Aldosteronism Hypernatremia

Aldosterone and other steroids with mineralocorticoid properties promote the reabsorption of sodium from the distal convoluted and cortical collecting renal tubules, loosely coupled to the excretion of potassium and hydrogen ion. Sodium reabsorption in the sweat and salivary glands, gastrointestinal mucosa, and across cell membranes in general is also increased. Excessive levels of aldosterone produced by tumors or overdosage with synthetic mineralocorticoids lead to hypernatremia, hypokalemia, metabolic alkalosis, increased plasma volume, and hypertension. 

Several relatively common disorders result in aldosterone secretion abnormalities and aberrations of electrolyte status. In Addison s disease, the adrenal cortex is often destroyed through autoimmune processes. One of the effects is a lack of aldosterone secretion and decreased Na+ retention by the patient. In a typical Addison s disease patient, serum [Na+] and [CL] are 128 and 96 meq/L, respectively (see Table 16.2 for normal values). Potassium levels are elevated, 6 meq/L or higher, because the Na+ reabsorption system of the kidney, which is under aldosterone control, moves K+ into the urine just as it moves Na+ back into plasma. Thus, if more Na+ is excreted, more K+ is reabsorbed. Bicarbonate remains relatively normal. The opposite situation prevails in Cushing s disease, however, in which an overproduction of adrenocorticosteroids, especially cortisol, is present. Glucocorticoids have mild mineralocorticoid activities, but ACTH also increases aldosterone secretion. This may be caused by an oversecretion of ACTH by a tumor or by adrenal hyperplasia or tumors. Serum sodium in Cushing s disease is slightly elevated, [K+] is below normal (hypokalemia), and metabolic alkalosis is present. The patient is usually hypertensive. A more severe electrolyte abnormality is seen in Conn s syndrome or primary aldosteronism, usually caused by an adrenal tumor. Increased blood aldosterone levels result in the urinary loss of K+ and H+, retention of Na+ (hypernatremia), alkalosis, and profound hypertension. 

Hypokalemia or hypernatremia occur with the overproduction of aldosterone (aldosteronism). Aldostenmism occurs after the age of 40 and results in increased Na resorption, increased blood volume, and increased urinary losses. In rare cases, hypokalemia occurs with the habitual consumption of large amounts of black licorice. Licorice contains glycyrrhizic add. This compound has a structure and an effect similar to those of aldosterone. 

In addition to vasodilatory responses, PGs have a number of other effects in the kidney. For example, PGs stimulate adenylate cyclase in juxtaglomerular cells, resulting in an increase in cAMP production this, in turn, increases renin release. Renin stimulates the release of aldosterone, which increases renal tubular secretion of potassium (Stillman Schlesinger 1990). PGs also enhance tubular excretion of sodium and water (Patrono Dunn 1987). By causing these effects in the kidneys, PGs can alter electrolyte homeostasis. Therefore, other renal side-effects of NSAID therapy can include hyperkalemia, hypernatremia and edema. Often these metabolic changes are not observed in individuals with normal renal function, but in the presence of pre-existing disease they can become clinically significant. 

The presence of excess TBW and hypernatremia indicates a net gain of water and Na, with Na gain in excess of water (see Figure 46-3). This condition is commonly observed in hospital patients receiving hypertonic saline or sodium bicarbonate. Other causes of hypervolemic hypernatremia include hyperaldosteronism and Cushing s syndrome (see Chapters 24 and 51). Excess aldosterone and cortisol (which also act as ligands for the distal tubule aldosterone receptor) results in excess Na and water retention. Corticosteroid therapy can have similar effects as weh. 

Common laboratory findings include hypokalemia (80% to 90%), suppressed renin activity, elevated plasma aldosterone concentrations, hypernatremia (>142 mEq/L), hypomagnesemia, and elevated bicarbonate concentration (>31 mEq/L). 

Conn s syndrome is apparently caused by an inability of the adrenal cortex to carry out 17a-hydroxylation during the biosynthesis of the hormones from cholesterol. Consequently, the disease is characterized by a high secretory level of aldosterone, which lacks a 17a-hydroxyl functional group. In addition, hypernatremia, polyuria, alkalosis, and hypertension are observed (12). 

Supplements may be provided if a lack of aldosterone or cortisol is present. The nurse must monitor for signs of overtreatment, which would include signs of hypernatremia and of Cushing syndrome owing to excess cortisol. 6... 

Reduced absorption from the Gl tract has many causes, some of which are diarrhea, insufficient dietary intake, damage to the small intestine that may inhibit absorption, and malnutrition. Some common causes of excessive loss in the urine include diureses owing to alcohol, loop diuretics, and glycosuria. Other factors that may lead to hypomagnesemia are hypersecretion of aldosterone (causing hypernatremia), ADH, or thyroid hormone and excessive vitamin D (causing hypercalcemia) and intravenous fluids. 

Sodium deprivation increases aldosterone secretion, probably by modifying the volume of the body fluids. This conclusion was reached because of observations that (1) the administration of water (with Pitressin to prevent diuresis) depresses aldosterone secretion in spite of the hyponatremia (2) if the body fluids are expanded by administering normal saline, aldosterone excretion is stimulated although the sodium levels of the blood are not modified and (3) dehydration leads to aldosterone secretion, although the reduction in body fluid volume resulting from dehydration is associated with hypernatremia. From these observations, changes in body fluid volume appear to affect aldoster-rone secretion, and it has been stated that the expansion of the body fluids reduces aldosterone secretion. This conclusion, which is based on experimental obser-... 

Hypernatremia is not an absolute finding in primary hyperaldosteronism, and a mechanism of renal adaptation has been proposed. Thus, in progressive aldosteronism, salt retention activates a nonaldoste-ronic mechanism of sodium regulation, which increases sodium excretion in the distal tubules without affecting the proximal tubule, thus reestablishing the balance between sodium intake and excretion. Whether the postulated natriuretic hormone [32] is involved remains to be seen (see Fig. 9-12). 

Excess of sodium in the body causes hypernatremia and its deficiency causes hyponatremia. H5rpernatremia causes hi blood pressure, h5rpertension, excessive sweating, lack of proteins and kidney damage. Sometimes it causes edema which may occur due to circulatory failure, excessive production of aldosterone and ADH harmone. 

The nutritional requirement is a reflection of obligatory losses (maintenance) and the needs of growth, pregnancy, and lactation. Abnormal losses owing to disease, or in animals such as humans and horses which sweat extensively, raise the requirement. The impact of equine sweating is different from that in humans. Human sweat always contains sodium at concentrations well below plasma levels (and when aldosterone secretion is raised, levels of sweat sodium fall very low) horse sweat is hypertonic but this helps to offset the osmotic effect of the increased respiratory water loss during exertion, i.e., it may be a defense against hypernatremia, rather than a potential cause of sodium depletion. Similarly hypernatremia in many species induces dehydration natriuresis - an appropriate defense. 

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