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Primary Splenic Tuberculosis in Transplant Candidates Yvonne Cummings, MD, Iluminado Cruz, MD, Joseph Kovi, MD, Clive Callender, MD, Martin Dillard, MD, and Adrian Hosten, MD Washington, D.C.
Caseous granulomatous lesions, consistent with tuberculosis, were found in the spleen in two of our renal transplant candidates. There was no clinical evidence of tuberculosis in either patient. Only one patient had a positive tuberculin skin test whose chest film showed hilar calcifications suggestive of healed granulomatous disease. Because of this incidental finding in the spleen, both patients were placed on antituberculous therapy. There has been no evidence of active tuberculosis in either patient despite the use of usual doses of immunosuppressive drugs. Splenectomy is routinely performed in our transplant center to protect the patients against the leukopenic effects of azathioprine. Caseous granulomatous lesions, consistent with tuberculosis, were found in the spleen in two of our transplant candidates. There was no apparent involvement of other organs in these two patients. These two cases are presented as examples of apparently isolated granulomas, presumably tuberculous in origin.
From the Renal Division of the Department of Medicine, the Transplant Service of the Department of Surgery, and the Department of Pathology, Howard University, College of Medicine, 2041 Georgia Avenue, NW, Washington, D.C. Requests for reprints should be addressed to Dr. Iluminado Cruz, Department of Medicine, Howard University Hospital, 2041 Georgia Avenue, NW Washington, D.C. 20060.
Case Reports Case 1 A 28-year-old black male was transferred to Howard University Hospital in September 1974. The patient claimed to have been well until six weeks prior to admission when, during a job interview, he developed paresthesias and loss of control of his lips. Shortly thereafter, he was admitted to a community hospital with complaints of nausea and vomiting, and was found to have 4+ proteinuria, pyuria, a blood urea nitrogen level of 134 mg/100 ml, and a serum creatinine level of 22 mg/100 ml. Serum complement was 110 mg/100 ml (normal 120 to 185 mg/100 ml). Lupus erythematosus (LE) cell preparation was negative on two occasions. Intravenous pyelography revealed poor visualization of both kid-
neys; when measured they were 11 cm each. There was no evidence of calyceal distortion or obstruction. The patient had a three-year history of intravenous drug abuse and had re-
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 70, NO. 3, 1978
ceived methadone treatment for two years. He denied drug usage for the two years prior to admission. He denied any known exposure to tuberculosis or history of hypertension or renal disease. Initial physical examination at Howard University Hospital was normal except for a blood pressure of 170/100 mg Hg. His hemoglobin was 8.5 gm%o. Blood urea nitrogen was 150 mg/100 ml, serum creatinine 22 mg/100 ml, sodium 133 mEq/liter, potassium 5.0 mEq/lliter, chloride 100 mEq/liter, and bicarbonate 12/mEq/liter. Urinalysis showed a specific gravity of 1.010, 3+ proteinuria, no glycosuria, a few white blood cells, many granular casts, and some white cell casts. No red blood cells, red cell casts, or oval fat bodies were seen. Twenty-four hour urine protein excretion was 4.2 gm. Chest x-ray revealed minimal cardiomegaly and hilar calcifications suggestive of healed granulomatous disease. The lung fields were clear. Renal tissue obtained by percutaneous biopsy contained only five glomeruli, three of which were completely hyalinized. The other two glomeruli showed changes of membranous glomerulonephritis. The patient was subsequently started on chronic hemodialysis, and in December of 1974, bilateral nephrectomy and splenectomy were done in preparation for a kidney transplant. Three weeks later, he received an ABO 167
0'
SW.
~40
Figure 1. Spleen. A large area of central caseous necrosis is surrounded by palisading epitheloid cells, by multinucleated Langhans giant cells, and huge numbers of lymphocytes. Hematoxylin and eosin, X 125.
compatible-4 HLA antigen matched kidney from his sister in whom the leukocyte crossmatch was negative prior to kidney transplant. About sixweeks post-transplant he developed ureteral necrosis and lost the allograft. He subsequently received a second, living, related-donor transplant which he rejected after 13 months. A third transplant, this time from a cadaver, is functioning well six months after retransplantation.
