Case Report

Post Transplanted Infective Endocarditis Motomaru MASUTANI, Kiyomitsu IKEOKA, Ryoutarou SASAKI, Susumu NAGASAWA, Seinosuke KAWASHIMA,Yorihisa MlTANl, Kazuhiro FUJITANI, Tadaaki IWASAKI, Yukio SAWADA*and Kunio UEMATSU* The patient, a 51-year-old man, was receiving immunosuppresants for 2 yr after renal allotransplantation. He had heart failure with aortic regurgitation, fever, anemia and a history of odontectomy on admission. He wasresistant to medical treatments and died from cerebral emboli. Onautopsy, vegetation of the aortic valve was identified. Progression of atherosclerosis, which may have been due to steroids and chronic rejection, was prominent. This report is the first case of infective endocarditis following organ transplantation in Japan. Such complications as infective endocarditis and atherosclerosis will be on the rise with the increase of numbers of organ transplantations.

Key words: Infective endocarditis,

Renal transplantation

Recently an improved survival rate after organ transplantation has been realized with the advent of


various new immunosuppresants, but infectious diseases as complications due to the use of these

A 51-year-old man with chronic renal failure received hemodialysis from 1982 and underwent

agents are important problems and presently are the most commoncause of death of organ recipients (1 , 2). Amongthe various infectious complications, infection of respiratory, urinary and digestive tracts

renal transplantation at the Department of Urology of Hyogo College of Medicine Hospital on July 25,

rarely reported. There are only a few published cases in Euro-US areas (6), and still no cases have been published yet in Japan (7, 8). Vascular accidents due

per day were administered orally as immunosuppressive agents. Two years later, he had

are frequent


while infective



to severe atherosclerosis are also reported as complications after organ transplantations (9). The use of immunosuppressive agents including steroids and chronic rejective reaction are presumed to be the


No hypertension

or cardiac

murmur was

pointed out at that time. Later, 50 mg azathioprine, 8 mg methylpredonisolone, and 150 mgmizoribine

nocturnal dyspnea and was diagnosed as congestive heart failure in May 1988. Although he transiently recovered with medical treatments, the symptoms of congestive heart failure recurred and he was admitted to our department for further examina-

cause of the rapid progression of atherosclerosis. The present report describes the first case in Japan of a transplant patient complicated with infective

tions. The patient had a history of odontectomy 4 months before.

endocarditis with severe aortic regurgitation who showed severe atherosclerosis, as proven in the autopsy examination, 2 yr after renal allotransplantation.

tion of the internal jugular vein rose to 7 cm H2O at 45 degrees of Fowler's position, and holosystolic murmur (Levine 4/6) of the apex coupled with a

Physical examination demonstrated that pulsa-


murmur (Levine

From The First Department of Internal Medicine, and *The Department of Pathology (Hospital), Nishinomiya Received

for publication

June 1, 1990;


for publication



at the


Hyogo College of Medicine,

14, 1991

Reprint requests should be addressed to MotomaruMasutani, MD,The First Department of Internal Medicine, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya 663, Japan 458

Jpn J Med Vol 30, No 5 (September,

October 1991)

Infective Endocarditis


space at the left sternal border were

audible. The blood pressure in the upper and lower limbs



mmHg and



respectively. His body temperature was 37.5°C. The results of routine laboratory tests demonstrated normocytic and normochromic anemia (the red-blood-cell count was 319 x 104, the hemoglobin 8.4 g/dl) and the existence of inflammation (erythrocyte sedimentation rate was 22 mm/h, C-reactive protein 1 + )à" The arterial gas analysis showed an oxygen tension of 63.4 mmHgindicating the presence of hypoxia (Table 1). Although there was no remarkable abnormality in chest roentgenographic findings prior to


(on March 23, 1987), cardiomegaly

with a cardio-thoracic



of 65% and

pulmonary congestion with bilateral pleural effusion were noted on admission. After hospitalization, the patient proved resistant to medical treatments, and an extended CTRand an increase in lung congestion werefound in the chest roentgenogramon November

18 (Fig.


Anelectrocardiogram obtained at the time of

renal transplantation (July 25, 1986) revealed no significant abnormalities, but exhibited left ventri-

cular hypertrophy at the time of admission (Fig. 2). An echocardiographic


showed a

dilated left ventricle (diastolic dimension, 65 mm; systolic dimension, 55mm) with mild hypertrophy

1987.3.23 1988.ll.9

(diastolic thickness, 12 mm). Although no definite vegetation showing a shaggy pattern in a M-mode echocardiogram was found in the aortic valve, the Table





at the time of admission.


