eMedicine Specialties > Radiology > Genitourinary

Hyperaldosteronism

Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, Consultant Radiologist, North Manchester General Hospital, The Pennine Acute NHS Trust, Manchester UK
Sumaira MacDonald, MBChB, PhD, MRCP, FRCR, Lecturer, Sheffield University Medical School; Endovascular Fellow, Sheffield Vascular Institute; Durre Sabih, MBBS, MSc, Visiting Faculty, Department of Nuclear Medicine, Pakistan Institute Applied Sciences and Nishtar Medical College; Director, Multan Institute of Nuclear Medicine and Radiotherapy; Muhammad Sohaib, MBBS, MSc, Senior Medical Officer, Assistant Professor, Department of Medical Sciences, Pakistan Institute of Engineering and Applied Sciences

Updated: Apr 8, 2008

Introduction

Background

Primary aldosteronism, also termed Conn syndrome, is clinically characterized by hypertension and hypokalemia. Primary aldosteronism was first described in 1955 as a syndrome related to the hypersecretion of aldosterone by an adrenal adenoma. Although primary aldosteronism accounts for 0.05-2% of cases of hypertension in the general population, recognition of the disease is important because patients readily respond to the removal of the adrenal gland tumor.

The most common cause of primary aldosteronism is an adrenal adenoma; most of the remaining cases result from adrenal gland hyperplasia. Adrenal carcinoma is an extremely rare cause of primary aldosteronism. In 75-90% of patients with a solitary aldosterone-producing tumor, surgical adrenalectomy corrects the hypertension and hypokalemia.

Axial enhanced CT scan in a 32-year-old woman who presented with hypertension shows a low-attenuating 2.8-cm suprarenal mass (A) (same patient as in Image 1 in Multimedia). Histologic results obtained after surgery confirmed a tumor due to Conn syndrome.

Longitudinal sonogram through the left kidney in a 32-year-old woman who presented with hypertension shows a 3-cm hypoechoic but solid mass superior to the upper pole of the kidney. Initially, the mass was regarded as a nonfunctioning adenoma unrelated to the patient's hypertension. Subsequently, mild hypokalemia developed. Surgical resection confirmed a tumor due to Conn syndrome.

Scintigram obtained by using iodine-131-6β-iodomethylnorcholesterol (NP-59) in a 59-year-old man with hypertension shows fairly intense radionuclide uptake in the right adrenal tumor (same patient as in Image 7 in Multimedia). At surgery, a Conn tumor was confirmed.

Pathophysiology

Clinical manifestations of primary hyperaldosteronism are caused by aldosterone excess in the renal tubules. Aldosterone promotes the excessive preservation of sodium at the expense of potassium loss. Sodium retention promotes water retention, an expansion in the extracellular volume, hypertension, and a suppression of renin production. Excessive potassium loss causes hypokalemic alkalosis, which may be associated with various complications, including muscular weakness, tetany, and abnormal electrocardiographic findings. In 65-89% of patients, primary aldosteronism occurs as a result of 1 or more aldosterone-producing adenomas (APAs). In 65-70% of patients, the aldosteronoma is solitary, while in 13% of patients, multiple adenomas are present, and in 6% of patients, microadenomatosis exists.^1,2,3,4

Adrenal carcinoma rarely causes primary aldosteronism and occurs in less than 1% of patients. Malignant adrenal tumors often secrete aldosterone in addition to glucocorticoids. These patients may present with hypertension or the manifestations of Cushing syndrome. Small aldosteronomas have an average size of 1.7 cm (range, 0.5-3.5 cm), the left adrenal gland is affected more often, and the tumors are bilateral in 6% of patients.

The diagnosis of primary aldosteronism is based on the typical biochemical findings of hypokalemia, hypernatremia, depletion of magnesium, elevated bicarbonate levels, low plasma pH, and elevated aldosterone levels in the serum and urine. However, this biochemical pattern is not unique to primary aldosteronism; it may be seen in secondary aldosteronism as well.

