The influence of indomethacin on renal acidification in normal subjects and in patients with sickle cell anemia.
Patients with sickle cell nephropathy have been shown to have a distal type of incomplete renal tubular acidosis. We evaluated renal tubular acidification before and after indomethacin administration because prostaglandins have been shown to inhibit the transepithelial potential difference in the collecting tubule and since we previously found indirect evidence of increased prostaglandin synthesis in patients with sickle cell nephropathy. Indomethacin did not change urine pH in the sickle cell anemia (SCA) patients or in the control subjects. It induced, however, an increase in titratable acid excretion particularly in the SCA patients. Ammonium excretion decreased after indomethacin in the SCA patients while it did not change significantly in the control subjects. In the SCA patients, net acid excretion did not rise after indomethacin. In contrast there was an increase in net acid excretion after indomethacin administration in the control subjects. We conclude from our study that the inability of patients with SCA to lower urine pH to a normal extent after ammonium chloride loading is not improved by indomethacin. The decrease in ammonium excretion after indomethacin administration in SCA might be due to an effect of the prostaglandin synthesis inhibitor indomethacin on ammoniagenesis.
D000138:Acidosis / Q000150:complications / Q000188:drug therapy*; D000293:Adolescent; D000328:Adult; D000755:Anemia, Sickle Cell / Q000150:complications / Q000188:drug therapy; D005260:Female; D006801:Humans; D007213:Indomethacin / Q000627:therapeutic use*; D007674:Kidney Diseases / Q000150:complications / Q000188:drug therapy*; D007684:Kidney Tubules; D008297:Male; D008875:Middle Aged
D007213:Indomethacin