Hypoaldosteronism - disease or normal response?

Article Abstract:

Hyperkalemia, an excess of potassium in the blood, may result from a variety of different physiological influences. It may result from kidney dysfunction, from a deficiency in aldosterone secretion or a deficiency in response to aldosterone, or a host of other factors. Aldosterone stimulates the resorption of sodium and the excretion of potassium in the distal tubules of the nephrons within the kidneys; inadequate potassium excretion may result from a congenital deficiency in aldosterone, the loss of aldosterone stimulation resulting from renin deficiency, the use of ACE inhibitors, or a variety of drugs which interfere with mineralocorticoid receptors, including spironolactone. Not all patients with hyperkalemia have kidney disease or aldosterone deficiency, however, and the term "pseudohypoaldosteronism" was coined to describe patients with hyperkalemia in the absence of either hypoaldosteronism or kidney dysfunction. Type I pseudohypoaldosteronism results from a deficiency in the receptors for aldosterone within the kidney; it is characterized salt wasting, hyperkalemia, low blood pressure, a lack of response to mineralocorticoid, and elevated plasma renin and aldosterone. A second form of pseudohypoaldosteronism has been recognized which has been dubbed type II. This form, which may occur sporadically or as a familial disease, is distinguished from type I by the presence of high blood pressure. It had previously been proposed that type II pseudohypoaldosteronism may result from a defect in the transport of chloride ions within the kidney nephron. This defect would change the voltage across the cell membranes of potassium-transporting cells and make it more difficult to excrete potassium. Now, in the February 14, 1991 issue of The New England Journal of Medicine, researchers have presented physiological evidence that a defect in chloride transport, a so-called ''chloride shunt,'' is indeed the cause of type II pseudohypoaldosteronism. The physiological response to infusion of sodium compounds was evaluated in three patients, a father and two of his children. The results not only support the notion of the chloride shunt, but provide further evidence that a single inherited defect may cause the type II syndrome. Fortunately, type II pseudohypoaldosteronism may be completely reversed with a low-sodium diet and diuretic treatment. (Consumer Summary produced by Reliance Medical Information, Inc.)

Case studies, Hypertension, Kidneys, Genetic disorders, Kidney, Chlorides, Endocrine gland diseases, Endocrine diseases, editorial, Hyperkalemia, Chlorides in the body

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Costimulatory B7 molecules in the pathogenesis of infectious and autoimmune diseases

Article Abstract:

T-cell costimulation involves two different signals, an important mechanism in disease immunity. The B7:CD28/CTLA-4 costimulatory pathway consists of the two ligands B7-1 and B7-2 binding to the two T cell receptors CD28 and CTLA-4. The immune response of chronic diseases can be visualized as a continuum from autoimmune diseases on one end to infectious diseases on the other extreme. B7 molecules may stimulate the production of helper T cells in autoimmune illness, while reductions in T cell ratios disable immunity in infections like lepromatous leprosy or microfilaremic filariasis. Further research may lead to innovative immunosuppressive therapies or vaccines.

Communicable diseases, Autoimmune diseases, Antigen receptors, T cell, T cell antigen receptors, Cellular signal transduction, Cellular immunity

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