Sodium disease/disorder effects

P3. Patrick, J., and Hilton, P. J., Characterization of sodium-transport disorders in disease Different effects upon sodium and potassium of changes in the sodium pump and in membranes permeability. Clin. Sci. Mol. Med. 57, 289 (1979). 

Many glomerular diseases, such as those associated with diabetes mellitus or systemic lupus erythematosus, exhibit renal retention of salt and water. The cause of this sodium retention is not precisely known, but it probably involves disordered regulation of the renal microcirculation and tubular function through release of vasoconstrictors, prostaglandins, cytokines, and other mediators. When edema or hypertension develops in these patients, diuretic therapy can be very effective. If heart failure is also present, see the warnings mentioned above. 

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. 

The autonomous, sustained production of AVP in the absence of known stimuli for its release is called SIADH. In this syndrome, plasma AVP concentrations are inappropriately increased relative to a low plasma osmolality and to a normal or increased plasma volume. SIADH may be the result of one of several factors production of vasopressin by a malignancy (such as a small cell carcinoma of the lung), the presence of acute and chronic diseases of the central nervous system, pulmonary disorders, or a side effect of certain drug therapies. In addition, as many as 10% of patients undergoing pituitary surgery have a transient SIADH approximately 8 to 9 days after surgery (when the patient is at home), which responds to water restriction (2 to 3 days) and resolves without recurrence. In SIADH, a primary excess of AVP, coupled with unrestricted fluid intake, promotes increased reabsorption of free water by the kidney. The result is a decreased urine volume and an increased urine sodium concentration and urine osmolality. As a consequence of water retention, these patients become modestly volume expanded. The increase in intravascular volume causes hemodilution accompanied by dilutional hyponatremia and a low plasma osmolality. Volume expan-... 

Several bisphosphonates are available in the United States. Etidronate sodium (Didronel) is used for treatment of Paget s disease and may be used parenterally to treat hypercalcemia. Because etidronate is the only bisphospho-nate that inhibits mineralization, it has been supplanted largely by pamidronate and zoledronate for treating hypercalcemia. Pamidronate (Aredia) is approved for management of hypercalcemia but also is effective in other skeletal disorders. Pamidronate is available in the United States only for parenteral administration. For treatment of hypercalcemia, it may be given as an intravenous infusion of 60 to 90 mg over 4 to 24 hours. 

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