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PubMed1998

Hormonal characteristics of primary aldosteronism due to unilateral adrenal hyperplasia.

A case of unilateral adrenocortical hyperplasia is presented. A 46-year-old woman with a 7-year history of hypertension and a 1-year-history of hypokalemia was diagnosed with primary aldosteronism. Computed tomography, magnetic resonance imaging, venous sampling and adosterol scintigraphy exhibited a functioning left adrenal mass. The plasma aldosterone concentration increased markedly when furosemide with upright posture and either captopril or adrenocorticotropin were administered. Plasma renin activity was suppressed below the detectable range. Aldosterone secretion displayed a circadian rhythm and was not suppressed by dexamethasone administration. The resected left adrenal mass was pathologically diagnosed as adrenocortical nodular hyperplasia. Unilateral adrenal hyperplasia involving the zona glomerulosa rarely has been reported, with varying and incompletely characterized hormonal characteristics. This case report and literature review suggest unilateral adrenal hyperplasia as a rare cause of hyperaldosteronism with characteristics intermediate between idiopathic hyperaldosteronism and aldosterone-producing adrenocortical adenoma, resembling the functional features of the adenoma more closely.

Adrenal Cortex↗

PubMedDate not supplied

Primary aldosteronism.

The basic clinical pathophysiology of primary aldosteronism (PAL) was described by Conn in terms of autonomous production of aldosterone, secondary suppression of renin and development of hypertension with hypokalaemic alkalosis. Conn recognised a normokalaemic form of the syndrome and suggested that it might masquerade as essential hypertension and be not uncommon. This was hotly disputed at the time, and normokalaemic PAL considered rare until recently, and, as a consequence, overlooked. The advent of a simple screening test, the aldosterone-renin ratio, led to recognition that normokalaemic forms are not uncommon. In fact, PAL may be the commonest specifically treatable and potentially curable form of hypertension so far identified. In all patients with PAL confirmed by lack of suppressibility ("autonomy") of aldosterone production, Familial Hyperaldosteronism Type I (FH-I, glucocorticoid-remediable hyperaldosteronism, reviewed elsewhere in this issue) should first be excluded by dexamethasone suppression or genetic testing. Capable of causing fatal stroke in young people affected by this dominantly inherited disorder, it can be reversed by doses of glucocorticoids such as dexamethasone which partially suppress endogenous ACTH without producing "steroid" side-effects. The remaining varieties of PAL may eventually also be shown to have a genetic basis, but are currently treated either by excision of a solitary aldosterone-secreting tumour or by antagonism of aldosterone's action in the renal tubule. It is possible that both adrenal cortices are genetically predisposed to overproduction of aldosterone in all varieties of PAL, whether because of anomalous regulation of aldosterone secretion or because of a tendency towards hyperplasia and neoplasia. Aldosterone-producing adenomas (APA's) can be divided into two main subtypes based on morphology and biochemical behaviour. The first subtype to be morphologically and biochemically characterised is composed predominantly of fasciculata-like cells and is unresponsive to angiotensin II (ALL-U-APA). The more recently characterised subtype is composed predominantly of glomerulosa-like cells, is responsive to angiotensin II (AII-R-APA) and could previously have been misdiagnosed as bilateral hyperplasia. The renin gene is often overexpressed in the second variety of adenoma, and in surrounding non-tumorous cortex, and the two subgroups show different allelic frequencies for RFLP's of the constitutive renin gene and the constitutive ANP gene locus. Unilateral, solitary, benign adrenal cortical adenomas producing aldosterone (APA's) represent a potentially surgically curable form of hypertension. Adrenal venous sampling (AVS) should always be performed because APA's are biochemically recognisable by adrenal venous steroid measurement before they are identifiable by computerised tomography or scintigraphy, and adrenal masses seen on CT may not be responsible for PAL. The secretory activity of adrenal masses must therefore be established by AVS before surgical removal. Discovery of an adrenal mass on CT requires formulation of a plan, whether or not it is found to be secreting hormones in excess. Independently of the treatment of the patient's hypertension, an apparently nonfunctioning adrenal mass ("incidentaloma") should be removed if 2.5 cm or more in diameter, because of the risk of cancer. Smaller masses require long-term follow-up. Primary aldosteronism not lateralising on AVS should be treated with low dose spironolactone, or with amiloride. For any such patients intolerant of medical treatment, laparoscopic removal of the adrenal showing higher production of aldosterone on AVS is an option worthy of consideration.The resultant reduction in mass of tissue autonomously secreting aldosterone should improve hypertension, as aldosterone productions falls below a critical level, and may even be curative in the short, medium or long term, depending on the rate of growth and activity of au

Humans↗

PubMed2003

Non-glucocorticoid-remediable aldosteronism in an infant with low-renin hypertension.

