Escape from sodium and potassium retaining actions of aspirin-like drugs used in a patient with Bartter's syndrome

Escape from sodium and potassium retaining actions of aspirin-like drugs used in a patient with Bartter's syndrome. An analysis was done with regard to the mode of escapes from sodium and potassium retaining actions of aspirin-like drugs in a patient with Bartter's syndrome. In the indomethacin therapy of the syndrome, there was a delay in the initiation of potassium escape as compared to sodium escape, whereas no delay was seen in the ibuprofen therapy. This delay was probably related to the direct or indirect inhibition of sodium-potassium exchange in the distal nephrons. The course of aspirin therapy went midway between the above two. In the spironolactone therapy, the mode of escape was a mirror image of the one in the indomethacin therapy. Also, in a patient with rheumatoid arthritis, but without Bartter's syndrome, the escapes from the effects of indomethacin were seen. In order to understand the effect of these drugs on potassium excretion in Bartter's syndrome, some other intrarenal events, such as the influence on chloride transport in the loop of Henle leading to potassium conservation, may have to be considered.