To the Editor.
—We have read with interest the article from Drs Smetana and Bar-Khayim published in the July 1985 issue of the Archives in which two further cases of isolated renal hypouricemia were described.1 We would like to make the following comments.According to the four-component model of renal urate excretion, any renal hypouricemia could be due to any of the following: diminished presecretory reabsorption; enhanced tubular secretion; decreased postsecretory reabsorption; or any combination of these. Discrimination between these different tubular defects can be done inbase to the responses observed in the pyrazinamide and probenecid pharmacological tests, as is summarized in the Table.There are, to our knowledge, 31 cases of isolated renal hypouricemia2 published anteriorly to the article by Drs Smetana and Bar-Khayim.1 Ten of these cases were classified as due to defective presecretory reabsorption, four to enhanced tubular secretion, six to defective
Gaspar GS, Puig JG, Mateos FA, Cabanillas AJ. Hypouricemia due to Renal Tubular Defect. Arch Intern Med. 1986;146(6):1241-1243. doi:10.1001/archinte.1986.00360180261060