kidney. Semipurified hog renin given in equipressor doses also causes renin depletion and stimulation of the zona glomerulosa, but no hypertension nor vascular disease. However, semipurified hog renin becomes as effective as the crude preparation after addition of retarding substances such as gelatin, oil, or cholesterol. Thus, a prolonged and sustained resorption of renin seems to be a prerequisite for the development of hypertension. Since hypertension takes place only after a latent period during which arterial pressure remains within the normal range, it does not appear that hypertension can be attributed to the acute pressor effect of renin. It is proposed as a working hypothesis that renin, through angiotensin, initiates nervous mechanisms which are responsible for the development of benign hypertension and that the acute pressor effect of angiotensin is more specifically associated with the malignant phase of hypertension.

The Response of Metabolic Alkalosis in Severe Hypertension to Antihypertensive Drugs

Case Studies1 February 1963The Response of Metabolic Alkalosis in Severe Hypertension to Antihypertensive DrugsMARK L. ARMSTRONG, M.D., ANNETTE E. FITZ, M.D., LOUIS SCHWARTZ, M.D.MARK L. ARMSTRONG, M.D.Search for more papers by this author, ANNETTE E. FITZ, M.D.Search for more papers by this author, LOUIS SCHWARTZ, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-58-2-336 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptA case of metabolic alkalosis that occurred in association with idiopathic malignant hypertension and disappeared after antihypertensive drug therapy is reported.Hypertensive disease per se has no connotation of electrolyte or acid-base disturbance. Even in the malignant phase of hypertension, electrolyte balance is usually normal (1), or only mildly changed (2), before renal insufficiency or congestive heart failure occurs. However, aldosterone excretion tends to increase throughout all levels of hypertension (3-5), and may increase remarkably in malignant hypertension (2). Against such a background, evidence (6-8) suggests that distinct alkalosis occasionally arises as a metabolic concomitant of hypertension.CASE REPORTA...

The treatment of malignant hypertension ∗

In malignant hypertension the blood pressure must be reduced as a matter of urgency and by the best means available. Difficulties such as renal impairment are encountered more frequently than in the less severe grades of hypertension; patients with malignant hypertension therefore require close observation and meticulous care. Although by these means the five-year survival rate can be vastly improved, it is difficult to obtain more than about 50 per cent. It is evident that the malignant phase of hypertension should, if possible, be prevented, and there is some evidence that it is in fact becoming less common. This may be due to the widespread use of antihypertensive drugs in less severe cases, a proportion of whom might otherwise have developed the malignant phase.

STUDIES ON EXPERIMENTAL HYPERTENSION

STUDIES ON EXPERIMENTAL HYPERTENSION