Biographical Memoirs

VOLUME 63



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Biographical Memoirs: Volume 63 Biographical Memoirs VOLUME 63

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Biographical Memoirs: Volume 63 This page in the original is blank.

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Biographical Memoirs: Volume 63 THOMAS ADDIS July 27, 1881–June 4, 1949 BY KEVIN V. LEMLEY AND LINUS PAULING THOMAS ADDIS was one of the early physician members of the National Academy of Sciences. As a physician-scientist, he had a distinctively quantitative and rigorous approach to clinical problems. His name is firmly connected to the study of kidney function and structure-function correlation and to the diagnosis and dietary treatment of the class of kidney disorders once collectively known as Bright's disease. During his life he developed a national and international reputation as a result of his research and his success in treating patients. His approach to diagnosis and treatment, however, never came into widespread clinical use and fell into almost total disuse in the United States soon after his death. The application of dietary therapy in renal disease is currently enjoying a considerable renaissance, and Addis's work is being rediscovered and appreciated once more for its rigor and clarity. [Statement by L.P., a friend and former patient of Tom Addis: Forty years ago I agreed to write the biographical memoir of Tom Addis. His widow, however, asked me not to include any mention of his political beliefs and activities. She said that she and her two children would not permit such mention, partly because of their fear for their own safety. This was at the start of the McCarthy period. I

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Biographical Memoirs: Volume 63 felt that a biographical memoir that did not mention this important aspect of Tom Addis's life should not be published, and I deferred writing the memoir. Now, after the death of Mrs. Addis, I feel free to publish the memoir, in the writing of which I have had the great benefit of collaboration with Dr. K. V. Lemley.] Tom Addis was born in Edinburgh, Scotland, on July 27, 1881. His mother was Cornelia Beers Campbell. His father, Thomas Chalmer Addis, was a Presbyterian minister. Addis was raised in a religious and rather ascetic environment with a great emphasis on moral values. In his youth he carried a bible in his pocket and was quite conversant about its contents. Decades after his naturalization as a U.S. citizen in 1917, he still considered his native Scotland and Edinburgh as "the most beautiful country and the most lovely town in the world." Addis was graduated from Watson's College in Edinburgh in 1900 and received the M.B.Ch.B. degree in 1905 from the Faculty of Medicine of the University of Edinburgh. Following three more years of hospital training in Edinburgh, Gloucester, and Bristol (including a year working and living in slums), he received the M.D. degree and was elected to membership in the Royal College of Physicians (Edinburgh). Two years of postdoctoral research in Berlin and Heidelberg followed (1909–11) as a Carnegie scholar and fellow. Addis returned to Scotland as registrar at Leith Hospital (Edinburgh) in 1911. Later in 1911 Addis accepted an appointment as chief of the Clinical Laboratory of the Department of Medicine of the newly organized Stanford University School of Medicine in San Francisco (the medical school moved to its current location on the Palo Alto campus in 1959). The new medical school dean, Dr. Ray Lyman Wilbur, brought Addis to Stanford on the recommendation of Sir Clifford Allbutt of the University of Cambridge, an event Wilbur

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Biographical Memoirs: Volume 63 later remembered as "among the more fortunate things which I did as a young dean of a young medical school." In 1913 Addis married Elesa Bolton Partridge, with whom he eventually had two daughters, Elesa and Jean. Mrs. Addis was a trained nurse and later a nurse-dietician in Addis's renal clinic at Stanford. Addis was promoted to associate professor of medicine in 1913. He served as a captain in the U.S. Army Medical Corps during World War I (1917–19) at Camp Lewis, Washington, as part of a medical contingent drawn from Stanford Medical School. Earlier, before the United States formally entered the war, Addis had come under the threat of prosecution by the U.S. Attorney's office in San Francisco, probably for violation of the neutrality laws (he was then still a British citizen). He benefited from the intervention of Dr. Wilbur, who was on leave from the medical school while working in the office of Herbert Hoover, President Wilson's wartime food administrator. Addis became professor of medicine in 1920 and served in that capacity until becoming professor emeritus in 1946. He also ran the Clinic for Renal Diseases at Stanford from 1921. He served as consultant to the surgeon general during World War II (1942–45), working on artificial substitutes for blood plasma with support from the Office of Scientific Research and Development (OSRD). After retirement, Addis continued to work in his laboratory at Stanford until the summer of 1948, when he moved to Los Angeles to continue his research, working with Dr. Jessie Marmorston in Harry Goldblatt's Institute for Medical Research at Cedars of Lebanon Hospital.1 Addis died at the age of sixty-seven at Cedars of Lebanon Hospital on June 4, 1949, in septic shock following surgery to remove a kidney infarcted as a result of thromboembolic disease.