The demonstration of suppressed renin levels is vital to the diagnosis.² A sodium chloride suppression test can be used to demonstrate the inability to suppress aldosterone secretion. This suppression testing involves the administration of large amounts of sodium chloride over 3-5 days, which causes hypokalemia in 80-90% of patients with primary aldosteronism. This response is associated with muscle weakness, cardiac arrhythmia, carbohydrate intolerance, and nephrogenic diabetes insipidus. Hypertension associated with primary aldosteronism is usually benign, but in rare cases, malignant hypertension may develop.⁴

An adrenal myelolipoma is a benign, fatty tumor that is not hormonally active, but in very rare cases, it is associated with functional adrenal disorders. Jung and colleagues reported a case of bilateral adrenal myelolipomas associated with primary hyperaldosteronism.⁵

Frequency

United States

In 0.05-2% of patients with hypertension, the condition is caused by primary aldosteronism.

Mortality/Morbidity

• In 75-90% of patients with a solitary APA, surgical adrenalectomy corrects hypertension and hypokalemia.
• Most other patients have idiopathic hyperaldosteronism associated with bilateral adrenal hyperplasia; in these patients, surgery rarely cures hypertension.

Sex

The male-to-female ratio is 1:2.

Age

Primary aldosteronism occurs in patients aged 30-50 years.

Anatomy

Since computed tomography (CT) scanning has become the standard technique in diagnostic adrenal imaging, differentiating normal from abnormal adrenal glands is essential. Normal adrenal glands are identified in almost all patients with the help of CT scans, whereas a normal left-sided gland is identified in 45% of patients and a normal right-sided gland is identified in 80% of patients with the help of ultrasonograms.^6,7

Cross-sectional images obtained by using CT scanning and MRI show the adrenal glands as thin, folded structures with an anteromedial ridge and 2 posterior or posterolateral limbs. These limbs, which appear winglike, are joined together at the superior aspect of the gland, placed at the upper pole of the kidney. Inferiorly, the limbs open, straddling the upper poles of the kidney. MRI scans can show the adrenal glands elegantly and in many planes. With standard CT scanning, only cross-sectional images may need to be interpreted. On the most cephalic CT scan section, the gland usually has a linear appearance with an anteroposterior orientation or a slanted, anterior-to-posterolateral orientation.^7,8,9,10,11

The midsections of the gland present a Y -shaped configuration. Occasionally, the anteromedial ridge is small or not well developed, resulting in an inverted, V -shaped gland. The normal adrenal limbs measure 3-6 mm in thickness, 4-6 cm in length, and 2-3 cm in width. The variation in size explains why some hyperfunctioning glands are seen to be normal in size on images and at surgery.

Presentation

Primary aldosteronism is characterized by moderate-to-severe hypertension without edema. Biochemically, the condition is associated with hypokalemia, metabolic alkalosis, and hyperaldosteronism not appropriately suppressed during volume expansion and depression of plasma renin activity. With hypokalemic alkalosis, various symptoms, including muscular weakness, polydipsia, polyuria, nocturia, paresthesia, tetany, headaches, and abnormal electrocardiographic features, may develop.^1,2,3,4,5

Other abnormalities that are associated with primary aldosteronism are subarachnoid hemorrhage, postural hypotension, and bradycardia. A neonatal, idiopathic form of hyperaldosteronism has been described that presents with functional gastrointestinal tract symptoms associated with hypokalemia and hypertension.

Preferred Examination

The workup in patients in whom primary aldosteronism is suspected usually starts with appropriate biochemical analysis, after which, thin-collimation CT scanning is performed.^1,6 If CT scan findings are equivocal, radionuclide studies and MRI should be performed.⁸ If doubt concerning the diagnosis remains and if CT scans do not show a mass in the adrenal glands, adrenal venous sampling is recommended.

Plain radiographs have no significant role. Ultrasonography has little to contribute unless the adrenal tumor is large, which is seldom the case. However, ultrasonography is an excellent modality for the investigation of hypertension.

