They were the second most common extrarenal complication except empyema (11/20, 55%). Two (10%) died and seven (35%) of the survivors developed long-term renal morbidity. Twelve of the 20 patients (60%) were diagnosed with SP-HUS. Younger age, female children, higher white blood cell count, higher alanine transaminase, higher lactate dehydrogenase and high incidence

of DIC were significantly common in SP-HUS cases. All SP-HUS cases were complicated with pleural effusion, empyema, learn more or both. Positive Thomsen-Freidenreich antigen (T-Ag) activation was 83% sensitive and 100% specific for SP-HUS, and a positive direct Coombs’ test was 58% sensitive and 100% specific. Conclusion:  Invasive pneumococcal infection is the most common cause of HUS in Taiwan.

Positive T-Ag activation and a direct Coombs’ test are rapid predictors of SP-HUS in children with invasive pneumonia. “
“Date written: June 2008 Final submission: June 2009 No recommendations possible based on Level I or II evidence. (Suggestions are based on Level III and IV evidence). Stable hypertensive kidney transplant recipients should be advised to restrict sodium intake to 80–100 mmol/day. (Level III evidence) The development of arterial hypertension is common after kidney transplantation. While the aetiological factors of post-transplant hypertension have not been clearly elucidated, it has been correlated with male sex, age, donor age, the presence of diabetes, weight gain, body mass index and delayed graft function.2 Calcineurin Fossariinae BTK inhibitor supplier inhibitors are known to contribute to hypertension and prednisone may also play a role.3,4 Post-transplant arterial hypertension is a risk factor for cardiovascular disease (CVD), which is a significant

cause of morbidity and mortality in the kidney transplant population.5 Hypertension appears to be one of the primary risk factors for carotid lesions in the kidney transplant recipients, with such lesions being associated with a five- to sixfold increase in myocardial infarction or stroke in the general population.6 In the non-transplant population, the relationship between blood pressure and risk of CVD events is continuous, consistent and independent of other risk factors. For each 20 mmHg rise in systolic blood pressure or 10 mmHg rise in diastolic blood pressure above 115/75 mmHg, the risk of CVD is doubled (in people aged 40–70 years).7 Conversely, a reduction of 5 mmHg diastolic blood pressure is associated with a 35–45% fall in risk of stroke.8 Treating hypertension successfully may significantly affect the progression of CVD in the transplant population in a similar manner. Recent studies have shown that hypertension is associated with chronic allograft nephropathy and acute rejection. An elevated blood pressure, even within the normal range, has been shown to adversely affect kidney graft survival.