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Biographical Memoirs: Volume 63 Addis published over 130 scientific and clinical papers as well as two important books, The Renal Lesion in Bright's Disease (1931, 4), with J. R. Oliver, and Glomerular Nephritis: Diagnosis and Treatment (1948). He received the following prizes and lectureships: a Carnegie research fellowship, the Gibbs Prize, and in 1942 the Cullen Prize (awarded by the Royal College of Physicians of Edinburgh for the "greatest benefit done to practical medicine in the previous four years"); he delivered the Harvey Lecture in 1928 and the Thayer Lectures in 1931 and was visiting fellow at the Rockefeller Institute in 1928. Addis was a member of the Association of American Physicians, the American Physiological Society, the Society for Experimental Biology and Medicine, the American Society for Clinical Investigation (president in 1930), and the National Academy of Sciences from 1944. He was also a fellow of the Royal College of Physicians (Edinburgh) and the American College of Physicians. Addis's students, colleagues, and co-workers over the years included Ray Lyman Wilbur, C. K. Watanabe, George D. Barnett, Jean R. Oliver, A. E. Shevky, M. C. Shevky, Marjorie G. Foster, Douglas R. Drury, B. A. Flyers, Leona Bayer, Lois L. MacKay, Eaton M. MacKay, Lee J. Poo, William Lew, David A. Karnofsky, Evalyn Barrett, Florence Walter, Horace Gray, David A. Rytand, Arthur L. Bloomfield, Richard W. Lippman, Jessie Marmorston, Leland J. Rather, Edward C. Persike, Eloise Jameson, Belding Scribner, Marcus A. Krupp, William Dock, B. O. Raulston, and Roy Cohn. ADDIS'S EARLY LABORATORY WORK (1909-19) Addis's early work was concerned with several different clinical problems. As with his later work, it was characterized by a high degree of methodological sophistication and a critical attitude toward current practice. His pragmatism

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Biographical Memoirs: Volume 63 and concern with practical clinical applications are also apparent throughout. His earliest work (part of it conducted during a Carnegie research fellowship in Germany) concerned blood coagulation. He showed convincingly that, contrary to earlier claims, oral administration of either citric acid or calcium lactate had no effect on blood coagulation in patients with a variety of diseases, both hemorrhagic and thrombotic. These studies used Addis's modification of a standard coagulation assay (McGowan's method), a modification that he validated by daily triplicate determinations of his own coagulation time over fifty days. He also contributed investigations into the pathogenesis of hereditary hemophilia, suggesting that the disease is due to a defect in the conversion of prothrombin to thrombin, rather than in the activity of the thrombin itself or (as was believed by Sahli and others) a cellular defect.2 After moving to Stanford, Addis conducted spectroscopic analyses with Wilbur of the hemoglobin breakdown products (bile pigments) in hemolytic disease states such as pernicious anemia. He also published several studies on diabetes mellitus, including an analysis of the different clinical methods for estimating the degree of acidosis (this was just before the advent of insulin therapy), a critique of the conventional preparation of the diabetic patient for surgery (which he held to be "a pure hypothesis, unsupported by any experimental work") together with a proposal for better perioperative management, and an approach to the early diagnosis of diabetes mellitus in patients incidentally found to have glycosuria. The latter was based on a graded increase in the "strain" imposed on the glucose-utilizing tissues by increasing daily glucose loads, an early form of glucose tolerance test in which glycosuria rather than blood sugar was measured, and an approach similar to that which he later employed in studying kidney function.3

