A case of normotensive primary aldosteronism with hypopituitarism, epilepsy, and medullary sponge kidney

1989 ◽  
Vol 121 (6) ◽  
pp. 797-801 ◽  
Author(s):  
Takeo Kuroda ◽  
Ken Okamura ◽  
Mototaka Yoshinari ◽  
Hiroshi Ikenoue ◽  
Kaori Sato ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Primary Aldosteronism ◽  
Metabolic Alkalosis ◽  
Plasma Renin ◽  
Normal Blood ◽  
Normal Blood Pressure ◽  
Medullary Sponge Kidney ◽  
High Potassium ◽  
Potassium Clearance

Abstract. A 55-year-old man with normotensive primary aldosteronism, hypopituitarism, epilepsy, and medullary sponge kidney is reported. Seventeen years before admission, he had been noted to have hypokalemia associated with high potassium clearance, suppressed plasma renin activity, metabolic alkalosis, and normal blood pressure as well as low urinary excretion of 17-hydroxycorticosteroids. He kept normotensive in spite of hyperaldosteronism until nine months after the initiation of replacement therapy with glucocorticoid and thyroxine for hypopituitarism, when he became hypertensive. Hypopituitarism seemed to play a role in keeping a normal blood pressure despite long-standing hyperaldosteronism.

scholarly journals Normal Blood Pressure and Plasma Renin Activity in Mice Lacking the Renin-binding Protein, a Cellular Renin Inhibitor

2000 ◽  
Vol 275 (20) ◽  
pp. 15357-15362 ◽  
Author(s):  
Christian Schmitz ◽  
Michael Gotthardt ◽  
Stephan Hinderlich ◽  
Jörg-Robert Leheste ◽  
Volkmar Gross ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Binding Protein ◽  
Protein A ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Inhibitor ◽  
Normal Blood ◽  
Normal Blood Pressure

Effect of Angiotensin II and Converting Enzyme Inhibitor (Captopril) on Blood Pressure, Plasma Renin Activity and Aldosterone in Primary Aldosteronism

1981 ◽  
Vol 61 (s7) ◽  
pp. 289s-293s ◽  
Author(s):  
F. Mantero ◽  
F. Fallo ◽  
G. Opocher ◽  
D. Armanini ◽  
M. Boscaro ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Primary Aldosteronism ◽  
Enzyme Inhibitor ◽  
Plasma Renin ◽  
Renin Activity ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitor ◽  
Idiopathic Hyperaldosteronism

1. Patients with idiopathic hyperaldosteronism (IHA) show a response of aldosterone to posture which is not present in patients with aldosterone-producing adenoma (APA). We have determined whether this could be explained by a different sensitivity to angiotensin II. 2. Angiotensin II was infused in gradually increasing doses in six patients with APA and in seven patients with IHA. No changes in aldosterone concentration were found at the end of each period in APA, whereas there was a significant increase in IHA; blood pressure rose by a similar extent in both groups. 3. In order to evaluate the role of endogenous angiotensin II, captopril, a converting enzyme inhibitor, was administered to six patients with APA and five patients with IHA at a dose of 75 mg/day for 1 week. There was a significant fall of mean blood pressure in IHA and only minimal changes in APA. Plasma renin activity and plasma and urinary aldosterone were unchanged in APA. In IHA there was a small increase in upright plasma renin activity and a slight decrease in both plasma and urinary aldosterone, but these changes were not significant. 4. These findings further support the idea that idiopathic hyperaldosteronism is a clinical state different from that occurring in primary aldosteronism due to adenoma, and may be more closely related to essential hypertension.

Renin and Aldosterone in Essential Hypertension

1971 ◽  
Vol 41 (4) ◽  
pp. 321-331 ◽  
Author(s):  
T. A. Kotchen ◽  
P. J. Mulrow ◽  
L. B. Morrow ◽  
P. M. Shutkin ◽  
N. Marieb
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Primary Aldosteronism ◽  
Plasma Renin ◽  
Upright Posture ◽  
Hypertensive Patients ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
History Of

