Non-Bacterial Thrombotic Endocarditis in a CAPD Patient
Author(s) -
K.B. Modi,
I. S. Henderson
Publication year - 1987
Publication title -
the nephron journals/nephron journals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 72
eISSN - 2235-3186
pISSN - 1660-8151
DOI - 10.1159/000184415
Subject(s) - medicine , endocarditis , peritoneal dialysis , cardiology , intensive care medicine
Dr. K.B. Modi, MD, MRCP, Renal Unit, Stobhill Hospital, Glasgow G21 3UW (UK) Dear Sir, We report a case of non-bacterial thrombotic endocarditis (NBTE or marantic endocarditis) causing cardiac failure and death in a patient with end-stage chronic renal failure managed with continuous ambulatory peritoneal dialysis (CAPD). The patient was a 60-year-old male who developed chronic renal failure due to accelerated hypertension detected in July 1979. Regular home haemodialysis was commenced in March 1981. He suffered from recurrent fluid overload and cardiac failure due to unsatisfactory control of systemic hypertension and excessive fluid-intake and required several admissions for ultrafiltration. He was noted to have a long systolic murmur, best heard at the aortic area, which was shown to be due to aortic valve sclerosis after clinical and echocardiographic assessment in March 1984. In August 1984, the patient chose to change from home haemodialysis to CAPD. With CAPD he had an initial improvement in dyspnoea but later developed progressive tiredness. Hypoal-buminaemia was a major problem in spite of high protein intake and repeated intravenous plasma protein supplementation. His PD effluent fluid revealed an albumin concentration of 22–26 g/litre and this persistently high albumin loss in PD fluid in the absence of peritonitis was considered to result from long-standing congestive cardiac failure. In March 1985, during an admission for investigation of progressive tiredness, lethargy, low-grade pyrexia and weight loss (9 kg over the previous 8 months), a short early diastolic murmur was noted. Repeat echocar-diogram revealed a tricuspid aortic valve with marked vegetations and left ventricular dilatation in addition to previously noted hypertrophy. Repeated blood cultures were negative. He died suddently during an attack of pulmonary oedema. Postmortem examination revealed a partially calcified tricuspid aortic valve, the valve cusps being covered by large, crumbling vegetations which were sterile on culture (fig. 1). The other cardiac valves were unremarkable apart from a calcified mitral valve ring. There was no evidence of recent myocardial infarction. To our knowledge, this is the first case of NBTE in a CAPD patient. NTBE is characterised by sterile, verruFig. 1. Postmortem examination of heart showing marantic vegetations. Non-Bacterial Thrombotic Endocarditis in a CAPD Patient 393
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