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Biographical Memoirs: Volume 63 Several studies were carried out during Addis's service in the Army Medical Corps during World War I. Measurements of blood pressure and pulse rates in recruits were used to construct tables of normal values for these parameters under conditions of basal and normal activity, exercise, and changes in position. UREA EXCRETION AND THE AMOUNT OF FUNCTIONING RENAL TISSUE (1916-25) Almost from the time of Richard Bright's first clinical and pathological descriptions in 1827 of the constellation of kidney ailments that so long bore his name, the fact that blood urea levels rise in diseases of the kidney had been known. Because the kidneys are the sole excretory organs for urea (formed in protein catabolism), blood urea concentrations rise whenever renal excretory function is compromised. As early as 1856, Picard recommended the measurement of blood urea as a diagnostic tool. Little more was done with these observations, though, until the turn of the century and the development of analytical procedures (principally by Folin, Wu, Van Slyke, and Marshall) capable of accurately determining urea concentrations in small samples of blood and urine. This ushered in an era of dynamic tests of kidney function using the rate of renal urea excretion and the blood urea concentration. From 1916 to 1925, Addis and his colleagues produced about thirty publications on the quantitative assessment of renal function through measurement of urea excretion. Two large series concerned renal function in man ("The Rate of Urea Excretion I–VIII") and in the rabbit ("The Regulation of Renal Activity I–XI"). In the human experiments, Addis, his students, and his co-workers were the subjects, supplying the specimens for literally hundreds of blood and urine urea determinations. In all these studies

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Biographical Memoirs: Volume 63 the goal was a functional assessment of the anatomic state of the normal and diseased kidney: "This would give us what we most need in clinical work—an anatomical foundation for early diagnosis, prognosis, and treatment. For functional studies have in the last resort no fundamental significance unless they are of such a nature that structural inferences may be drawn from them." In this attitude, Addis continued in an intellectual tradition dating back to Richard Bright and René Laennec, two of the pioneers in clinical-pathologic correlation. Bright in particular had sought to understand kidney disease "by reference to Morbid Anatomy" (as he stated it in his famous Reports on Medical Cases). Addis saw himself faced with "the problem of the relation between renal function and structure, the problem which Bright set before himself nearly a century ago." Given the very poor level of understanding of kidney physiology at the time, it is not surprising that Addis and many of his contemporaries sought a bedrock of reliable knowledge in the relatively better understood pathology of the kidney. In the first paper in this series, Addis and Watanabe examined the previous quantitative theory of Ambard and Weill (1912) against their more complete and carefully obtained data and found that although it was qualitatively suggestive, it did not "allow . . . even a rough prediction of the rate of urea excretion" (1916, 1). This motivated a very long paper by Addis (1917) in which he described his own test to assess "the work of the kidney." In it he outlined the characteristics of an ideal substance for testing the secretory (i.e., excretory) function of the kidney: It must be "a true end-product . . . incapable of chemical alternation within the body . . . whose only path of excretion [is] through the kidneys"; its blood concentration should also be susceptible to alteration by systemic administration.4 Earlier attempts at a functional assessment of renal

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Biographical Memoirs: Volume 63 had foundered on the high normal variability of renal excretory function, variability arising largely from the changing excretory needs of the body.5 Addis and his colleagues were convinced that such high variability was found only in short-term studies of renal function and was due to a changing balance in the factors that normally regulate renal activity. Over twenty-four-hour periods, the forces tended to cancel one another, leading to a greater stability in the measured renal function. The fundamental index of function that Addis and his colleagues settled on was the ratio U·V/B, the Addis urea ratio, where U is the urine urea concentration, V is the urine volumetric flow rate, and B is the blood urea concentration. Thus, the product U·V is the urinary excretion rate of urea. The urea ratio was approximately constant in a given individual (and reflected the functioning renal mass), at least for urine flows over about two milliliters/minute, the augmentation limit of Van Slyke. Many of the later papers in this series were dedicated to describing factors that contribute to the short-term variability in renal excretory function, so that these could be controlled during clinical examinations. Later Addis extended the urine collection period to twenty-four hours and thus overcame much of this variability. The principal factors uncovered were the state of diuresis, diet (particularly caffeine, protein, and amino acids), exercise, and certain hormones (adrenalin and hormones of the posterior pituitary gland). Among the factors subject to external control was the blood urea concentration B. It was established that the variation in the ratio U·V/B decreases with increasing blood urea concentrations. Addis's interpretation of this finding was that the "strain" of excreting greater amounts of urea would push the kidney to the maximum work of which it was capable.6 Thus, patients were studied after receiving