1. The renin-aldosterone system was studied in seventy-one selected hypertensive patients. Nine (13%) were diagnosed as having primary aldosteronism. Of the twenty-three patients who presented with a history of unprovoked hypokalaemia, the incidence of primary aldosteronism was 40%. 2. Renin and aldosterone responses to the combined stimuli of a low sodium diet and the upright posture were suppressed in patients with essential hypertension. There was no evidence that the suppression was due to abnormal adrenal function, sympathetic neuropathy, or the level of the blood pressure. The mechanism of the suppressed plasma renin activity response and its significance in the pathogenesis of hypertension are unknown.

scholarly journals Rare Variant of Bartter Syndrome with Sensorineural Deafness

2016 ◽  
Vol 35 (3) ◽  
pp. 293-294
Author(s):  
Rajesh Kumar ◽  
Pankaj Kumar ◽  
Manoj Kumar
Keyword(s):  
Blood Pressure ◽  
Sodium Chloride ◽  
Rare Variant ◽  
Metabolic Alkalosis ◽  
Sensorineural Deafness ◽  
Bartter Syndrome ◽  
Normal Blood ◽  
Normal Blood Pressure ◽  
Renal Tubular Disorder ◽  
Renal Tubular

Bartter syndrome is an inherited renal tubular disorder characterized by hypokalemia, hypochloremic metabolic alkalosis, hyperreninemia, hyper-prostaglandinism, normal blood pressure, with increased urinary loss of sodium, chloride, potassium, calcium and prostaglandins. There are five known type of Bartter syndrome, out of which type 4 and 5 are very rare. We are presenting here a case of Bartter syndrome with sensorineural hearing loss.J Nepal Paediatr Soc 2015;35(3):293-294.

scholarly journals Intraoperative Hypertensive Crisis in a Patient with Normotensive Primary Aldosteronism. Lessons from a Clinical Case

2019 ◽  
pp. 1-7
Author(s):  
Agnieszka Kuzior ◽  
Manuel Esteban Nivelo-Rivadeneira ◽  
Paula Fernandez-Trujillo-Comenge ◽  
Esperanza Perdomo-Herrera ◽  
Alba Lucia Tocino-Hernandez ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Primary Aldosteronism ◽  
Peak Plasma ◽  
Left Kidney ◽  
Hypertensive Crisis ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renal Oncocytoma ◽  
Adequate Treatment

Primary hyperaldosteronism is the most frequent cause of secondary hypertension. However, it can also be found in apparently normotensive patients, often associated with recurrent hypokalemia and isolated hypertensive episodes. We hereby present the case of a normotensive 50-year-old female patient with a surgical left kidney mass; however, after anaesthetic induction, surgery was aborted due to a severe hypertensive crisis. She was referred to our Hypertension Outpatient Clinic to rule out pheochromocytoma/ paraganglioma. The anamnesis revealed unexplained episodes of hypokalemia. Ambulatory blood pressure monitoring showed normal mean values of blood pressure and heart rate, with an isolated hypertensive peak. Plasma glucose, ions, creatinine, lipids, metanephrines and chromogranin A were normal, but plasma aldosterone was clearly elevated with suppressed plasma renin activity and high aldosterone/renin activity ratio. Primary aldosteronism was confirmed by the captopril test. Abdominal CT was compatible with left adrenal hyperplasia. Treatment with low-dose spironolactone was well tolerated and resulted in normal blood pressure, normokalemia and unsuppressed plasma renin activity. The patient underwent successful laparoscopic removal of a renal oncocytoma.  We conclude that normotensive primary aldosteronism is not harmless; it can be associated with severe hypokalemia, anxiety, depression, hypertensive crisis and cardiovascular damage. Patients can also develop resistant hypertension. Adequate treatment can decisively improve the survival and quality of life of the patients with primary aldosteronism, but a correct diagnosis is needed first. Therefore, it must be considered as a diagnostic possibility in normotensive patients with unexplained hypokalemia or isolated hypertensive episodes.

scholarly journals SAT-563 The Unsuppressed Plasma Renin Activity May Not Enough for Management of Non-Surgically Treated Primary Aldosteronism

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Takamasa Ichijo ◽  
Moe Hayasaka ◽  
Takayuki Suzuki ◽  
Ayako Suzuki ◽  
Manabu Saito ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Primary Aldosteronism ◽  
Cardiovascular Events ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Aldosterone Concentration ◽  
Significant Difference ◽  
The Mean