Limitations of Techniques

Hypersecreting adrenal glands may appear to be normal in size on images, because the size of the adrenal gland may be compared to a normal measurement and because the healthy adrenal gland varies considerably in size. The adrenal glands also vary in size and weight as a result of illness or stress. This size discrepancy is a particular problem with APAs, because they are often small and difficult to detect. In one series, the average diameter of an APA was 18 mm, and 20% of tumors were smaller than 1 cm.

In earlier generations of CT scanners, the sensitivity for detecting APAs was 50-70%. In current CT scanners, the sensitivity has been improved to 82-88%. Diagnosis by using CT scans is hampered by the detection of ipsilateral or contralateral, nonfunctioning adenomas, which leads to a false-positive diagnosis of adrenal hyperplasia. CT scanning is not reliable in distinguishing between hyperplasia and adenoma in patients with multiple, bilateral nodules.^6,7,12,13

Differential Diagnoses

Other Problems to Be Considered

Nonfunctioning adrenal adenoma associated with incidental hypertension
Secondary hyperaldosteronism associated with an incidental, nonfunctioning adenoma
Idiopathic hyperaldosteronism
Liddle syndrome (pseudohyperaldosteronism)
Gordon syndrome (pseudohyperaldosteronism type II, familial hypertensive hyperkalemia)
Secondary hyperaldosteronism due to an extra-adrenal stimulus from hyperreninemia (adrenal embryologic rest neoplasms in a kidney or ovary)

Radiography

Findings

Conventional radiography has no role in the diagnosis of APA.

Computed Tomography

Findings

Axial enhanced CT scan in a 32-year-old woman who presented with hypertension shows a low-attenuating 2.8-cm suprarenal mass (A) (same patient as in Image 1 in Multimedia). Histologic results obtained after surgery confirmed a tumor due to Conn syndrome.

Axial nonenhanced CT scan through the adrenal glands in 56-year-old man shows multiple nodules in both glands, although biochemical results indicated primary aldosteronism. The patient received medical treatment.

Axial enhanced CT scan in a 56-year-old man shows no enhancement of the adrenal masses (same patient as in Image 3 in Multimedia).

Axial nonenhanced CT scan through the adrenal glands in a 60-year-old patient who presented with hypertension and hypokalemia shows a bilobulated tumor in the right adrenal gland.

Axial enhanced CT scan through the adrenal glands in a 60-year-old patient who presented with hypertension and hypokalemia shows minor tumor enhancement (same patient as in Image 5 in Multimedia). Note the normal left adrenal gland.

A 59-year-old man was referred for renal ultrasonography as a part of the workup for newly diagnosed hypertension. The sonogram depicted a 3-cm right adrenal mass, which was regarded as an incidentaloma (not shown). Axial enhanced CT scan through the adrenal gland shows minor patchy enhancement in a right adrenal tumor.

The mean attenuation level in adrenal adenomas is -2.2 HU. Among hyperfunctioning adenomas, aldosteronomas have the lowest attenuation levels. In patients with primary hyperaldosteronism, CT scan findings may be normal, or scans may show nodular or multinodular glands.

Degree of Confidence

CT scanning has a sensitivity of 60-80% in detecting APAs. CT appears more reliable at revealing tumors larger than 1 cm. Conversely, 20% of tumors may be missed. In one series, the average diameter of an APA was 18 mm, and 20% tumors were smaller than 1 cm. With earlier-generation CT scanners, the sensitivity for detecting APAs was 50-70%. The sensitivity of current scanners has been improved to 82-88%. The specificity of CT scanning in the detection of APAs is 77%.^6,7,12,13

False Positives/Negatives

CT scan findings of ipsilateral or contralateral, nonfunctioning adenomas lead to a false-positive diagnosis of adrenal hyperplasia. CT scanning is not reliable in distinguishing hyperplasia from adenoma in patients with multiple, bilateral nodules.

