Abnormal Renal Sodium Handling in Essential Hypertension. Relation to Failure of Renal and Adrenal Modulation of Responses to Angiotensin II

such as benign disorders of the stro1rtte:st11!1al and tract, and infectious diseases. To observe the course of both tumor markers postoperatively in an attempt to determine whether the operation itself alters their levels, the authors measured the preoperative and postoperative values in patients who were operated upon for benign diseases. The level of the tumor marker tissue polypeptide antigen increased distinctly after surgical trauma. The increase began 3 to 6 days postoperatively and lasted for more than 6 weeks. Carcinoembryonic antigen showed no comparable reaction. W. W. H. 3 figures, 5 references

DISEASES OF BLOOD VESSELS, HYPERTENSION AND RENOV ASCULAR SURGERY Abnormal Renal. Sodium Handling in Essential Hypertension. Relation to Failure of Renal and Adrenal Modulation of Responses to Angiotensin II N. K. HOLLENBERG, T. MOORE, D. SHOBACK, J. REDGRAVE, S. RABINOWE AND G. H. WILLIAMS, Departments of Med-

icine and Radiology, Harvard Medical School, and Brigham and Women's Hospital, Boston, Massachusetts Amer. J. Med., 8Jl: 412-418 (Sept.) 1986 The authors studied 61 patients between 25 and 60 years old with normal renin essential hypertension. All antihypertensive medications were discontinued at least 10 days before hospitalization. The patients were divided into 2 groups: group 1-25 patients received 200 mEq. sodium daily for the first 36 to 48 hours after hospitalization and then 10 mEq. sodium for at least 5 days, and group 2-36 patients received 10 mEq. sodium from the time of hospitalization for at least 5 to 6 days. Renal and adrenal responsiveness to angiotensin II was assessed by measurement of the para-aminohippurate clearance and plasma aldosterone before and during infusion of 3 ng./kg. angiotensin II per minute. This test identifies patients with esse~tial hypertension in whom renal and adrenal responses are abnormal (nonmodulating group). In group 1 the half-time of sodium excretion was 24.5 ± 1.8 hours in the normal modulating while it was prolonged to 36.6 ± 2.1 hours in the nonmodulating patients. In group 2 the shift in sodium intake from 10 to 200 daily resulted in an increase in sodium excretion in both groups. The nonmodulating showed a '"'""v""'u",v" at which external sodium balance was achieved. These patients also had greater cumulative sodium I/~,,~"~~, more weight gain and a greater frequency of blood pressure increase. Patients with normal renin essential hypertension and a limited ability to handle a sodium load presumably had an abnormality in the control of renal and adrenal function by angiotensin II. F. T. A. 5 figures, 3 tables, 32 references

TRANSPLANTATION Renal Tubular Function in Cyclosporine-Treated Patients A.G. PALESTINE, H. A. AUSTIN, III AND R. B. NUSSENBLATT,

Section of Clinical stitute and National Institutes of Health,

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Amer. J. Med., 81: 419-424 (Sept.) 1986 Since nephrotoxicity frequently is observed in patients who receive cyclosporin the authors studied renal tubular function in 32 consecutive patients treated with cyclosporin for bilateral autoimmune uveitis. The dose of cydosporin began at 10 mg./ kg. per day and was increased to a maximum of 1 7 mg./kg. per day if no therapeutic response was noted after 2 to 4 weeks. The dose was decreased to maintain the serum creatinine level at less than 2 mg./dl. and less than twice the pre-treatment value. The serum cyclosporin level was determined 24 hours after the previous dose. Fanconi's syndrome (aminoaciduria, glycosuria, hypophosphatemia, hypouricemia and hypokalemia) and lysozymuria are indicative of proximal tubule dysfunction. These conditions were not observed during 3 to 6 months of treatment. There was an elevation in serum creatinine, uric acid and potassium levels. With the mild decrease in the glomerular filtration rate the fractional excretion of magnesium was slightly higher and that of calcium was lower than pre-treatment values. These findings were compatible with the mild azotemia that evolved concurrently in these patients. The alterations in tubular function that could be considered specific for cydosporin nephrotoxicity were not observed. Since cyclosporin has a potential therapeutic value further studies are necessary to identify early clinical and/or morphological changes that could improve the diagnosis and treatment of the associated nephrotoxicity. F. T. A. 3 figures, 29 references

URODYNAMICS, PHYSIOLOGY AND EMBRYOLOGY Benign Pro§tatic Hyperplasia Treated by Castration o:r the LH-RH Analogue Buse:relilll.: A Report on 6 Cm.es

F. H.

SCHROEDER, M. WESTERHOF, R. J. L. H. BOSCH AND K. H. KURTH, Department of Urology, Erasmus Uni-

versity Rotterdam, Rotterdam, The Netherlands Eur. Urol., 12: 318-321 (Sept.-Oct.) 1986 The authors report on 6 elderly men unsuitable for transurethral prostatic resection (mostly because of severe cardiac disease) who were treated for benign prostatic hyperplasia and urinary retention by castration or the luteinizing hormonereleasing hormone analogue buserelin (1). All 6 men experienced a marked decrease in prostatic volume during 2 to 3 months. The prostatic volume as measured by transrectal ultrasonography decreased an average of 31.4 per cent (range 19 to 55 per cent) in 5 patients. All patients were able to void to completion and became free of a catheter. The wide variation in prostatic volume depletion may be owing to individual variations in the ratio of epithelial to stromal elements in benign prostatic hyperplasia, since regressive changes after castration previously have been shown to occur in epithelial elements. To date it is unknown which changes induced by surgical or pharmacological castration are responsible for these prostatic changes. H. McC. S. 1 figure, 1 table, 10 references