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Biographical Memoirs: Volume 63 an acute oral urea load. Tests of renal function were in addition conducted in a fasting state and during a water diuresis (which Van Slyke had also shown decreases variability). Through such efforts to suppress or stabilize regulatory influences, the coefficient of variation for urea ratios in a single individual in Addis's lab was reduced to 5.1 percent. Addis conceived of the excretory capability of the kidney as the result of two factors: the total functioning mass of secretory tissue (the relatively constant factor) and the level of renal activity (the variable factor). The influence of renal mass on excretory function was suggested by the observation that the body weights (and hence the kidney weights) of rabbits and men fall in approximately the same proportion as their urea ratios (35:1 and 33:1, respectively). This was also suggested by studies of the urea ratio in animals with reduced functional mass as a result of nephrectomy7 or graded damage to the kidney in experimental uranium nephritis.8 Interestingly, Addis and his colleagues did find that the ratio U·V/B somewhat overestimated kidney weight (approximately 17 percent) after compensatory hypertrophy. The discrepancy was rectified in a morphological study by Jean Oliver in which he showed that a disproportionately large amount of renal hypertrophy following uninephrectomy was due to hypertrophy in the proximal convoluted tubules. At that time, renal excretory function was thought to be primarily a secretory process (the importance of glomerular filtration was not yet fully appreciated), and the most effective portion of the nephron for urea secretion was considered to be the convoluted tubule. The evolution of all kidney studies was considerably advanced by the development of the concept of renal clearance. The first expression of the clearance concept, viz., that the Addis urea ratio expresses the virtual volume of blood freed of urea by the action of the kidney in a unit of

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Biographical Memoirs: Volume 63 Clinical methods of estimating the degree of acidosis in diabetes. Calif. State J. Med. 11:440–42. With R. L. Wilbur. Urobilin: Its clinical significance. Trans. Assoc. Am. Physicians 28:617–82. 1914 With R. L. Wilbur. Urobilin: Its clinical significance. Arch. Int. Med. 13:235–86. 1915 A working hypothesis of hemoglobin pigment metabolism. Arch. Int. Med. 15:413–37. The preparation of diabetic patients for operation. JAMA 64:1130–34. 1916 With C. K. Watanabe. The rate of urea excretion. First paper. A criticism of Ambard and Weill's laws of urea excretion. J. Biol. Chem. 24:203–20. The effect of intravenous injections of fresh human serum and of phosphated blood on the coagulation time of the blood in hereditary hemophilia. Proc. Soc. Exp. Biol. Med. 14:19–23. With C. K. Watanabe. The rate of urea excretion. II. The rate of excretion of administered urea in young healthy adults on a constant diet. J. Biol. Chem. 27:249–66. With C. K. Watanabe. The volume of urine in young healthy adults on a constant diet. J. Biol. Chem. 27:267–72. With G. D. Barnett. The effect of pituitrin and adrenalin on the urea-excreting function of the kidney. Proc. Soc. Exp. Biol. Med. 14:49. With C. K. Watanabe. A method for the measurement of the urea-excreting function of the kidneys. J. Biol. Chem. 28:251–69. 1917 With C. K. Watanabe and J. R. Oliver. The function of the kidneys under strain in uranium nephritis and the relationship between anatomy and function under these conditions . Proc. Soc. Exp. Biol. Med. 14:147. With A. E. Shevky. Sources of error in the estimation of dextrose by the colorimetric picrate method. Proc. Soc. Exp. Biol. Med. 15:79.

