RT Journal
A1 SLOAND JA, Izzo JL, JR
T1 Cystinuria: Failure of captopril to reduce cystine excretion-reply
JF Archives of Internal Medicine
JO Archives of Internal Medicine
YR 1989
FD March 1
VO 149
IS 3
SP 713
OP 717
DO 10.1001/archinte.1989.00390030153036
UL http://dx.doi.org/10.1001/archinte.1989.00390030153036
AB In Reply.—We are most encouraged to see that our findings1 have prompted other investigators to research the effects of captopril therapy on cystine excretion in cystinuria. The individual case study performed by Dahlberg and Jones demonstrates a close correlation between urinary cystine determinations as quantitated both by the ion exchange–triketohydrindene hydrate (Ninhydrin) method and the phosphotungstic method that we used. The reason for the discrepancy between their results and those we obtained is unclear. As suggested by these authors, both the excretion of cystine and the effect of a vasoactive drug such as captopril on that excretion is probably multifactorial. Genetic subtypes of cystinuria could account not only for differing renal tubular handling of cystine, dibasic amino acid, and, possibly, captopril, but also for intestinal transport of these substances.2 Alternatively, their patient, who had such high levels of urinary cystine, may not have received enough captopril to