Aldosterone Escape

 

Mrs. R. Deepa

Associate Professor, College of Nursing, Sri Ramakrishna Institute of Paramedical Sciences, Coimbatore.

 

ABSTRACT:

The adrenal glands are located on the top of your kidneys, and produce adrenaline, cortisol, aldosterone, and other steroid hormones that enable the body to respond to stress. Conn's disease is a condition in which the adrenal glands produce too much aldosterone. It is frequently caused by a benign (non-cancerous) tumor of an adrenal gland. High blood pressure (hypertension) is often the only symptom of Conn's disease. In some cases, the condition can lower the level of the mineral potassium in a patient's blood. This can lead to muscle weakness, headaches, and the passing of large amounts of urine. The secondary effects of the hypertension are important – complications such as renal and retinal damage (microvascular disease) are more likely with poorly controlled hypertension which is usually the case with Conn’s syndrome – hence early detection is important.

 

 

 

INTRODUCTION:

CASE HISTORY:

Mr. Issac Abraham, 64 years who admitted in a private hospital with postural hypotension, giddiness anorexia and nausea. He is a known case of bilateral adrenal hyperplasia, hypertensive since three years, recently underwent prostatectomy. On the day of admission, he was hemodynamically stable. Investigations reveals numerous pus cells present in urinalysis, albumin was trace and some bacterial infections. Bloodpressure was little high during hospitalization. Other renal parameters were normal. He was treated by anti-hypertensives, anti-inflammatory and potassium sparing diuretics.

 

BRIEF VIEW:

Conns syndrome is named after Jerome W. Conn (1907-1994), the American endocrinologist who first described adenomas as a cause of the condition in 1955.

 

INTRODUCTION:

In physiology, aldosterone escape is a term that has been used in two different aspects namely escape from the sodium- retaining effects of excess aldosterone and inability of ACE inhibitor therapy to reliably suppress aldosterone release. Aldosterone initially results in an increase in Na+ reabsorption in these patients through stimulation of ENaC channels in principal cells of the renal collecting tubules. Increased ENaC channels situated in the apical membranes of the principal cells allow for more Na+ reabsorption, which may cause a transient increase in fluid reabsorption as well. Electrolyte homeostasisis maintained in these patients, which excludes the possibility that other Na+ transporters elsewhere in the kidney are being shut down.

 

Normally Na+ and water are reabsorbed from the tubules and dumped into the interstitium. From there, Starling forces dictate the gradient for movement of water and Na+ into the peritubular capillaries. Because hydrostatic pressures in the tubules, interstitium and peritubular capillaries are normally equivalent, oncotic pressures govern flow. Typically, oncotic pressures are higher in the peritubular capillaries, because protein composition in the interstitium is nominal; therefore, Na+ and water leave the interstitial space and enter the capillaries. When hydrostatic pressures are raised in the peritubular capillaries such as seen in hyperaldosteronism, Starling forces begin to favor " backflow" of Na+ and water from the interstitium into the tubules- thus, increasing Na+ excertion. It is how the patients with increased levels of aldosterone are able to maintain Na+ balance and avoid an edematous state.

 

DEFINITION:

It is known as primary aldosteronism or Conns syndrome. It refers to the excess production of the hormone aldosterone from the adrenal glands, resulting in low renin levels.

 

INCIDENCE:

About 33% of cases are due to adrenal adenoma that produces aldostrone and 66% of cases are due to an enlargement of both adrenal glands. It is present in about 10% of people with high blood pressure. It occurs more often in women than men. Often it begins in those between 30 and 50 years of age. 40% of people with an adrenal aldostrone producing adnoma have somatic gain-of-function mutations in a single gene (KCNJ5). Adenomas without this mutation tend to occur in older men with resistant hypertension. Other genes commonly mutated in aldosterone producing adenomas are ATP1A1, ATP2B3, CACNA1D and CTNNB1.

 

TERMINOLOGY:

·         Primary hyperaldosteronism: cause is in the adrenal gland

·         Secondary hyperaldosteronism: cause is extra adrenal

·         Tertiary hyperaldosteronism: cause is renal juxtaglomerular cells

 

ETIOLOGY:

Ÿ  Primary hyperaldosteronism: Idiopathic adrenal hyperplasia, adrenal adenomas, rarely adrenal carcinoma

Ÿ  Secondary hyperaldosteronism: Increased levels of plasma renin from non-adrenal pathology which includs CCF, pregnancy, renal artery stenosis, nephrosclerosis, gypoalbuminemia, ovarian tumor and hyperthyroidism.

Ÿ  Tertiary hyperaldosteronism: Hypertrophy and hyperplasia of renal juxtaglomerular cells, autosomal recessive and Bartter syndrome.

Ÿ  Glucocorticoid suppressible hyperaldosteronism

Ÿ  Early onset of hypertension and severe target organ damage.

 

PATHOPHYSIOLOGY:

Aldostrone stimulates sodium-potassium ATPase in muscle cells. Increasing intracellular potassium and also increases sodium reabsorption all along the intestine and nephron, possibly due to to widespread stimulation of sodium-potassium ATPase. Finally, epithelial cells of sweat gland ducts and distal colon surface respond exactly the same as the principal cells of the nephron. These responses are important in climate adaptation and as a cause of constipation with elevated aldostrone.

 

The sodium retention leads to plasma volume expansion and elevated blood pressure. It will lead to increased GFR and cause a decrease in renin release from the juxtaglomerular apparatus in the kidney decreasing sodium reabsorption and returning sodium renal excretion to near normal levels allowing sodium to escape the effect of mineralocorticoids.

 

DIAGNOSIS:

·         Plasma aldosterone concentration to plasma renin activity (ratio >30 is strongly suggestive )

·         Serum aldostrone level, urine aldosterone levels and

·         Saline suppression test, ambulatory salt loading test or fludrocortisone suppression test.

·         CT scan or cross sectional imaging - confirm the adrenal abnormality, adrenal cortical adenoma, adrenal carcinoma, bilateral adrenal hyperplasia.

·         Adrenal venous sampling if surgery is needed.

·         High serum sodium, low serum potassium, metabolic alkalosis.

 

TREATMENT:

·         Surgical removal of adrenal gland

·         Spironolactone drug therapy

·         Antiandrogen therapy

 

COMPLICATIONS:

Risk rates of stroke, cardiovascular disease, kidney failure and abnormal heart rhythms.

 

REFERENCES:

1.      eMedicine- Hyperaldosteronism imaging.

2.      Radiopedia supporter

3.      "aldostronism" at Dorland's Medical Dictionary

4.      "Hyperaldostronism, eMedicine Paediatrics: General Medicine "

5.      Journal of Acute Disease- volume 5, issue 3, 1 May 2016, pages 264-266

6.      Prakash ES (2005). "Aldosterone escape" or refractory hyperaldosteronism? "MedGenMed.7 (3):25. PMC1681639.

7.      Funder etal. Endocrine society case detection, diagnosis and treatment of patients with conns syndrome: an endocrine society clinical practice guideline J Clin Endocrinol Metab.2008.

 

 

 

 

Received on 07.12.2018         Modified on 29.12.2018

Accepted on 29.01.2019      ©A&V Publications All right reserved