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Biographical Memoirs: Volume 63 With C. I. Watanabe. The rate of urea excretion. III. The effect of changes in blood urea concentration on the rate of urea excretion. J. Biol. Chem. 29:391–98. With C. K. Watanabe. The rate of urea excretion. IV. The effect of changes in the volume of urine on the rate of urea excretion. J. Biol. Chem. 29:399–404. With C. K. Watanabe. The causes of variation in the concentration of urea in the blood of young healthy adults. Arch. Int. Med. 19:507–17. With G. D. Barnett. Urea as a source of blood ammonia. J. Biol. Chem. 30:41–46. With A. E. Shevky. The return of urea from the kidney to the blood. Am. J. Physiol. 43:363–70. The ratio between the urea content of the urine and of the blood after the administration of large quantities of urea; an approximate index of the quantity of actively functioning kidney tissue. J. Urol. 1:263–87. The early diagnosis of diabetes: A simple method involving strain on the capacity of the tissues to utilize glucose. JAMA 69:109–11. 1918 With G. D. Barnett and A. E. Shevky. The regulation of renal activity: I. Regulation of urea excretion by the concentration of urea in the blood and in the urine. Am. J. Physiol. 46:1–10. With A. E. Shevky and G. Bevier. The regulation of renal activity: II. Regulation of urea excretion by anatomical factors. Am. J. Physiol. 46:11–21. With G. D. Barnett and A. E. Shevky. The regulation of renal activity: III. Regulation of urea excretion by unknown factors. Am. J. Physiol. 46:22–27. With G. D. Barnett and A. E. Shevky. The regulation of renal activity: IV. Regulation of urea excretion by adrenalin. Am. J. Physiol. 46:39–51. With G. D. Barnett and A. E. Shevky. The regulation of renal activity: V. Regulation of urea excretion by pituitrin. Am. J. Physiol. 46:52–62. With M. G. Foster and G. D. Barnett. The regulation of renal activity: VI. The effect of adrenalin and pituitrin on the action of the kidney under strain. Am. J. Physiol. 46:84–89.

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Biographical Memoirs: Volume 63 With A. E. Shevky and G. Bevier. The regulation of renal activity: VII. The balance between the regulation by adrenalin and by pituitrin . Am. J. Physiol. 47:129–46. With A. E. Shevky. The rate of color production in alkaline solutions of dextrose and picrate. J. Biol. Chem. 35:43–51. With A. E. Shevky. A modification of the picrate method for blood sugar determinations. J. Biol. Chem. 35:53–59. With C. K. Watanabe and J. R. Oliver. Determination of the quantity of secreting tissue in the living kidney. J. Exp. Med. 28:359–76. 1919 A pulse rate standard for recruits. JAMA 72:181–85. With W. J. Kerr. The relative frequency in recruits with and without thyroid enlargement of certain signs and symptoms which occur in neurocirculatory asthenia. Arch. Int. Med. 23:316–33. The future of the teaching of clinical medicine. Edinburgh Med. J. 23:235–43. 1922 Determination of the extent and nature of the renal lesion in Bright's disease. Calif. State J. Med. 20:90–93. Blood pressure and pulse rate levels. First paper. The levels under basal and daytime conditions. Arch. Int. Med. 29:539–53. Blood pressure and pulse rate reactions. Second paper. Arch. Int. Med. 30:240–68. Protein restriction in Bright's disease. Med. Clin. North Am. 6:209–12. Renal function and the amount of functioning tissue. The ratio: Urea in one hour's urine after giving urea and water. Urea in 100 c.c. of blood. Arch. Int. Med. 30:378–85. With A. B. Spalding and A. E. Shevky. The extent of the renal lesion in the toxemias of pregnancy. Am. J. Obstet. Gynecol. 4:350–61. With M. G. Foster. Specific gravity of the urine. Arch. Int. Med. 30:555–58. With M. D. Shevky. A test of the capacity of the kidney to produce a urine of high specific gravity. Arch. Int. Med. 30:559–62.

