Treatment of cystinuria / Wilson G. Smillie, M.D. Boston.

  • Wilson G. Smillie
Date:
1915
Catalogue details

Licence: In copyright

Credit: Treatment of cystinuria / Wilson G. Smillie, M.D. Boston. Source: Wellcome Collection.

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    diet. In the subsequent treatment of their patient, Folin was able by these means, to keep him free from symptoms for over a year. Most patients, however, chafe under the restrictions of a low protein diet, and are willing even to suffer from renal colic, rather than bear the monotony of the nitrogen-poor regimen. Furthermore 30 to 50 gm. of protein a day is minimum for normal metabolism, and this amount causes a considerable excretion of cystin. Cystin is so readily soluble in weak alkali, that it seemed plausible to treat cystinuria by the addition of sodium bicarbonate to the diet. This empirical treatment only needed a patient for its justification. Curiously enough two of these cases were studied at about the same time and treated by the same method, one by Klemperer and Jacoby2 in Berlin and one by myself. The report of Klemperer’s case, how¬ ever, was published in March, 1914, and since this treatment was similar to mine, though my conclusions are at variance from his, it was thought advisable to defer publishing my studies for a year, meanwhile keeping the patient under observation. Klemperer’s patient had a typical history and symptom-complex. The studies are briefly reported. The patient was first placed on a rich protein diet. No estimation of the nitrogen intake or of the urinary nitrogen is recorded. The cystin both precipitated and in solution was determined by Gaskell’s3 method. They found a total of 716 mg. of cystin on the fifth day of the high protein diet. The patient was then put on a very low protein diet for three days. The average excretion of cystin was 78 mg. This they called the “endogenous cystin.” Finally a mixed diet was given. The nitrogen intake or excretion is not stated. From 6 to 10 gm. of sodium bicar¬ bonate were added to the diet each day. The cystin both in the precipi¬ tate and in solution rapidly decreased and on the fifth day none was present in the urine. These results are very striking, and their con¬ clusions are that the alkali does not act as a solvent for cystin, but actually influences metabolism of the body so that cystin is not excreted or even formed. The patient studied by us had a characteristic history. Patient 812, a white printer, unmarried, aged 22, was entered as complaining of gravel present in the urine for twenty months. Family History.—The patient’s father is living and is said to have tabes dorsalis. His mother, one brother and three sisters are living and well. No tuberculosis, cancer, diabetes or kidney trouble occur in the family. He denies venereal disease. He uses a moderate amount of tea, coffee and tobacco, but no alcohol. Past History.—Patient’s health has always been poor. He had scarlet fever with a cardiac complication at an early age. At 8 years of age he had rheumatic 2. Klemperer and Jacoby: Therap. d. Gegenw., 1914, lv, 101. 3. Gaskell, J. F.: Jour. Physiol., London, 1907, xxxvi, 142.
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