RBC 319xlO4/mm3, Hb 8.4g/dl, Ht 28.5%, Plat 19.8x lO4/mm3 WBC 6,900/mm3 (st. 1, seg. 74, lym. 18, eo. 1, ba. 3, mo.3) TP 6.14g/dl, Alb. 3.75g/dl, T-bil 0.62mg/dl, D-bil 0.25mg/dl GOT 19KU, GPT 17KU, LDH 459U, ALP 2.35BLU, FBS 106mg/dl BUN 42.9mg/dl, CRN 1.70mg/dl, Ccr. 39.4ml/min Na 143.5mEq/l, K 3.7mEq/l, Cl 107.2mEq/l, T-Cho. 212mg/dl HDL-Cho. 31mg/dl, TG 102mg/dl, ESR 22mm/h, CRP (+) CH50 40U/ml, VDRL (-), TPHA (-), HBs-Ag (-), HBs-Ab (-)


Blood Gas analysis

pH 7.506, 22.3 SAT 94.0%,



Po2 63.4mmHg,


BE -0.0

Urinalysis Specific gravity 1.020, pH 5.5, Sugar (-), l OOmg/dl Occult Blood (-), Sediments; nothing particular



Fig. 1. Sequential chest roentgenograms. Congestive heart failure progressed after hospitalization to medical treatments.

Jpn J Med Vol 30, No 5 (September,

October 1991)

and was resistant 459

Masutani et al

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Fig. 2. An electrocardiogram hypertrophy on admission.

Fig. 3. Two dimensional echocardiograms revealed no vegetation of the aortic valve but deformity and insufficient closure in diastole (upper). Color flow imaging showed severe aortic regurgitation

showing left ventricular

which progressed after hospitalization PC-G 1200x10"unit

| CZON8g



SB-PC 16g IFMOX4g~

Globulin2.5g [



DOA 10y DOB 10y


Digitoxin0.1mg Furosemide 120mg Nifedipine 80mg |



Apnea Consiousness clear

ESR (mm/1hr)(/nl) 40









å #"'


O^^^-CTR 65%

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CTR 63%






CTR 67%

Fig. 4. Clinical course of the patient. SB-PC,






C%*^-^^ CTR 63%









JJ. >|

WBC B.T. (°C)


CTR 63%

W A^>P


i% A-^P


25 days

PCG, benzylpeni-



flomoxef; DOA,dopamine hydrochloride; DOB, dobutamine hydrochloride; HD, hemodialysis; E-COM, extra-corporeal

ultra filtration method; ESR,erythrocyte sedimentation rate; WBC, white blood cell; B.T., body temperature; CTR, cardio-thoracic 460


Jpn J Med Vol 30, No 5 (September,

October 1991)

Infective Endocarditis

valve exhibited deformity and an increase in echo intensity, which was accompanied by insufficient valvular closure in diastole in the short axis view. Aortic regurgitation (grade 4) was observed on color flow imaging, and the aortic valvular deformity and

regurgitation progressed after hospitalization (Fig.

3). The color flow imaging also revealed moderate mitral regurgitation. The mitral valve, however, did not show deformity, calcification or prolapse. From the time of admission, as shown in Fig. 4, catecholamines such as dopamine and dobutamine and diuretics were employedfor treating congestive heart failure, and antibiotics including 1,200 x 104 units of benzylpenicillin per day were injected for suspected





gestive heart failure was transiently recovered with the use of antibiotics and extra-corporeal ultra filtration method (ECUM),unconsciousness occurred suddenly, followed by cardiopulmonary arrest which lead to death on December 12.

The gross anatomicopathological findings showed destruction of the aortic valve accompanied by a small vegetation (2x3x3 mm). The hematoxylin-eosin stained histological findings of the vegetation revealed precipitated fibrin suggesting the presence of previous inflammation, without

definite bacteria (Fig. 5). Multiple cerebral infarction was also found (Fig. 6). The renal artery which had been transplanted from a 21-year-old man, and

Fig. 6. Multiple cerebral the vegetation, was found.

Jpn J Med Vol 30, No 5 (September,


October 1991)

Fig. 5. Destruction of the aortic valve accompanied by a small vegetation. Histological findings revealed precipitated fibrin without definite bacteria (hematoxylin-eosin stain, X400).


to be due to emboli from


Masutani et al


very few transplantations

are being per-

formed in Japan compared with other advanced countries, therefore the cases of endocarditis are few, but would increase with the increase of transplantations.

In the present case, the pathological findings of the vegetation did not show any bacteria within it, and, therefore, diagnostic differentiation from nonbacterial thrombotic endocarditis was required (10). Based on the following, we diagnosed the patient as infective endocarditis with aortic regurgitation with a complication of multiple cerebral emboli: 1) Fig. 7. The transplanted renal artery and the abdominal aorta showed severe progression

of atherosclerosis.


the abdominal aorta showedsevere progression of atherosclerosis (Fig. 7). A severe coronary stenosis due to atherosclerosis was seen at the proximal portion of the left anterior descending coronary artery. There were no abnormal findings in the

transplanted kidney itself.


2 yr

matic improvement was observed after administration of antibiotics, 4) the destruction of the aortic valve wasmoresevere than that commonlyobserved in nonbacterial



5) non-

bacterial thrombotic endocarditis is generally formed such as malignant

tumors. In the present case, the patient was in good condition in spite of the presence of aortic regurgita-

the use of immunosuppresants has

decreased the frequency of rejective reaction in recipients and leads to an improved success ratio in organ transplantation,

and steroids

which easily lead to infection, 3) transient, sympto-

under consumptive diseases



he had a history of odontectomy, 2) he had received

the increase in infectious

tion on admission. It was additionally noted that progression of atherosclerosis was conspicuous on autopsy.