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Biographical Memoirs: Volume 63 1923 With D. R. Drury. The rate of urea excretion. V. The effect of changes in blood urea concentration on the rate of urea excretion. J. Biol. Chem. 55:105–11. With D. R. Drury. The rate of urea excretion. VII. The effect of various factors other than blood urea concentration on the rate of urea excretion. J. Biol. Chem. 55:629–38. With D. R. Drury. The rate of urea excretion. VIII. The effect of changes in urine volume on the rate of urea excretion. J. Biol. Chem. 55:639–51. The clinical significance of abnormalities in urine volume. Arch. Int. Med. 31:783–96. With F. B. Taylor and D. R. Drury. The regulation of renal activity. VIII. The relation between the rate of urea excretion and the size of the kidneys. Am. J. Physiol. 65:55–61. 1924 With D. C. Stafford. Diastase determinations in urine and blood as a method for the measurement of the functional capacity of the kidney. Q. J. Med. 17:151–61. With H. Sharlit and W. G. Lyle. The specific gravity of the urine. Arch. Int. Med. 33:109–17. With B. A. Meyers and J. Oliver. The regulation of renal activity. IX. The effect of unilateral nephrectomy on the function and structure of the remaining kidney. Arch. Int. Med. 34:243–57. With M. G. Foster. The concentrating capacity of the kidney. Arch. Int. Med. 34:462–80. 1925 Urea determinations in blood and urine. J. Lab. Clin. Med. 10:402–9. With B. A. Meyers and L. Bayer. The regulation of renal activity. XI. The rate of phosphate excretion by the kidney; the effect of variation in the concentration of phosphate in the plasma on the rate of phosphate excretion. Am. J. Physiol. 72:125–42. Renal failure casts. JAMA 84:1013–15. With L. L. MacKay and E. M. MacKay. Compensatory hypertrophy of the kidney: The effect of pregnancy and of lactation. Proc. Soc. Exp. Biol. Med. 22:536–37.

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Biographical Memoirs: Volume 63 A clinical classification of Bright's disease. Trans. Assoc. Am. Phys. 40:101–15. A clinical classification of Bright's disease. JAMA 85:163–67. 1926 The number of formed elements in the urinary sediment of normal individuals. J. Clin. Invest. 2:409–15. Effect of some physiological variables on the number of casts, red blood cells and white blood cells and epithelial cells in the urine of normal individuals. J. Clin. Invest. 2:417–21. With L. L. MacKay and E. M. MacKay. Phosphate and kidney weight. Proc. Soc. Exp. Biol. Med. 24:130. With E. M. MacKay and L. L. MacKay. The effect on the kidney of the long continued administration of diets containing an excess of certain food elements. I. Excess of protein and cystine. J. Biol. Chem. 71:139–56. With E. M. MacKay and L. L. Mackay. The effect on the kidney of the long continued administration of diets containing excess of certain food elements. II. Excess of acid and of alkali. J. Biol. Chem. 71:157–66. 1927 With L. L. MacKay and E. M. MacKay. Do high protein diets increase weight of kidney because they increase nitrogen excretion? Proc. Soc. Exp. Biol. Med. 24:336–37. With L. L. MacKay and E. M. MacKay. Influence of age on degree of renal hypertrophy produced by high protein diets. Proc. Soc. Exp. Biol. Med. 24:335–36. 1928 Compensatory hypertrophy of the lung after unilateral pneumonectomy. J. Exp. Med. 47:51–56. An error in the urease method for the determination of urea. Proc. Soc. Exper. Biol. Med. 25:365–67. With E. M. MacKay and L. L. MacKay. Factors which determine renal weight. V. The protein intake. Am. J. Physiol. 86:459–65. With E. M. MacKay and L. L. MacKay. Factors which determine renal weight. VI. Influence of age on the relation of renal