A 6-week-old male with severe hypertension is presented. He was found to have hyperaldosteronism and a negative long polymerase chain reaction (PCR) test for glucocorticoid-remediable aldosteronism. His mother and maternal grandfather also had severe hypertension. A case is made for the possible diagnosis of familial hyperaldosteronism type II at a very early age.

Drug Resistance↗

PubMed1975

Bartter's syndrome. New insights into pathogenesis and treatment.

Discussed here is a patient with normotension, hypokalemic alkalosis, hyperreninemia, hyperaldosteronism, juxtaglomerular cell hyperplasia and insensitivity to the pressor effects of angiotensin (Bartter's syndrome). The hyperreninemia and hyperaldosteronism were both suppressible with volume expansion. Hypokalemia was correctible both short-term with potassium chloride infusions and long-term with spironolactone. Nevertheless, the abnormal pressor response to infused angiotensin could not be corrected by these maeuvers, suggesting that this defect is likely to be of primary pathophysiologic significance. We found that potassium loading markedly stimulated aldosterone excretion. This may explain the inadequacy of potassium supplementation alone to correct the hypokalemia and the observed "escape" from the potassium conserving effects of spironolactone seen in patients with Bartter's syndrome. The administration of propranolol in large doses only partially suppressed the marked hyperreniemia of our patient and failed to prevent a subsequent rise in the renin level which was associated with spironolactone therapy. In contrast, suppression of the renin level to normal was demonstrated by sodium loading. It is suggested that patients with Bartter's syndrome be treated simultaneously with large doses of spironolactone and a high sodium intake.

Adult↗

PubMed1994

Pathophysiology of potassium absorption and secretion by the human intestine.

When normal people ingest 90 mEq/day of K+ in their diet, they absorb about 90% of intake (81 mEq) and excrete an equivalent amount of K+ in the urine. Normal fecal K+ excretion averages about 9 mEq/day. The vast majority of intestinal K+ absorption occurs in the small intestine; the contribution of the normal colon to net K+ absorption and secretion is trivial. K+ is absorbed or secreted mainly by passive mechanisms; the rectum and perhaps the sigmoid colon have the capacity to actively secrete K+, but the quantitative and physiological significance of this active secretion is uncertain. Hyperaldosteronism increases fecal K+ excretion by about 3 mEq/day in people with otherwise normal intestinal tracts. Cation exchange resin by mouth can increase fecal K+ excretion to 40 mEq/day. The absorptive mechanisms of K+ are not disturbed by diarrhea per se, but fecal K+ losses are increased in diarrheal diseases by unabsorbed anions (which obligate K+), by electrochemical gradients secondary to active chloride secretion, and probably by secondary hyperaldosteronism. In diarrhea, total body K+ can be reduced by two mechanisms: loss of muscle mass because of malnutrition and reduced net absorption of K+; only the latter causes hypokalemia. Balance studies in patients with diarrhea are exceedingly rare, but available data emphasize an important role for dietary K+ intake, renal K+ excretion, and fecal K+ losses in determining whether or not a patient develops hypokalemia. The paradoxical negative K+ balance induced by ureterosigmoid anastomosis is described. The concept that fecal K+ excretion is markedly elevated in patients with uremia as an intestinal adaptation to prevent hyperkalemia is analyzed; we conclude that the data do not convincingly show the existence of a major intestinal adaptive response to chronic renal failure.

Adaptation, Physiological↗

PubMed1994

Aldosteronoma in childhood: a review of clinical features and management.

Primary hyperaldosteronism is rare in children and usually results from bilateral adrenocortical hyperplasia. Adrenal adenoma causing primary hyperaldosteronism (aldosteronoma) in children is even rarer, with only eight reported cases in children under 18 years of age. Aldosteronoma is a very rare, correctable cause of childhood hypertension. A review of all the reported cases, including that of the authors, is presented. Also discussed are the available biochemical and radiological investigations, the preoperative medical management, the surgical treatment, and the postoperative management.