Magnetic Resonance Imaging

Findings

Early experience with MRI in the diagnosis of APA has been encouraging. APAs are iso-intense or hypo-intense relative to the liver on T1-weighted images; they are slightly hyperintense on T2-weighted images. Chemical-shift imaging is a useful method for the characterization of adrenal masses. It is based on the principle that fat protons precess faster than do water protons. Chemical-shift MRI is highly sensitive and specific for the differentiation of benign from malignant adrenal tumors, because benign adrenal tumors contain fat, while malignant adrenal tumors rarely do. With chemical-shift imaging, the signal intensity has been found to decrease on out-of-phase images in 86% of patients with APAs and in 89% of patients with bilateral adrenal hyperplasia.^8,9,10,11

Degree of Confidence

A sensitivity of 70-100% and a specificity of 64-100% have been reported in the detection of APAs with MRI.^8,9,10,11

False Positives/Negatives

False-positive diagnoses have occurred in cases of idiopathic hyperaldosteronism, bilateral nodular hyperplasia, primary hypertension, and primary hypertension associated with nonfunctioning adrenal adenoma.

Ultrasonography

Findings

Longitudinal sonogram through the left kidney in a 32-year-old woman who presented with hypertension shows a 3-cm hypoechoic but solid mass superior to the upper pole of the kidney. Initially, the mass was regarded as a nonfunctioning adenoma unrelated to the patient's hypertension. Subsequently, mild hypokalemia developed. Surgical resection confirmed a tumor due to Conn syndrome.

Degree of Confidence

Ultrasonographic findings contribute little to the diagnosis unless the adrenal tumor is large, which is seldom the case. However, ultrasonography is an excellent modality for the investigation of hypertension.

False Positives/Negatives

The exact sensitivity of ultrasonography in the diagnosis of APA is not known, but it appears to be low. Similar to other types of cross-sectional imaging, ultrasonography may incidentally demonstrate nonfunctioning masses in the adrenal glands.

Nuclear Imaging

Findings

Scintigram obtained by using iodine-131-6β-iodomethylnorcholesterol (NP-59) in a 59-year-old man with hypertension shows fairly intense radionuclide uptake in the right adrenal tumor (same patient as in Image 7 in Multimedia). At surgery, a Conn tumor was confirmed.

Degree of Confidence

CT scanning is an excellent modality for the detection of APAs; bilateral hyperplasia is usually inferred by the absence of an adrenal tumor. In contrast, NP-59 scanning provides a specific diagnosis of adrenal hyperplasia. Accuracy and sensitivity of 80-95% can be obtained. Smaller adenomas, which are not clearly depicted on CT scans, can be detected on NP-59 scans.¹³

False Positives/Negatives

Primary aldosteronism must be clinically and biochemically diagnosed before the radionuclide study is performed, because secondary hyperaldosteronism produces bilateral tracer uptake that is indistinguishable from that of primary, autonomous, bilateral hyperplasia. In addition, all drugs that disturb the renin-angiotensin-aldosterone axis must be withdrawn before imaging. The extremely rare mineralocorticoid-secreting carcinoma also demonstrates NP-59 uptake.¹³

Scintigraphy must be performed in the appropriate clinical setting, because NP-59 uptake has been described in benign, nonsecretory adenoma, as well as in metastatic lung cancer, metastatic colon cancer, lymphoma, myelolipoma, ganglioneuroma, adrenal cysts, and adrenocortical carcinoma. Tracer uptake at extra-adrenal sites also has been reported.¹³

Angiography

Findings

Because APAs are small and are not usually vascular, selective adrenal angiography is seldom helpful. However, adrenal phlebography has a useful role in the investigation of APA, because the splaying of veins around APAs can help in identifying even small tumors. If contrast medium is refluxed into the veins of the APA, a wheel-spoke pattern is seen in the intratumoral veins. Because APAs are small, a vigorous retrograde venous injection is usually required to detect the tumors; this vigorous injection is not without risk, because extravasation may occur.