Case 2 A 39-year-old black male construction worker was referred to the Howard University Hospital Renal Service in March 1973 for evaluation of his renal function. The patient was originally seen in his workers' union medical clinic in 1966, and was found to have 4+ proteinuria and a blood pressure of 130/90 mm Hg. Intravenous pyelogram at that time did not outline the kidneys. A retrograde pyelogram revealed small kidneys bilaterally. Over the next six 168
years, the patient developed sustained hypertension, progressive renal insufficiency, and persistent proteinuria. During this period, he received intermittent treatment for his hypertension. On initial evaluation in the Renal Clinic, he offered no complaints. He was a well-developed, well-nourished male in no obvious distress. Vital signs were normal except for a blood pressure of 186/124 mm Hg. Examination of the eyes revealed grade II hypertensive changes. The lungs were clear, and cardiovascular examination was within normal limits. Laboratory examination revealed levels of blood urea nitrogen of 51 mg/100 ml, serum creatinine of 4.8 mg/100 ml, and serum electrolytes, normal. The ASO titer and LE cell preparation were negative. Serum complement was 124 mg/100 ml and 24-hour urine protein excretion was 6.4 gm. Chest x-ray showed minimal cardiomegaly and clear lung fields. Electrocardiogram revealed left ventricular hypertrophy by voltage criteria. The patient refused kidney biopsy.
Over the next seven months, he was followved in the Renal Clinic. His blood pressure was poorly controlled because of failure to take his medications as prescribed. He was lost to followup, and was not seen again until March 1974 when he was admitted to the hospital for uncontrolled hypertension. His blood pressure was 210/140 mm Hg. He developed progressive azotemia and symptoms of uremia which were controlled with dietary manipulation and other conservative measures. He began chronic hemodialysis in August 1974. The patient did well on hemodialysis and was admitted to the hospital for a cadaveric kidney transplant in January 1975. Splenectomy was done at the time of transplantation. He rejected this allograft after three months and was returned to dialysis. A second cadaveric kidney transplant was performed in July 1975. In January 1976, because of uncontrolled hypertension his native kidneys were removed without amelioration of his hypertension. He is currently 18 months posttransplant and although moderately azotemic with blood urea nitrogen of 47 mg/100 ml and serum creatinine of 5.3 mg/100 ml, he is asymptomatic.
Pathological Studies The kidneys of both patients were free from any lesions suggestive of tuberculosis. The spleens were normal both in size and gross morphologic appearance. Microscopic study revealed scattered areas of granulomatous tissues. Hematoxylin and eosin-stained sections showed the following characteristics: a broad area of central caseous necrosis surrounded by an inflammatory reaction composed of palisading epitheloid cells, Langhan giant cells, and varying numbers of lymphocytes (Figure 1). Special stains did not reveal the presence of fungi or bacteria in these lesions. A Ziehl-Neelsen stain for acidfast bacilli was negative. Based on the histological appearance of these lesions, a diagnosis of caseous granulomatous disease of the spleen, consistent with tuberculosis, was made. Both patients were placed on isoniazid continuously from the time of their first kidney transplant. There has been no evidence of active tuberculosis in these patients despite their large
JOURNAL OF THE NATIONAL MEDICAL
ASSOCIATION,
VOL. 70, NO. 3,
1978
doses of immunosuppressive agents. Tuberculin skin test was positive in the first patient.