Adenoma↗

PubMed1995

Primary aldosteronism--some genetic, morphological, and biochemical aspects of subtypes.

Primary aldosteronism is the commonest cause of potentially curable hypertension when diagnosed in both florid and less florid forms. Genetic screening, so far available only for glucocorticoid-suppressible hyperaldosteronism, permits diagnosis from birth, before any biochemical or clinical abnormalities appear. Biochemical screening using the aldosterone-to-renin ratio permits diagnosis in the absence of raised aldosterone or of hypokalemia. Primary aldosteronism occurs in several familial forms. As well as the variety described in 1966 which is ACTH-dependent and glucocorticoid-suppressible, and not so far associated with tumors, another variety described in 1991 is not glucocorticoid-suppressible and is frequently associated with aldosterone-producing adenomas (APAs). Primary aldosteronism due to adrenocortical hyperplasia, adenoma, or carcinoma can also occur as part of the multiple endocrine neoplasia syndromes, where normoplasia, hyperplasia, benign neoplasia, and malignant neoplasia can exist in the same patient in the same endocrine gland(s) at the same time. The morphology of adrenocortical hyperplasia causing primary aldosteronism ranges from glomerulosa-like (idiopathic hyperplasia of the adrenals) to fasciculata-like (glucocorticoid-suppressible hyperaldosteronism). The morphology of adrenocortical neoplasia causing primary aldosteronism can also be either predominantly glomerulosa-like or fasciculata-like, in our experience equally often. Varying morphology of APAs is associated with varying responses of aldosterone to angiotensin II. Tumors predominantly fasciculata-like are unresponsive to angiotensin II, whereas those predominantly glomerulosa-like are responsive to angiotensin II. Both subtypes can be seen in a single family. Primary aldosteronism represents a spectrum of genetic disorders resulting in hyperplasia or neoplasia, but all are associated with some degree of autonomy of aldosterone production, independent of the renin-angiotensin system.

Adrenal Gland Neoplasms↗

PubMed1993

Differential diagnosis in primary aldosteronism.

The diagnosis of primary aldosteronism (PA) is based on the finding of the combination of elevated urinary and/or plasma aldosterone and suppressed renin activity in patients with hypertension and hypokalemia. However, PA consists of a number of subsets, and diagnostic criteria for a correct identification of surgically remediable forms are of great interest. The methods and the results concerning our series of 113 patients with PA are presented in this review. Aldosterone producing adenoma (APA) and idiopathic hyperaldosteronism (IHA) were the most frequent forms, 51 and 44%, respectively. They had similar blood pressure levels, but hypokalemia was most frequently found in APA. Urinary and upright plasma aldosterone were similar, but supine plasma aldosterone was lower in IHA. Plasma aldosterone response to upright posture and angiotensin II infusion was absent in most cases of APA and present in IHA, but occasionally renin-responsive adenoma were found. Captopril failed to decrease plasma aldosterone in most patients with APA, and in a subgroup of patients with IHA. Patients with adenoma also had higher values of the aldosterone precursor 18-hydroxy-corticosterone, and of atrial natriuretic peptide, probably as a consequence of a greater degree of volume expansion. Among morphological studies, CT scan and adrenal radiocholesterol scintiscan provided similar results (85% accuracy): adrenal veins catheterization clarified almost all the remaining cases. Among the subsets of PA, 3 familiar cases of dexamethasone-suppressible hyperaldosteronism were recognized, with characteristically high levels of aldosterone, 18-hydroxy-corticosterone, 18-hydroxy-cortisol and 18-oxo-cortisol, due to the genetic abnormalities of the 11-18 hydroxylase system. Isolated cases of primary adrenal hyperplasia (with all functional tests resulting compatible with APA, but no tumour at surgery) and aldosterone producing carcinoma (1 case) have also been reported in the present study.

Diagnosis, Differential↗

PubMed2004

[Hypertension: the main causes revisited].

Does "essential" mean "ignorance"? The historical demonstration made by Jerome Conn who was the first to describe primary hyperaldosteronism, back in 1954, shows how an outstanding diagnostic route has enlightened our knowledge. Using the examples of hyperaldosteronism and reno-vascular hypertension, a reflex ion is made to arouse our curiosity. In the end, the term "essential" is only the cover-up of what we yet have to learn.