Extravasation is a particular problem if the catheter is wedged into the vein. Extravasation can be painful and has been associated with adrenal infarction. Adrenal vein thrombosis is also a known complication of adrenal phlebography, which has been linked to adrenal infarction. Adrenal insufficiency has been described as a result of bilateral adrenal infarction. Adrenal vein thrombosis is more likely to occur if the catheter is wedged in the adrenal vein and left there for several minutes during the procedure.

The most useful technique in the investigation of primary aldosteronism is adrenal venous sampling.^7,9,14 Blood samples are obtained from both adrenal veins for aldosterone level analysis; hormone level ratios are compared with each other and with levels in the inferior vena cava below the adrenal veins. In experienced hands, this technique can achieve a high sensitivity; however, it is a time-consuming procedure that necessitates prolonged cannulation of adrenal veins and increases the risk of adrenal vein thrombosis. In addition, the adrenal veins are small, and collecting 7 mL of blood for sampling is not easy. This is particularly a problem when blood is collected from the right adrenal vein, in which a short vein enters the inferior vena cava directly.

Some venous samples thus acquired may be diluted by blood from the inferior vena cava on the right and from the phrenic or renal vein on the left. To overcome the problem of dilution, cortisol levels can be measured from the same samples. A low cortisol level suggests dilution by nonadrenal blood, whereas a high cortisol level indicates a relatively pure sample. When aldosterone and cortisol are measured in blood samples from the same site, an aldosterone-cortisol ratio that corrects the concentration of aldosterone for dilution can be calculated.

Degree of Confidence

An accuracy of 95% and a sensitivity of 75% have been reported with adrenal venous sampling. Adrenal venous sampling is required for the definitive diagnosis of primary aldosteronism and for the detection of laterality of the adrenal lesion.¹⁴

Zarnegar and colleagues conducted a study of 59 patients with biochemically diagnosed hyperaldosteronism who subsequently underwent unilateral adrenalectomy.¹⁵ Clinical decision in proceeding to surgery was based on CT scanning alone (n=30) or on CT scanning and adrenal venous sampling (n=29). The authors found that in the 2 groups, adrenalectomy had similar clinical effects. CT scanning can be used to reliably diagnose adenomas larger than 1.0 cm. The authors recommended that adrenal venous sampling be reserved for cases in which CT scan findings are equivocal or in which both of the patient's adrenal glands are abnormal.

False Positives/Negatives

The dilution of blood from the inferior vena cava on the right and from the renal or phrenic vein on the left can lead to erroneous results in adrenal venous sampling.

Intervention

Although primary aldosteronism accounts for 0.05-2% of cases of hypertension in the general population, recognition of the disease is important because patients readily respond to the removal of the adrenal gland tumor. In 75-90% of patients with a solitary APA, surgical adrenalectomy corrects hypertension and hypokalemia.

Most other patients have idiopathic hyperaldosteronism associated with bilateral adrenal hyperplasia. In these patients, surgery rarely cures hypertension; instead, patients with idiopathic hyperaldosteronism are usually treated medically.¹⁶ Therefore, differentiating primary aldosteronism caused by APAs from idiopathic hyperaldosteronism is essential.

Multimedia

Media file 1: Longitudinal sonogram through the left kidney in a 32-year-old woman who presented with hypertension shows a 3-cm hypoechoic but solid mass superior to the upper pole of the kidney. Initially, the mass was regarded as a nonfunctioning adenoma unrelated to the patient's hypertension. Subsequently, mild hypokalemia developed. Surgical resection confirmed a tumor due to Conn syndrome.

Media file 2: Axial enhanced CT scan in a 32-year-old woman who presented with hypertension shows a low-attenuating 2.8-cm suprarenal mass (A) (same patient as in Image 1 in Multimedia). Histologic results obtained after surgery confirmed a tumor due to Conn syndrome.

Media file 3: Axial nonenhanced CT scan through the adrenal glands in 56-year-old man shows multiple nodules in both glands, although biochemical results indicated primary aldosteronism. The patient received medical treatment.

Media file 4: Axial enhanced CT scan in a 56-year-old man shows no enhancement of the adrenal masses (same patient as in Image 3 in Multimedia).