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Biographical Memoirs: Volume 63 weight to the protein intake and the degree of renal hypertrophy produced by high protein diets. Am. J. Physiol. 86:466–70. The renal lesion in Bright's disease. Harvey Lecture Series. Am. J. Med. Sci. 176:617–37. 1929 The renal lesion in Bright's disease. Harvey Lecture Series. 23:222–50 1930 With B. O. Raulston. A reversible form of experimental uremia. Trans. Assoc. Am. Physicians 45:318–20. 1931 With L. L. MacKay and E. M. MacKay. Factors which determine renal weight. XII. The nitrogen intake as varied by the addition of urea to the diet. J. Nutr. 4:379–83. Haemorrhagic Bright's disease. I. Natural history. Bull. Johns Hopkins Hosp. 49:203–24. Haemorrhagic Bright's disease. II. Prognosis, etiology and treatment. Bull. Johns Hopkins Hosp. 49:271–85. With J. R. Oliver. The Renal Lesion in Bright's Disease. New York: Hoeber. 1932 Proteinuria and cylinduria. Proc. Calif. Acad. Med. 2:38–52. Hypertrophy of the gastrointestinal tract and high residue diets. Am. J. Physiol. 99:417–23. With E. M. MacKay and L. L. MacKay. The degree of compensatory renal hypertrophy following unilateral nephrectomy. I. The influence of age . J. Exp. Med. 56:255–65. 1933 Science and practice in Bright's disease. Ann. Int. Med. 6:1077–79. 1935 Compensatory hypertrophy of paired organs after one has been removed. International Physiology Congress, 15th Summaries of Communications, p. 4. Total body and organ proteins—changes under varying dietary con-

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Biographical Memoirs: Volume 63 ditions. International Physiology Congress, 15th Summaries of Communications, p. 4. 1936 With L. J. Poo, W. Lew, and D. W. Yuen. Gravimetric methods for the determination of total body protein and organ protein. J. Biol. Chem. 113:497–504. With L. J. Poo and W. Lew. The quantities of protein lost by the various organs and tissues of the body during a fast. J. Biol. Chem. 115:111–16. With L. J. Poo and W. Lew. Protein loss from liver during a two-day fast. J. Biol. Chem. 115:117–18. With L. J. Poo and W. Lew. The rate of protein formation in the organs and tissues of the body. I. After casein refeeding. J. Biol. Chem. 116:343–52. 1938 With L. L. MacKay and E. M. MacKay. The degree of compensatory renal hypertrophy following unilateral nephrectomy. I. The influence of the protein intake. J. Exp. Med. 67:515–19. With D. Karnofsky, W. Lew, and L. J. Poo. The protein content of the organs and tissues of the body after administration of thyroxine and dinitrophernol and after thyroidectomy. J. Biol. Chem. 124:33–41. 1939 The treatment of chronic renal insufficiency. J. Urol. 41:126–36. Metabolism of intraperitoneally injected serum protein. Proc. Soc. Exp. Biol. Med. 40:336–38. With F. Walter. Organ work and organ weight. J. Exp. Med. 69:467–83. With L. J. Poo and W. Lew. Protein anabolism of organs and tissues during pregnancy and lactation. J. Biol. Chem. 128:69–77. With W. Lew. Age and the rate of venous enlargement under increased venous pressure. Proc. Soc. Exp. Biol. Med. 42:602–3. With W. Lew. Diet and death in acute uremia. J. Clin. Invest. 18:773–75. 1940 With D. D. Lee, W. Lew, and L. J. Poo. The protein content of the

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Biographical Memoirs: Volume 63 organs and tissues at different levels of protein consumption. J. Nutr. 19:199–205. With D. D. Lee, W. Lew, and L. J. Poo. The utilization of parenterally administered horse serum by the rat. Am. J. Physiol. 128:544–46. With W. Lew. The restoration of lost organ tissue; rate and degree of restoration. J. Exp. Med. 71:325–33. With W. Lew. Protein consumption and the restoration of lost organ tissue. J. Exp. Med. 71:563–68. Theory and practice in the dietetic treatment of glomerular nephritis. J. Am. Diet. Assoc. 16:306–12. With L. J. Poo, W. Lew, and D. D. Lee. Protein anabolism in the organs and tissues of pregnant rats at different levels of protein consumption. J. Nutr. 19:505–15. With D. W. Yuen, L. J. Poo, and W. Lew. Protein anabolism in the heart, kidney and liver after consumption of various food proteins. Am. J. Physiol. 129:685–90. Treatment of nephritis by rest. J. Mo. State Med. Assoc. 37:458–60. The osmotic work of the kidney and the treatment of glomerular nephritis. Trans. Assoc. Am. Phys. 55:223–29. 1942 With J. Sugarman, M. Friedman, and E. Barrett. The distribution, flow, protein and urea content of renal lymph. Am. J. Physiol. 138:108–12. Proteinuria. Trans. Assoc. Am. Physicians. 57:106–8. 1943 The effect of variation in food protein consumption on the protein of the organs and tissues of the body. Pac. Sci. Congr. Proc. 6:677–79. 1945 Renal degenerations due to protein reabsorption by the kidney. Stanford Med. Bull. 3:67–69. 1946 With E. Barrett, W. Lew, L. J. Poo, and D. W. Yuen. Danger of intravenous injection of protein solutions after sudden loss of renal tissue. Arch. Int. Med. 77:254–59.

