Risk factors for systemic emboli in infective endocarditis.

A retrospective study was undertaken to analyse the risk factors for systemic emboli in infective endocarditis. Patients (n = 80; 70% males; mean age 65 years; range 20-91 years) with infective endocarditis, as defined by the Duke criteria and diagnosed using transoesophageal echocardiography during the period January 1995 to March 2001, were included. The average time between the start of the illness and the beginning of antibiotic treatment was 55 days (range 0-405 days). The pathogens identified were streptococci (n = 47), staphylococci (n = 11), enterococci (n = 9), and others (n = 4). In nine cases, blood cultures were sterile. Thirty patients with at least one embolic episode were compared with 50 control patients. According to univariate analysis, the main risk factor for systemic emboli was the size of the vegetation (12.4 mm vs. 7.8 mm; p = 0.0005). The risk of emboli was 57% when the vegetation measured > 10 mm and only 22% when it was < 10 mm (p = 0.003). The mobility of the vegetation was also a risk factor: 48% if the vegetation was mobile; and 9% if fixed (p = 0.003). Sex, age, pathogen, antibiotic treatment, type of valve and the number and position of the vegetations were not found to be risk factors. With multivariate analysis, only mobility was identified as a risk factor. Overall, mobile vegetations > 10 mm in size were associated with an increased risk of embolic episodes in infective endocarditis.

[Cerebral angiitis and Goodpasture's syndrome]. / Angéite cérébrale et syndrome de Goodpasture.

Goodpasture's syndrome is a form of rapidly progressive glomerulonephritis with pulmonary hemorrhage in the presence of antiglomerular basement membrane antibodies. Concomittant central nervous system manifestations are exceptionally reported. We report such a case of an 55-year-old woman who developed fluctuant neurobehavioral manifestations over a 9 months period. Angiography showed cerebral arterial distal lesions compatible with the diagnosis of angiitis. The antiglomerular basement membrane antibody titer was elevated. Search for anti-neutrophil cytoplasmic antibody was negative. After the reintroduction of cyclophosphamide agent, clinical evolution was favourable. Clinical cerebral manifestations in our case are probably du to a angiitis. Few cases are reported in the literature. The role of antiglomerular basement membrane antibody in the development of the cerebral angiitis is possible.

Excessive body weight as a new independent risk factor for clinical and pathological progression in primary IgA nephritis.

Experimental evidence suggests a role for obesity in the formation and progression of some glomerular lesions, but data for human glomerulonephritis are lacking. In a cohort of 162 incident patients with biopsy-proven immunoglobulin A (IgA) nephropathy, we assessed whether the presence of an elevated body mass index (BMI >/= 25 kg/m(2)) at the time of the first renal biopsy (RB1) correlated with clinical data at RB1 (24-hour proteinuria, arterial hypertension, and renal function), pathological data (global optical score [GOS] with detailed pathological indices), and clinical progression to both arterial hypertension and chronic renal failure (CRF). In both univariate and multivariate analyses, the presence of an elevated BMI at RB1 was significantly associated with the severity of pathological renal lesions (GOS and vascular, tubular, and interstitial indices). Hypertension-free survival was significantly less in overweight patients (P: < 0.0001) compared with those with normal weight. In a Cox regression analysis for hypertension-free survival including 24-hour proteinuria greater than 1 g, GOS, and metabolic parameters, only elevated BMI and GOS were independent factors for the development of arterial hypertension. CRF-free survival was also significantly less in patients with an excessive BMI. In a multivariate Cox regression analysis for CRF-free survival, hypertension, GOS, and BMI at RB1 were independent risk factors for CRF. In IgA nephropathy, excessive body weight and/or BMI are underestimated predictive factors for the development of arterial hypertension and, ultimately, CRF.