Media file 5: Axial nonenhanced CT scan through the adrenal glands in a 60-year-old patient who presented with hypertension and hypokalemia shows a bilobulated tumor in the right adrenal gland.

Media file 6: Axial enhanced CT scan through the adrenal glands in a 60-year-old patient who presented with hypertension and hypokalemia shows minor tumor enhancement (same patient as in Image 5 in Multimedia). Note the normal left adrenal gland.

Media file 7: A 59-year-old man was referred for renal ultrasonography as a part of the workup for newly diagnosed hypertension. The sonogram depicted a 3-cm right adrenal mass, which was regarded as an incidentaloma (not shown). Axial enhanced CT scan through the adrenal gland shows minor patchy enhancement in a right adrenal tumor.

Media file 8: Scintigram obtained by using iodine-131-6β-iodomethylnorcholesterol (NP-59) in a 59-year-old man with hypertension shows fairly intense radionuclide uptake in the right adrenal tumor (same patient as in Image 7 in Multimedia). At surgery, a Conn tumor was confirmed.

References

1. Gallay BJ, Ahmad S, Xu L, et al. Screening for primary aldosteronism without discontinuing hypertensive medications: plasma aldosterone-renin ratio. Am J Kidney Dis. Apr 2001;37(4):699-705. [Medline].

2. Pratt JH. Low-renin hypertension: more common than we think?. Cardiol Rev. Jul-Aug 2000;8(4):202-6. [Medline].

3. Leung AM, Sasano H, Nishikwa T, et al. Multiple unilateral adrenal adenomas in a patient with primary hyperaldosteronism. Endocr Pract. Jan-Feb 2008;14(1):76-9. [Medline].

4. Pimenta E, Calhoun DA. Resistant hypertension and aldosteronism. Curr Hypertens Rep. Nov 2007;9(5):353-9. [Medline].

5. Jung SI, Kim SO, Kang TW, et al. Bilateral adrenal myelolipoma associated with hyperaldosteronism: report of a case and review of the literature. Urology. Dec 2007;70(6):1223.e11-3. [Medline].

6. Mayo-Smith WW, Boland GW, Noto RB, et al. State-of-the-art adrenal imaging. Radiographics. Jul-Aug 2001;21(4):995-1012. [Medline]. [Full Text].

7. Magill SB, Raff H, Shaker JL, et al. Comparison of adrenal vein sampling and computed tomography in the differentiation of primary aldosteronism. J Clin Endocrinol Metab. Mar 2001;86(3):1066-71. [Medline]. [Full Text].

8. Wang JH, Wu HM, Sheu MH, et al. High resolution MRI of adrenal glands in patients with primary aldosteronism. Chung Hua I Hsueh Tsa Chih (Taipei). Jun 2000;63(6):475-81. [Medline].

9. Rossi GP, Sacchetto A, Chiesura-Corona M, et al. Identification of the etiology of primary aldosteronism with adrenal vein sampling in patients with equivocal computed tomography and magnetic resonance findings: results in 104 consecutive cases. J Clin Endocrinol Metab. Mar 2001;86(3):1083-90. [Medline]. [Full Text].

10. Rossi GP, Chiesura-Corona M, Tregnaghi A, et al. Imaging of aldosterone-secreting adenomas: a prospective comparison of computed tomography and magnetic resonance imaging in 27 patients with suspected primary aldosteronism. J Hum Hypertens. Aug 1993;7(4):357-63. [Medline].

11. Sohaib SA, Peppercorn PD, Allan C, et al. Primary hyperaldosteronism (Conn syndrome): MR imaging findings. Radiology. Feb 2000;214(2):527-31. [Medline]. [Full Text].

12. Nocaudie-Calzada M, Huglo D, Lambert M, et al. Efficacy of iodine-131 6beta-methyl-iodo-19-norcholesterol scintigraphy and computed tomography in patients with primary aldosteronism. Eur J Nucl Med. Oct 1999;26(10):1326-32. [Medline].