History, 20th Century↗

PubMed2004

Clinical manifestation of aldosteronoma.

Formerly, fewer than 1% of patients with hypertension were believed to have primary hyperaldosteronism; however, recent studies have suggested a higher prevalence, in 5% to 10% of patients with hypertension. Hypokalemia is not necessary for the diagnosis and is probably a sign of more advanced disease. The best diagnostic test is the plasma aldosterone concentration to plasma renin activity (PAC/PRA) ratio. Excess aldosterone level has a deleterious effect on the cardiovascular system. Aldosteronomas should be differentiated from idiopathic hyperaldosteronism (IHA),because they are curable by laparoscopic adrenalectomy.

Adenoma↗

PubMed2005

Clinical outcomes of laparoscopic adrenalectomy for lateralizing nodular hyperplasia.

BACKGROUND: Nodular adrenal hyperplasia (NAH) may mimic the biochemical characteristics of an aldosterone-producing adenoma. The authors evaluated the outcomes of unilateral laparoscopic adrenalectomy in the setting of lateralizing aldosterone hypersecretion by NAH. METHODS: Retrospective review of consecutive patients who underwent a laparoscopic adrenalectomy for primary hyperaldosteronism owing to NAH was performed. Patient demographics, perioperative symptoms, medications, radiographic findings, and serum chemistries were analyzed. Response to operation was classified according to postoperative control of hypertension and hypokalemia as resolved, improved, or refractory. RESULTS: From January 1999 to October 2004, 15 patients underwent a laparoscopic unilateral adrenalectomy for hyperaldosteronism owing to lateralizing NAH. Nine (60%) patients presented with > or =5 years of hypertension, including 8 (53%) patients with labile or malignant hypertension. Ten (67%) patients had hypokalemia. Abdominal imaging results were normal in 9 (60%) patients. All patients underwent adrenal venous sampling (94% successfully), which revealed an average adjusted aldosterone ratio of 17.6 (range, 1.2 to 75.9). At a mean follow-up of 26 (range, 4 to 58) months, hypertension had resolved in 4 (27%), improved in 8 (53%), and was refractory in 3 (20%) patients. Hypokalemia resolved in all patients. There were no complications, conversions, or mortalities. CONCLUSION: This series shows that unilateral adrenalectomy for lateralizing NAH results in eradication of hypokalemia and resolution or significant improvement in hypertension in 80% of patients at long-term follow-up. When lateralization of aldosterone production is noted, laparoscopic adrenalectomy provides significant clinical improvement even in patients with a pathologic diagnosis of NAH.

Adrenal Glands↗

PubMed1996

Secondary hypertension: evaluation and treatment.

Most patients with hypertension in the United States have essential (primary) hypertension (95%), the cause of which is unknown. The remaining 5% of adults with hypertension have the secondary form of hypertension, the cause and pathophysiologic process of which are known. Internists and other primary care physicians refer to this as treatable or curable hypertension, because the hypertension can be managed or even controlled with medications. Similarly, the condition is called surgical hypertension by surgeons in the belief that once the cause is determined and identified, surgical intervention will result in cure of hypertension. Secondary causes of hypertension include renal parenchymal disease, renovascular diseases, coarctation of the aorta, Cushing's syndrome, primary hyperaldosteronism, pheochromocytoma, hyperthyroidism, and hyperparathyroidism. Occasionally included in this category are alcohol- and oral contraceptive-induced hypertension and hypothyroidism, but these conditions are not discussed herein. The evaluation of secondary hypertension is of interest and can bring together different facets of anatomy, physiology, pharmacology, and radiology in the medical and surgical treatment of these disorders. Despite enthusiasm that can be generated in the evaluation of these conditions, evaluation can be expensive and should not be conducted for all patients with hypertension. Features that aid in the diagnosis of secondary hypertension include the following: 1. Onset of hypertension before the age of 20 or after the age of 50 years. The presence of hypertension at a young age may suggest coarctation of the aorta, fibromuscular dysplasia, or an endocrine disorder. Hypertension found for the first time after the age of 50 years may suggest the presence of renovascular hypertension caused by atherosclerosis. 2. Markedly elevated blood pressure or hypertension with severe end-organ damage, as in grade III or IV retinopathy. These findings suggest the presence of renovascular hypertension or pheochromocytoma. 3. Specific body habitus and ancillary physical findings. For example, truncal obesity and purple striae occur with hypercortisolism, and exophthalmos is associated with hyperthyroidism. 4. Resistant or refractory hypertension (poor response to medical therapy usually necessitating use of more than three antihypertensive medications from three different classes). 5. Specific biochemical test that suggest the existence of certain disorders, such as hypercalcemia in hyperparathyroidism, hyperglycemia in Cushing's syndrome and pheochromocytoma, and unprovoked hypokalemia with renin-producing tumors, primary hyperaldosteronism, or renin-mediated renovascular hypertension. 6. Other characteristics that may suggest secondary hypertension such as abdominal diastolic bruits (renovascular hypertension), decreased femoral pulses (coarctation of the aorta), or bitemporal hemianopias (Cushing's disease). A combination of a good history and physical examination, astute observation, and accurate interpretation of available data usually are helpful in the diagnosis of a specific causation.