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Biographical Memoirs: Volume 63 1947 With E. Barrett, L. J. Poo, and D. W. Yuen. The relation between the serum urea concentration and the protein consumption of normal individuals. J. Clin. Invest. 26:869–74. With E. Barrett. The serum creatinine concentration of normal individuals. J. Clin. Invest. 26:875–78. With E. Barrett and J. T. Menzies. A clinical method for the approximate determination of serum creatinine concentration. J. Clin. Invest. 26:879–82. 1948 With H. Gray and E. Barrett. Food protein effect on plasma specific gravity, plasma protein, and hematocrit value. J. Exp. Med. 87:353–68. With H. Gray. Rat colony testing by Zucker's weight-age relation. Am. J. Physiol. 153:35–40. With E. C. Persike. Food protein consumption in glomerulonephritis; effect on proteinuria and concentration of serum protein. Arch. Int. Med. 81:612–22. Glomerular Nephritis: Diagnosis and Treatment. New York: Macmillan. 1949 With E. Barrett, R. I. Boyd, and H. J. Ureen. Renin proteinuria in the rat. I. The relation between the proteinuria and the pressor effect of renin. J. Exp. Med. 89:131–40. With R. I. Boyd. Adrenalectomy and renin proteinuria in the rat. Fed. Proc. 8:1. With F. L. Reichert, V. Richards, E. Holman, A. L. Bloomfield, D. A. Rytand, and J. K. Lewis. The medical and surgical treatment of hypertension. Ann. Surg. 129:349–57. The mechanism of proteinuria. Proc. Natl. Acad. Sci. USA 35:194–98. With E. C. Persike. Increased rate of urea formation following removal of renal tissue. Am. J. Physiol. 158:149–56. 1950 With H. Gray. Body size and organ weight. Growth 14:49–80. With H. Gray. Body size and suprarenal weight. Growth 14:81–92. With H. Gray. Body size and gonad weight. Growth 14:93–106. With E. C. Persike, R. W. Lippman, F. L. Reichert, and V. Richards.

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Biographical Memoirs: Volume 63 Surgical treatment for hypertensive complications of advanced renal disease. Arch. Int. Med. 83:348–54. With J. Marmorston, H. C. Goodman, A. L. Sellers, and M. Smith. Effect of adrenalectomy on spontaneous and induced proteinuria in the rat. Proc. Soc. Exp. Biol. Med. 74:43–46. With L. J. Rather. Renin proteinuria in the rat. II. Evidence that renin does not interfere with the tubular resorption of purified human hemoglobin or bovine albumin. J. Exp. Med. 91:567–72. With E. Barrett, L. J. Poo, H. J. Ureen, and R. W. Lippman. The relation between protein consumption and diurnal variations of the endogenous creatinine clearance in normal individuals. J. Clin. Invest. 30:206–9. With R. W. Lippman, W. Lew, L. J. Poo, and W. Wong. Effect of dietary protein consumption upon body growth and organ size in the rat. Am. J. Physiol. 165:491–6. With E. Barrett, L. J. Poo, and H. J. Ureen. Prerenal proteinuria. I. Particle size. Arch. Int. Med. 88:337–45. With E. Jameson. Prerenal proteinuria. III. Electrophoretic studies. Arch. Int. Med. 88:350–55. 1952 With R. W. Lippman, W. Lew, L. J. Poo, and W. Wong. Effect of diet upon body growth and organ size in the rat after partial nephrectomy. Am. J. Physiol. 168:114–20.

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