On the Nature of the Urinary Volume Response To Diuretic Agents by Patients with Edema

¹ Cornell University Medical College; Hospital for Joint Diseases and Medical Center; Cardiovascular Research Unit of the Beth Israel Medical Center; Lincoln Hospital; New York, N.Y.
² Phelps Clinic Research Foundation, El Reno, Oklahoma.
³ Cornell University Medical College; Hospital for Joint Diseases and Medical Center; Cardiovascular Research Unit of the Beth Israel Medical Center; Lincoln Hospital; New York, N.Y.

The response to a diuretic agent has a dysphasic character. It is a D-AD phenomenon, a diuretic response associated with an antidiuretic reaction. Evidence points to a hormonal factor, aldosterone, as being responsible for the antidiuretic reaction, as demonstrated by the competitive inhibition of the effect of aldosterone by spirolactone and other steroids.

The diphasic response is not confined to any special diuretic. It is applicable to drug diuresis in general. The response of the patient with edema is similar to that of the normal individual without edema.

Evaluation of a diuretic calls for the algebraic sum of two opposing effects to yield the net diuresis. The amount of edema, the dose of the drug, and the initial diuretic response are deciding factors. This formulation points the way to successful adjustment in the event of failure to clear edema.

The relative dominance of factors D and AD shows individual differences. Dominance of the AD factor is often responsible for the paradox of so-called intractable edema in an individual who is very sensitive to the drug. It is also often responsible for progressive decline in diuretic response to a series of doses, and for the paradox of increasing edema by the use of a diuretic. These may be overcome by the use of spirolactone (Aldactone) and other steroids which block the salt-retaining properties of aldosterone.

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