Discussion Secondary tuberculosis of the spleen is commonly associated with miliary tuberculosis. However, socalled primary tuberculosis of the spleen, in which the disease is apparently confined to that organ, has been reported only rarely.1-3 The term primary in this instance does not imply that the original focus of infection necessarily occurred in the spleen. Rather, it suggests that the point of entry either did not develop gross pathology or healed without leaving evidence of active disease while the disease became localized in the spleen. The splenic lesions become potential sources for dissemination of the disease. ' In 1912, Winternitz' reported 51 of these cases found in the literature. He was of the opinion that the portal of entry was the gastrointestinal tract. In 1933, Shands2 reported on an additional 30 cases found in the literature and described three cases of his own. He found no evidence of pulmonary tuberculosis on chest x-ray, but noted calcification in the area of the spleen on x-ray examination. Operative findings supported the diagnosis of splenic tuberculosis and it was suggested that x-ray examination of the abdomen was a useful tool in the preoperative diagnosis of these patients. Prior to this time, the diagnosis of primary splenic tuberculosis was usually made at autopsy, or at exploratory surgery. Fung et al,4 in 1973, reported a case of splenic tuberculosis presenting as pyrexia of unknown origin. An indium scan of the spleen revealed a large filling defect. It was concluded that indium scanning was useful, although by no means specific, in the diagnosis of splenic tuberculomas, and should be done in all suspected cases. Characteristically, the disease runs a chronic course. The patient is usually in the third or fourth decade of life, and complains of malaise, weight loss, and pain in the area of the spleen. The patient is usually thin and appears to be ill. In most instances the spleen is enlarged and tender and may have obvious nodules.'3 Other laboratory data are typically nonspecific; the erythrocyte sedimentation rate may be elevated,
and the patient is usually anemic. ' In contrast to the above, there is a smaller group of patients in which the presenting symptoms are much more striking and characteristic of an acute infectious process.' These patients usually present with chills, fever, backache, and collapse. Death is inevitable without prompt treatment. Transplantation patients are susceptible to numerous infections with both common and uncommon pathogens and indeed most transplant related deaths are due to infections.' It is well known that both corticosteroids and cytotoxic agents depress cell-mediated immunity, and that uremia itself can also depress cell-mediated immunity.7 Surprisingly, very few cases of tuberculosis have been encountered in patients after transplantation. The disease was identified in only three of approximately 400 patients who received a transplant at the University of Colorado Medical Center in a ten-year period ending 1974.8 Two patients whose spleens, removed in preparation for renal transplantation, were incidentally found to contain lesions consistent with tuberculosis. The only other tissue available for study, namely the kidney, did not show similar lesions. However, of the many diseases such as histoplasmosis, brucillosis, and cat-scratch fever, which are capable of producing caseating granulomas, tuberculosis is the most likely, even though we were unsuccessful in demonstrating organisms. The presence of healed granulomas on chest x-ray and the fact that the patients originated from an area endemic in tuberculosis lead to that possibility. Both patients have been on prophylactic isoniazid therapy since transplantation and neither has developed active tuberculosis. It has been suggested that all transplant candidates be skin tested for tuberculosis prior to transplant and that those with positive tests receive chemoprophylaxis while on immunosuppressive agents.9 However, Rolley et al'° tested the delayed cutaneous hypersensitivity of 69 uremic patients to dinitrochlorobenzene (DNCB), and found that 62 percent were negative. They concluded that an equal number could also be negative on tuberculin skin testing and, thus, negative results could give one a false sense of security prior to transplant.
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 70, NO. 3, 1978
Tuberculosis is endemic in the population served by our hospital, with the area ranking third nationally in reported cases of tuberculosis (personal communication). However, recent tuberculin skin testing of our chronic hemodialysis population revealed only five positive results in the 48 patients tested. Additionally, one patient recently diagnosed as having active tuberculosis has had persistently negative tuberculin skin tests before and after therapy. Thus, the use of tuberculin skin testing in uremic patients remains, at best, unsatisfactory in determining those patients who should receive chemoprophylaxis after transplantation. Pretransplant splenectomy as a means of protecting against the leukopenic effects of azathioprine is a controversial subject in the literature. At our transplant center, it is routinely done in addition to careful administration of the immunosuppressive therapy. If indeed the patients in this report had splenic tuberculosis, then this incidental finding would seem to provide a secondary reason for splenectomy in those patients drawn from populations in which tuberculosis is endemic. At least, splenectomy should be considered for such patients if they have calcified granulomas on routine chest x-ray.