13. Hwang I, Balingit AG, Georgitis WJ, et al. Adrenocortical SPECT using iodine-131 NP-59. J Nucl Med. Aug 1998;39(8):1460-3. [Medline]. [Full Text].

14. Nishikawa T, Saito J, Omura M. Adrenal venous sampling is absolutely requisite for definitively diagnosing primary aldosteronism as well as for detecting laterality of the adrenal lesion. Hypertens Res. Nov 2007;30(11):1009-10. [Medline]. [Full Text].

15. Zarnegar R, Bloom AI, Lee J, et al. Is adrenal venous sampling necessary in all patients with hyperaldosteronism before adrenalectomy?. J Vasc Interv Radiol. Jan 2008;19(1):66-71. [Medline].

16. Moo TA, Zarnegar R, Duh QY. Prediction of successful outcome in patients with primary aldosteronism. Curr Treat Options Oncol. Aug 2007;8(4):314-21. [Medline].

17. Haenel LC 4th, Hermayer KL. A case of unilateral adrenal hyperplasia: the diagnostic dilemma of hyperaldosteronism. Endocr Pract. Mar-Apr 2000;6(2):153-8. [Medline].

18. Stowasser M. Primary aldosteronism: rare bird or common cause of secondary hypertension?. Curr Hypertens Rep. Jun 2001;3(3):230-9. [Medline].

Keywords

primary hyperaldosteronism, primary aldosteronism, Conn syndrome, aldosterone hypersecretion, adrenal adenoma, adrenal gland tumor, adrenal gland hyperplasia, aldosterone-producing tumor, adrenal gland carcinoma, aldosterone excess, aldosterone-producing adenoma, APA, aldosterone-producing adrenal adenoma, aldosteronoma, secondary aldosteronism, idiopathic hyperaldosteronism

Contributor Information and Disclosures

Author

Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, Consultant Radiologist, North Manchester General Hospital, The Pennine Acute NHS Trust, Manchester UK
Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR is a member of the following medical societies: American Institute of Ultrasound in Medicine, Royal College of Physicians, Royal College of Physicians and Surgeons of the United States, Royal College of Radiologists, and Royal College of Surgeons of England
Disclosure: Nothing to disclose.

Coauthor(s)

Sumaira MacDonald, MBChB, PhD, MRCP, FRCR, Lecturer, Sheffield University Medical School; Endovascular Fellow, Sheffield Vascular Institute
Sumaira MacDonald, MBChB, PhD, MRCP, FRCR is a member of the following medical societies: British Medical Association, Royal College of Physicians, and Royal College of Radiologists
Disclosure: Nothing to disclose.

Durre Sabih, MBBS, MSc, Visiting Faculty, Department of Nuclear Medicine, Pakistan Institute Applied Sciences and Nishtar Medical College; Director, Multan Institute of Nuclear Medicine and Radiotherapy
Disclosure: Nothing to disclose.

Muhammad Sohaib, MBBS, MSc, Senior Medical Officer, Assistant Professor, Department of Medical Sciences, Pakistan Institute of Engineering and Applied Sciences
Disclosure: Nothing to disclose.

Medical Editor

John L Haddad, MD, Clinical Associate Professor, Department of Radiology, Weill Medical College of Cornell University; Director of Body MRI, Department of Radiology, Methodist Hospital in Houston
John L Haddad, MD is a member of the following medical societies: American College of Radiology, American Medical Association, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

Joshua A Becker, MD, Professor, Department of Radiology, New York University School of Medicine
Joshua A Becker, MD is a member of the following medical societies: Society of Uroradiology
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, Resolution Imaging Medical Corporation
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

Eugene C Lin, MD, Consulting Radiologist, Virginia Mason Medical Center; Clinical Assistant Professor of Radiology, University of Washington School of Medicine
Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, and Society of Nuclear Medicine
Disclosure: Nothing to disclose.

Basil Issa, MBBCh, MRCP, Consulting Staff, North Manchester Heath Care NHS Trust, contributed to this article.

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)