Atherosclerosis is hypothesized to be closely related

disease has posed a new problem, resulting in highest cause of death in the early and late phase of the posttransplantation period (1 , 2). The sites of infection in the late phase consist of the urinary tract (29.4%),

to lipid,

two contain the prominent lesions. The reported causal organisms are E. coli, Klebsiella and Enterobacter for urinary tract infection, and Klebsiella, Enterobacter, Candida albicans, Haemaphilus and Pseudomonas aeruginosa for

tolerance lead to chronic induced




hemorheology, and viral infection (1 1). With the long-term administration of steroids, the serum level of cholesterol and triglyceride increase is coupled

the respiratory tract (23.0%) and others; the former

with a decrease in HDLcholesterol level. Glucose

respiratory infection, in which opportunistic infection is prominent (5, 6). However, cases of infective

transplanted renal artery but in systemic arteries and causes injury to vascular endothelial cells and the formation of atherosclerosis (9). The calcified aorta

endocarditis after organ transplantation are rarely

reported, and no such reports have been published in Japan (7, 8). Although the reason is unclear, such cases maybe included in statistical reports under sepsis. The occurrence of sepsis is more frequent in the early phase of the post-transplantation period, while it occupies 11% of the late phase infections. The causal organisms are mainly Klebsiella, Enterobacter 462

and Pseudomonas aeruginosa



is reported

is also impaired (12, 13). These changes the progression of atherosclerosis. The rejective reaction after transplantation vascular inflammation not only in the

as one of the relative

risk factors


infective endocarditis (14). Therefore, the development of atherosclerosis due to transplantation might be the trigger of infective endocarditis in this case. In the near future, circulatory complications such as high degree atherosclerosis and infective endocarditis will likely increase with the increasing numbersof organ transplantations in Japan. We must elucidate a countermeasure to these complicaJpn J Med Vol 30, No 5 (September,

October 1991)

Infective Endocarditis tions.

1. Characteristics of post-transplant infection as compared with pairmatched hemodialysis patients. Nippon Touseki Gakkai Zasshi 21: 647, 1988 (in Japanese).


1) Sugimoto H, AkiyamaN, Otsubo O. Clinical study on 228 renal transplants. Nippon Geka Gakkai Zasshi 90:

8) Hida M. Autopsy findings in 68 fatal renal transplant recipients, collected from the annuals of pathological autopsy cases in Japan. Tokai J Exp Clin Med 13: 23, 1988.

2) Vanrenterghem Y, Rorls L, Lerut T, Waer M, Gruwez J, Michielsen P. Long-term prognosis after cadaveric kidney transplantation. Transplant Proc 19: 3762, 1987. 3) Murphy JF, McDonald F, Dawson M, Reite A, Turcotte

9) Satoh T, Nakamura K. Mansei kyozetsu hannou no rinsyou to byouri. Nippon Rinsyou 43: 41, 1985 (in



(in Japanese).


thrombotic endocarditis. AmHeart J 92: 723, 1976. infection in renal transplant recipients. Arch Intern Med 136: 670, 1976. ll) Tanaka K. Zyukuzyoukouka kenkyu no sinpo to seiingakusetsu no hensen, syogaihannousetsu wochusin ni. 4) Rifkind D, Marchioro TL, Wddell WR, Starzl TE. Nippon Rinsyou 46: 5, 1988 (in Japanese). Infectious diseases associated with renal homotrans- 12) Ettinger WH, Goldberg AP, Applebaum-Bowden D, J, Fekety

Jr R. Factors


the frequency


plantation. J Am Med Assoc 189: 397, 1964. 5) Uchida H, Yokota K. Zin-isyoku no gappeisyou, Kansensyou. Medicina 15: 1446, 1978 (in Japanese).

10) Deppisch LM, Fayemei OA. Nonbacterial

Hazzard WR. Dyslipoproteinemia in systemic lupus erythematosus, effect of corticosteroids. AmJ Med 83: 503, 1987.

6) Nicholls A, Edward N, Gatto GR. Staphylococcal septicaemia, endocarditis, and osteomyelitis in dialysis and renal transplant patient. Postgrad Med J 56: 642, 1980.

13) Mathew TH. Recurrence of disease following renal transplantation. AmJ Kidney Dis 12: 85, 1988. 14) Gregoratos G. Infective endocarditis, in: Cardiology, Parmley WW, Chatterjee K, Eds. J.B. Lippincott 7) Umetani N, Saka S, Inoue K, Kamata K, Okubo M. Company, Philadelphia, 1987. Infectious complications in renal transplant recipients.

Jpn J Med Vol 30, No 5 (September,

October 1991)


Post transplanted infective endocarditis.

The patient, a 51-year-old man, was receiving immunosuppressants for 2 yr after renal allotransplantation. He had heart failure with aortic regurgitat...
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