Literature Cited 1. Winternitz MC: Tuberculosis of the spleen. Arch Intern Med 9:680-697, 1912 2. Shands HR: Chronic primary tuberculosis of the spleen. Am J Surg 20:707-721, 1933 3. McGowan WB: Primary tuberculosis of the spleen. Cent Afr J Med 11:39-40, 1965 4. Fung WP, Siew CO, Lee YS: Splenic tuberculosis presenting as pyrexia of unknown origin. Med J Aust 1:446-448, 1973 5. Aird l: Companion in Surgical Studies. Edinburgh, Livingstone, 1949, p 864 6. Rattazzi LC, Simmons RL, Spanos PK, et al: Successful management of miliary tuberculosis after renal transplantation. Am J Surg 130:359-361, 1975 7. Oliver WA: Tuberculosis in renal transplant patients. Med J Aust 1:828-829, 1976 8. Neff TA, Hudgel DW: Miliary tuberculosis in a renal transplant recipient. Am Rev Resp Dis 108:677-678, 1973 9. Thomas PA, Manko MA: Chemoprophylaxis for the prevention of tuberculosis in the immunosuppressed renal allograft recipient. Transplantation 20:76-77, 1975 10. Rolley RT, Sterioff S, Williams GM, et al: Assessment of immunocompetency by DNCB sensitization prior to human renal allotransplantation. Surg Forum 25:268-270, 1974 11. Starzl TE, Marchioro TL, Talmage DW, et al: Splenectomy and thymectomy in human renal homotransplantation. Proc Soc Exp Biol Med 11e:929-932, 1963
169
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:::..
.
....
Primary Splenic Tuberculosis in Transplant Candidates Yvonne Cummings, MD, Iluminado Cruz, MD, Joseph Kovi, MD, Clive Callender, MD, Martin Dillard, MD, and Adrian Hosten, MD Washington, D.C.
Caseous granulomatous lesions, consistent with tuberculosis, were found in the spleen in two of our renal transplant candidates. There was no clinical evidence of tuberculosis in either patient. Only one patient had a positive tuberculin skin test whose chest film showed hilar calcifications suggestive of healed granulomatous disease. Because of this incidental finding in the spleen, both patients were placed on antituberculous therapy. There has been no evidence of active tuberculosis in either patient despite the use of usual doses of immunosuppressive drugs. Splenectomy is routinely performed in our transplant center to protect the patients against the leukopenic effects of azathioprine. Caseous granulomatous lesions, consistent with tuberculosis, were found in the spleen in two of our transplant candidates. There was no apparent involvement of other organs in these two patients. These two cases are presented as examples of apparently isolated granulomas, presumably tuberculous in origin.
From the Renal Division of the Department of Medicine, the Transplant Service of the Department of Surgery, and the Department of Pathology, Howard University, College of Medicine, 2041 Georgia Avenue, NW, Washington, D.C. Requests for reprints should be addressed to Dr. Iluminado Cruz, Department of Medicine, Howard University Hospital, 2041 Georgia Avenue, NW Washington, D.C. 20060.