Adult↗

PubMed2003

Laparoscopic partial adrenalectomy in patients with aldosterone-producing adenomas: indications, technique, and results.

OBJECTIVES: To report the indications, technique, and results in patients with primary hyperaldosteronism due to aldosterone-producing adrenal adenoma treated by laparoscopic partial adrenalectomy. Laparoscopy has become the technique of choice in adrenal surgery, but adrenalectomy is the standard procedure. Only a few studies have reported on partial adrenalectomy, and the indications and technique have not yet been clearly defined. METHODS: From June 1995 to December 2001, 13 patients presented with hyperaldosteronism and a single adrenal adenoma (Conn's syndrome) and were treated with laparoscopic partial adrenalectomy. The mean age was 60 years, and the average tumor size was 2.1 cm in diameter. A transperitoneal approach was used in all patients, tumors were resected with safety margins by endoshears, and hemostasis was achieved by bipolar coagulation and finally by sealing with fibrin glue. RESULTS: All procedures were finished laparoscopically, and no conversion was necessary. No major intraoperative or postoperative complication was observed. The histologic examination showed adenomas with negative surgical margins in all cases. Postoperative computed tomography revealed a normal blood supply for the remaining adrenal tissue. Blood pressure and aldosterone levels were unremarkable at follow-up, and no local recurrence was observed. CONCLUSIONS: Laparoscopic partial adrenalectomy for aldosterone-producing adenomas is a minimally invasive procedure with a low complication rate. It provides the benefit of retaining functional tissue on the side of the affected adrenal gland. Therefore, we recommend laparoscopic partial adrenalectomy for patients with small, potentially benign, tumors of the adrenal gland, even with a healthy contralateral adrenal gland.

Adrenal Gland Neoplasms↗

PubMed1990

The transtubular potassium concentration in patients with hypokalemia and hyperkalemia.

It is advantageous to make an independent assessment of the potassium (K) secretory process and the luminal flow rate in the renal cortex to evaluate K handling by the kidney during hypokalemia or hyperkalemia. The transtubular potassium concentration gradient (TTKG) is a semiquantitative index of the activity of the K secretory process. The purpose of this study was to define expected values for the TTKG in normal subjects with hypokalemia or following an acute K load. During hypokalemia of non-renal origin, the TTKG was 0.9 +/- 0.2; in contrast, the TTKG was significantly higher during the hypokalemia of hyperaldosteronism, 6.7 +/- 1.3. The TTKG was 11.8 +/- 3.6, 2 hours after normokalemic subjects received 0.2 mg 9 alpha-fludrocortisone (9 alpha-F). To obtain expected values during hyperkalemia, normal subjects ingested 50 mmol potassium chloride; 2 hours later, the TTKG was 13.1 +/- 3.8. Therefore, the expected value for the TTKG must be interpreted relative to the concentration of K in the plasma. Circumstances were also defined where the TTKG is low despite hyperaldosteronism, namely, during a water diuresis and pre-existing hypokalemia.

Desoxycorticosterone↗

PubMed2001

Aldosteronoma in a dog with polyuria as the leading symptom.