Abstract It is well known the primary aldosteronism (PA) is most common endocrinological hypertension and accounted for 10% among all hypertension population, and it develops cardiovascular disease more frequently than blood pressure matched essential hypertension. Those patients with bilateral hyperaldosteronism, called idiopathic hyperaldosteronism (IHA), or unwilling for surgical treatment are treated by mineralcorticoid receptor antagonists (MRAs). Although it had been unclear how titrate MRAs to prevent atherosclerotic cardiovascular events, a managemental target for those patients was recently reported as plasma renin activity (PRA) ≥ 1.0 ng/ml/hr to prevent cardiovascular events (Hundemer GL, et. al. Lancet Diabetes Endocrinol. 2018 Jan;6(1):51-59). Thus, we investigated 77 cases of adrenal venous sampling performed patients with PA and followed up for 3 years in our hospital since 2007, including 24 males and 53 females, and their mean age was 56.3 ± 12.5 years old. All patients underwent AVS and showed bilateral hyperaldosteronism and treated with MRAs and followed up more than 3 years. We collected blood pressure, serum sodium and potassium concentration, estimated glomerular filtration ratio (eGFR), PRA, plasma aldosterone concentration (PAC), atherosclerotic parameter, such as mean intima media thickness (IMT), brachial-ankle pulse wave velocity (baPWV) and ankle-brachial index (ABI). We evaluated the relationship of those patients’ PRA and aldosterone to renin ratio (ARR) with eGFR, IMT, baPWV, and ABI. The change of mean IMT after 3 year-follow up were 0.03 ± 0.11 mm vs. 0.06 ± 0.09 mm for well controlled (PRA ≥ 1.0 ng/ml/hr) and poorly controlled (PRA < 1.0 ng/ml/hr), respectively, and no significant difference between them. In the other hand, the change of mean IMT after 3 year-follow up showed 0.03 ± 0.10 mm vs. 0.08 ± 0.10 mm for well controlled (PRA ≥ 1.0 ng/ml/hr and ARR <20) and poorly controlled (PRA < 1.0 ng/ml/hr or ARR ≥ 20), respectively, and the mean IMT increase was significantly lower in this group. The mean IMT increase showed significantly lower only with PRA ≥ 1.0 ng/ml/hr and ARR <20 rather than PRA ≥ 1.0 ng/ml/hr alone. In our results, both PRA ≥ 1.0 ng/ml/hr and ARR<20 are important to prevent or improve atherosclerosis, rather than only PRA ≥ 1.0 ng/ml/hr and should be titrated MRAs to achieve this target. In conclusion, our result revealed the titration of MRAs is important to prevent atherosclerotic cardiovascular event and not only PRA ≥ 1.0 ng/ml/hr, but both PRA and ARR <20 should be achieved.

MINERALOCORTICOID EXCESS IN TWO BROTHERS WITH DWARFISM, HYPOKALAEMIC ALKALOSIS AND NORMAL BLOOD PRESSURE

1967 ◽  
Vol 55 (4) ◽  
pp. 661-672 ◽  
Author(s):  
H. K. A. Visser ◽  
H. J. Degenhart ◽  
E. Desmit ◽  
W. S. Cost
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
Plasma Renin ◽  
High Plasma ◽  
Normal Blood ◽  
Normal Blood Pressure ◽  
Primary Defect ◽  
High Sodium ◽  
Regular Control ◽  
Renal Tubular

ABSTRACT Using isotope dilution methods the secretion rates of cortisol, aldosterone, deoxycorticosterone, corticosterone and 18-hydroxycorticosterone were determined in two brothers (76/12 and 108/12 years old) with dwarfism, chronic hypokalaemia alkalosis, tendency to hyponatraemia and normal blood pressure. Both patients showed a decreased response of the blood pressure to infused angiotensin. The urinary excretion of cortisol, cortisone, corticosterone, 11-dehydrocorticosterone and their tetrahydrometabolites as well as of aldosterone was determined. In general, results were in agreement with those of the secretion rate studies. The results suggest a relatively small mineralocorticoid excess (mainly corticosterone) to high plasma-renin concentrations. The differences in both the plasma-renin concentrations and the steroid secretory rates during low and high sodium intake indicate that the renin-angiotensin-mineralocorticoid system is still under regular control, although the normal regulatory process is severely disturbed. The primary defect in these patients is probably not a relative insensitivity of the arterial walls to the pressor effect of angiotensin as suggested by Bartter et al. (1962), but rather a renal tubular defect in the re-absorption of sodium.

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