Case Reports Case 1 A 28-year-old black male was transferred to Howard University Hospital in September 1974. The patient claimed to have been well until six weeks prior to admission when, during a job interview, he developed paresthesias and loss of control of his lips. Shortly thereafter, he was admitted to a community hospital with complaints of nausea and vomiting, and was found to have 4+ proteinuria, pyuria, a blood urea nitrogen level of 134 mg/100 ml, and a serum creatinine level of 22 mg/100 ml. Serum complement was 110 mg/100 ml (normal 120 to 185 mg/100 ml). Lupus erythematosus (LE) cell preparation was negative on two occasions. Intravenous pyelography revealed poor visualization of both kid-
neys; when measured they were 11 cm each. There was no evidence of calyceal distortion or obstruction. The patient had a three-year history of intravenous drug abuse and had re-
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 70, NO. 3, 1978
ceived methadone treatment for two years. He denied drug usage for the two years prior to admission. He denied any known exposure to tuberculosis or history of hypertension or renal disease. Initial physical examination at Howard University Hospital was normal except for a blood pressure of 170/100 mg Hg. His hemoglobin was 8.5 gm%o. Blood urea nitrogen was 150 mg/100 ml, serum creatinine 22 mg/100 ml, sodium 133 mEq/liter, potassium 5.0 mEq/lliter, chloride 100 mEq/liter, and bicarbonate 12/mEq/liter. Urinalysis showed a specific gravity of 1.010, 3+ proteinuria, no glycosuria, a few white blood cells, many granular casts, and some white cell casts. No red blood cells, red cell casts, or oval fat bodies were seen. Twenty-four hour urine protein excretion was 4.2 gm. Chest x-ray revealed minimal cardiomegaly and hilar calcifications suggestive of healed granulomatous disease. The lung fields were clear. Renal tissue obtained by percutaneous biopsy contained only five glomeruli, three of which were completely hyalinized. The other two glomeruli showed changes of membranous glomerulonephritis. The patient was subsequently started on chronic hemodialysis, and in December of 1974, bilateral nephrectomy and splenectomy were done in preparation for a kidney transplant. Three weeks later, he received an ABO 167
0'
SW.
~40
Figure 1. Spleen. A large area of central caseous necrosis is surrounded by palisading epitheloid cells, by multinucleated Langhans giant cells, and huge numbers of lymphocytes. Hematoxylin and eosin, X 125.
compatible-4 HLA antigen matched kidney from his sister in whom the leukocyte crossmatch was negative prior to kidney transplant. About sixweeks post-transplant he developed ureteral necrosis and lost the allograft. He subsequently received a second, living, related-donor transplant which he rejected after 13 months. A third transplant, this time from a cadaver, is functioning well six months after retransplantation.
Case 2 A 39-year-old black male construction worker was referred to the Howard University Hospital Renal Service in March 1973 for evaluation of his renal function. The patient was originally seen in his workers' union medical clinic in 1966, and was found to have 4+ proteinuria and a blood pressure of 130/90 mm Hg. Intravenous pyelogram at that time did not outline the kidneys. A retrograde pyelogram revealed small kidneys bilaterally. Over the next six 168
years, the patient developed sustained hypertension, progressive renal insufficiency, and persistent proteinuria. During this period, he received intermittent treatment for his hypertension. On initial evaluation in the Renal Clinic, he offered no complaints. He was a well-developed, well-nourished male in no obvious distress. Vital signs were normal except for a blood pressure of 186/124 mm Hg. Examination of the eyes revealed grade II hypertensive changes. The lungs were clear, and cardiovascular examination was within normal limits. Laboratory examination revealed levels of blood urea nitrogen of 51 mg/100 ml, serum creatinine of 4.8 mg/100 ml, and serum electrolytes, normal. The ASO titer and LE cell preparation were negative. Serum complement was 124 mg/100 ml and 24-hour urine protein excretion was 6.4 gm. Chest x-ray showed minimal cardiomegaly and clear lung fields. Electrocardiogram revealed left ventricular hypertrophy by voltage criteria. The patient refused kidney biopsy.