In a 10-year-old castrated male shorthaired German pointer polyuria was associated with slight hypokalemia, hypophosphatemia and alkalosis, as well as elevated plasma concentrations of a glucocorticoid-inducible iso-enzyme of alkaline phosphatase. Repeated measurements of urinary corticoids and normal suppressibility of the hypothalamus-pituitary-adrenocorticial axis excluded glucocorticoid excess. Urine osmolality (Uosm) did not increase during administration of the vasopressin analogue desmopressin. At the time water deprivation had caused Uosm to rise from 300 to 788 mOsm/kg, there was also plasma hypertonicity. During hypertonic saline infusion the osmotic threshold for vasopressin release was increased. The combination of elevated plasma aldosterone concentrations and unmeasurably low plasma renin activity pointed to primary hyperaldosteronism. As initially computed tomography (CT) did not reveal an adrenocortical lesion, the dog was treated with the aldosterone antagonist spironolactone. This caused Uosm to rise in a dose-dependent manner. However, well-concentrated urine was only achieved with doses that gave rise to adverse effects. Once repeated CT, using 2-mm-thick slices, had revealed a small nodule in the cranial pole of the left adrenal, unilateral adrenalectomy was performed which resolved the polyuria completely. Also the plasma concentrations of kalium, aldosterone and renin activity returned to within their respective reference ranges. The adrenocortical nodule had the histological characteristics of an aldosteronoma, with the non-affected zona glomerulosa being atrophic.In this dog with primary hyperaldosteronism the polyuria was characterized by vasopressin resistance and increased osmotic threshold of vasopressin release, similar to the polyuria of glucocorticoid excess. The possibility is discussed that the polyuria of glucocorticoid excess is actually a mineralocorticoid effect.

Adrenalectomy↗

PubMed2000

Pathophysiology and diagnosis of primary aldosteronism.

The pathophysiology of primary aldosteronism still remains unknown. In mRNA and protein levels, overexpression of aldosterone synthase (P-450aldo) is recognized, although abnormalities and defects of DNA and its upper stream have not been detected. Several candidate genes responsible for pathogenesis of primary aldosteronism, such as renin, angiotensin receptor type II, etc., have been proposed, but no decisive genes have been found. A relatively reliable screening for hyperaldosteronism is a determination of the ratio of the plasma aldosterone level to the plasma renin activity. For differentiating several types of aldosteronisms, the simplest test is the response of plasma aldosterone to two hours in an upright posture: plasma aldosterone rises in most patients with idiopathic hyperaldosteronism. In contrast, in cases of autonomous aldosterone-producing tumor, most patients show no response or even a decrease in plasma aldosterone concentration. The size and location of the aldosterone-producing adenoma are determined by using computed tomography.

Humans↗

PubMed2001

Anomalous left adrenal venous drainage directly into the inferior vena cava.

Primary hyperaldosteronism is a potential cause of hypertension. Unilateral adrenal adenoma and bilateral adrenal cortical hyperplasia are the most common causes of primary hyperaldosteronism. Adrenal venous sampling is employed as the gold standard test to differentiate between these two different causes when the results of other studies in the work-up protocol are non-diagnostic or ambiguous. Adrenal venous sampling can be a challenging procedure, especially in the presence of anomalous venous drainage patterns. Knowledge of normal adrenal venous anatomy, as well as possible variants, is therefore important to ensure a successful procedure. The authors describe an unusual variant of left adrenal venous drainage directly into the IVC.

Adrenal Gland Diseases↗

PubMed1997

Fourier analysis of circadian blood pressure profile in secondary hypertension.

Different types of statistical methods have been used for circadian blood pressure (BP) rhythm analysis in secondary forms of hypertension. In the present study, we used the two-step statistical approach by Fourier analysis with four harmonics for the parametrization of the diurnal BP pattern in secondary hypertension. In 43 essential hypertensives (EH), eight patients with aldosterone producing adenoma (APA), 25 with idiopathic hyperaldosteronism (IHA), four with glucocorticoid remediable hyperaldosteronism (GRH) and seven with renovascular hypertension (RVH), 24-h ambulatory BP was measured. The diurnal BP and heart rate (HR) rhythm was present in more than 70% of patients with secondary hypertension, without significant differences with EH and despite the attenuation in the degree of the nocturnal BP fall. In conclusion, the statement that secondary hypertension is characterized by an abnormal diurnal rhythm of BP is a gross over-simplification. Our findings suggest that the two-step method with four harmonics Fourier analysis may represent a useful method and a more complete statistical approach to providing circadian parametrization of the 24-h profile in secondary hypertension.

Blood Pressure↗