Clinical Aspects of Diuretics

In a healthy human subject, changes in dietary intake or variations in the extrarenal loss of fluid and electrolytes are followed relatively rapidly by adjustments in the rate of renal excretion, thus maintaining the normal volume and composition of extracellular fluid in the body. Edema is an increase in extracellular fluid volume. In almost every case cf edema encountered in clinical medicine, the underlying abnormality involves a decreased rate of renal excretion. One of the factors influencing the normal relationship between the volume of interstitial fluid and the circulating plasma is the pressure within the small blood vessels. In diseases of hepatic origin (e.g., cirrhosis), the pressure relationships are dis turbed primarily within the portal circulation and ascites results. In congestive heart failure, pressure-flow relationships may be disturbed more in the pulmonary or systemic circulation and edema may be localized accordingly.

There is overwhelmingevidence to indicate that the primary disturbance of the kidney is in its ability to regulate sodium excretion, which underlies the pathogenesis of edema. Three approaches are available when edema fluid accumulates because of excessive reabsorption of sodium and other electrolytes by the renal tubules. First, one can attempt to correct the primary disease if possible; second, one can reduce renal absorption of electrolytes by the use of drugs; and third, one can restrict sodium intake to a level that corresponds to the diminished renal capacity for sodium excretion. Cardiac decompensation is one of the most common causes of edema. Treatment consists of full digitalization, which should be considered the primary therapeutic agent. Diuretic drugs have a secondary though very important role because it has been shown that blocking excessive electrolyte reabsorption in the renal tubule alleviates the symptoms of cardiac failure and also improves cardiac function. Diuretics are also used in the treatment of hypertension.

Diuretic therapy may lead to a number of metabolic and electrolyte disorders. In general, these disturbances are mild but can be life-threatening in certain cases. Some of the common adverse effects observed with diuretic treatment are hypokalemia, hyperuri-cemia, and glucose intolerance. Diuretics that possess a site of action proximal to the collecting tubules, such as the loop and thiazide diuretics, induce potassium loss; an average loss cf 0.5-0.7 meq/L generally results with long-term therapy (30). In most young hypertensive patients, this reduction does not present any problem; however, in older patients or patients with preexisting heart disease, it may lead to the occurrence of ventricular arrhythmias. Combinations with potassium-sparing diuretics are frequently used to minimize the effect. Dietary potassium supplements may also be prescribed. In patients receiving long-term diuretic therapy, serum uric acid concentrations increase on average 1.3 mg/L as the result of a decrease in extracellular volume and increased urate reabsorption from the filtrate. Some patients may experience an attack of gout, or those with preexisting gout or excessive uric acid production may experience more frequent attacks. A number of studies have shown that some patients who have undergone long-term diuretic therapy have elevated blood levels of glucose and that their tolerance to glucose decreases (31). The mechanism of the diuretic-induced glucose intolerance is unknown. Some other side effects that are observed with diuretic treatment are increases in cholesterol levels in men and post-menopausal women (32), ototoxicity, and hy-pomagnesemia.

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