Abstract
SINCE 1810, when Wollaston1 first described a urinary calculus composed entirely of cystine, the pathogenesis of cystinuria has been the subject of controversy. Most current concepts date from the observations that the urine of these patients contains large amounts of lysine, arginine2 , 3 and ornithine4 as well as cystine, whereas the plasma levels of these amino acids are not elevated.3 , 5 , 6 These findings led Dent and Rose3 to conclude that the gross cystinuria characteristic of this disease was due to defective tubular reabsorption rather than impaired metabolism of cystine. The renal clearances of the 4 di-amino acids were shown to be abnormally . . .
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