Over the next seven months, he was followved in the Renal Clinic. His blood pressure was poorly controlled because of failure to take his medications as prescribed. He was lost to followup, and was not seen again until March 1974 when he was admitted to the hospital for uncontrolled hypertension. His blood pressure was 210/140 mm Hg. He developed progressive azotemia and symptoms of uremia which were controlled with dietary manipulation and other conservative measures. He began chronic hemodialysis in August 1974. The patient did well on hemodialysis and was admitted to the hospital for a cadaveric kidney transplant in January 1975. Splenectomy was done at the time of transplantation. He rejected this allograft after three months and was returned to dialysis. A second cadaveric kidney transplant was performed in July 1975. In January 1976, because of uncontrolled hypertension his native kidneys were removed without amelioration of his hypertension. He is currently 18 months posttransplant and although moderately azotemic with blood urea nitrogen of 47 mg/100 ml and serum creatinine of 5.3 mg/100 ml, he is asymptomatic.
Pathological Studies The kidneys of both patients were free from any lesions suggestive of tuberculosis. The spleens were normal both in size and gross morphologic appearance. Microscopic study revealed scattered areas of granulomatous tissues. Hematoxylin and eosin-stained sections showed the following characteristics: a broad area of central caseous necrosis surrounded by an inflammatory reaction composed of palisading epitheloid cells, Langhan giant cells, and varying numbers of lymphocytes (Figure 1). Special stains did not reveal the presence of fungi or bacteria in these lesions. A Ziehl-Neelsen stain for acidfast bacilli was negative. Based on the histological appearance of these lesions, a diagnosis of caseous granulomatous disease of the spleen, consistent with tuberculosis, was made. Both patients were placed on isoniazid continuously from the time of their first kidney transplant. There has been no evidence of active tuberculosis in these patients despite their large
JOURNAL OF THE NATIONAL MEDICAL
ASSOCIATION,
VOL. 70, NO. 3,
1978
doses of immunosuppressive agents. Tuberculin skin test was positive in the first patient.
Discussion Secondary tuberculosis of the spleen is commonly associated with miliary tuberculosis. However, socalled primary tuberculosis of the spleen, in which the disease is apparently confined to that organ, has been reported only rarely.1-3 The term primary in this instance does not imply that the original focus of infection necessarily occurred in the spleen. Rather, it suggests that the point of entry either did not develop gross pathology or healed without leaving evidence of active disease while the disease became localized in the spleen. The splenic lesions become potential sources for dissemination of the disease. ' In 1912, Winternitz' reported 51 of these cases found in the literature. He was of the opinion that the portal of entry was the gastrointestinal tract. In 1933, Shands2 reported on an additional 30 cases found in the literature and described three cases of his own. He found no evidence of pulmonary tuberculosis on chest x-ray, but noted calcification in the area of the spleen on x-ray examination. Operative findings supported the diagnosis of splenic tuberculosis and it was suggested that x-ray examination of the abdomen was a useful tool in the preoperative diagnosis of these patients. Prior to this time, the diagnosis of primary splenic tuberculosis was usually made at autopsy, or at exploratory surgery. Fung et al,4 in 1973, reported a case of splenic tuberculosis presenting as pyrexia of unknown origin. An indium scan of the spleen revealed a large filling defect. It was concluded that indium scanning was useful, although by no means specific, in the diagnosis of splenic tuberculomas, and should be done in all suspected cases. Characteristically, the disease runs a chronic course. The patient is usually in the third or fourth decade of life, and complains of malaise, weight loss, and pain in the area of the spleen. The patient is usually thin and appears to be ill. In most instances the spleen is enlarged and tender and may have obvious nodules.'3 Other laboratory data are typically nonspecific; the erythrocyte sedimentation rate may be elevated,
