Adverse effects of sodium restriction with concurrent medication use

Abstract 

Although dietary sodium restriction is advocated commonly for the treatment of high blood pressure and espoused to be the solution to the high prevalence of hypertension in this country, there are a number of clinical situations in which reduced sodium intake may be more hazardous for the patient than the condition it is being prescribed to treat. Sodium restriction is known to enhance the antihypertensive action of many blood pressure-lowering drugs, and along with thiazide diuretics it can reduce urinary calcium excretion in patients who form hypercalciuric stones. However, adverse consequences of sodium restriction in a variety of conditions are being identified increasingly, particularly in patients with impaired sodium conservation mechanisms. Ischemic and nephrotoxic injuries are more readily induced in states of sodium depletion caused by impaired renal hemodynamics and activation of the renin-angiotensin system. Acute renal failure can be precipitated by sodium restriction and concomitant use of any of a number of commonly used medications. The renal tubular reabsorption of drugs such as lithium is enhanced by sodium restriction and can result in toxic blood levels of these drugs. It has been found that activation of the renin-angiotensin system by sodium depletion in experimental models promotes the growth of cysts in cystic renal disease. Therefore, in a given patient the recommendation to reduce sodium intake should include careful consideration of both potential benefits and possible adverse consequences.

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