and the patient is usually anemic. ' In contrast to the above, there is a smaller group of patients in which the presenting symptoms are much more striking and characteristic of an acute infectious process.' These patients usually present with chills, fever, backache, and collapse. Death is inevitable without prompt treatment. Transplantation patients are susceptible to numerous infections with both common and uncommon pathogens and indeed most transplant related deaths are due to infections.' It is well known that both corticosteroids and cytotoxic agents depress cell-mediated immunity, and that uremia itself can also depress cell-mediated immunity.7 Surprisingly, very few cases of tuberculosis have been encountered in patients after transplantation. The disease was identified in only three of approximately 400 patients who received a transplant at the University of Colorado Medical Center in a ten-year period ending 1974.8 Two patients whose spleens, removed in preparation for renal transplantation, were incidentally found to contain lesions consistent with tuberculosis. The only other tissue available for study, namely the kidney, did not show similar lesions. However, of the many diseases such as histoplasmosis, brucillosis, and cat-scratch fever, which are capable of producing caseating granulomas, tuberculosis is the most likely, even though we were unsuccessful in demonstrating organisms. The presence of healed granulomas on chest x-ray and the fact that the patients originated from an area endemic in tuberculosis lead to that possibility. Both patients have been on prophylactic isoniazid therapy since transplantation and neither has developed active tuberculosis. It has been suggested that all transplant candidates be skin tested for tuberculosis prior to transplant and that those with positive tests receive chemoprophylaxis while on immunosuppressive agents.9 However, Rolley et al'° tested the delayed cutaneous hypersensitivity of 69 uremic patients to dinitrochlorobenzene (DNCB), and found that 62 percent were negative. They concluded that an equal number could also be negative on tuberculin skin testing and, thus, negative results could give one a false sense of security prior to transplant.
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 70, NO. 3, 1978
Tuberculosis is endemic in the population served by our hospital, with the area ranking third nationally in reported cases of tuberculosis (personal communication). However, recent tuberculin skin testing of our chronic hemodialysis population revealed only five positive results in the 48 patients tested. Additionally, one patient recently diagnosed as having active tuberculosis has had persistently negative tuberculin skin tests before and after therapy. Thus, the use of tuberculin skin testing in uremic patients remains, at best, unsatisfactory in determining those patients who should receive chemoprophylaxis after transplantation. Pretransplant splenectomy as a means of protecting against the leukopenic effects of azathioprine is a controversial subject in the literature. At our transplant center, it is routinely done in addition to careful administration of the immunosuppressive therapy. If indeed the patients in this report had splenic tuberculosis, then this incidental finding would seem to provide a secondary reason for splenectomy in those patients drawn from populations in which tuberculosis is endemic. At least, splenectomy should be considered for such patients if they have calcified granulomas on routine chest x-ray.
Literature Cited 1. Winternitz MC: Tuberculosis of the spleen. Arch Intern Med 9:680-697, 1912 2. Shands HR: Chronic primary tuberculosis of the spleen. Am J Surg 20:707-721, 1933 3. McGowan WB: Primary tuberculosis of the spleen. Cent Afr J Med 11:39-40, 1965 4. Fung WP, Siew CO, Lee YS: Splenic tuberculosis presenting as pyrexia of unknown origin. Med J Aust 1:446-448, 1973 5. Aird l: Companion in Surgical Studies. Edinburgh, Livingstone, 1949, p 864 6. Rattazzi LC, Simmons RL, Spanos PK, et al: Successful management of miliary tuberculosis after renal transplantation. Am J Surg 130:359-361, 1975 7. Oliver WA: Tuberculosis in renal transplant patients. Med J Aust 1:828-829, 1976 8. Neff TA, Hudgel DW: Miliary tuberculosis in a renal transplant recipient. Am Rev Resp Dis 108:677-678, 1973 9. Thomas PA, Manko MA: Chemoprophylaxis for the prevention of tuberculosis in the immunosuppressed renal allograft recipient. Transplantation 20:76-77, 1975 10. Rolley RT, Sterioff S, Williams GM, et al: Assessment of immunocompetency by DNCB sensitization prior to human renal allotransplantation. Surg Forum 25:268-270, 1974 11. Starzl TE, Marchioro TL, Talmage DW, et al: Splenectomy and thymectomy in human renal homotransplantation. Proc Soc Exp Biol Med 11e:929-932, 1963
169
