Prebiotic Therapy with Inulin Associated with Low Protein Diet in Chronic Kidney Disease Patients: Evaluation of Nutritional, Cardiovascular and Psychocognitive Parameters.

A relationship between dysbiotic gut microbiome and chronic kidney disease (CKD) has been recently documented; it contributes to CKD-related complications, including cardiovascular disease. Aim: We tested how a low-protein diet (LPD)-with or without oral inulin supplementation as a prebiotic-modulates some inflammatory, atherosclerosis and endothelial dysfunction indices and nutritional markers, as well as psychocognitive functions in CKD patients. We conducted a prospective, case-control study on CKD patients on conservative therapy, divided in two groups: the intervention group treated with LPD (0.6 g/kg/day) plus inulin (19 g/day) and a control group treated with LPD without inulin, for six consecutive months. Clinical and hematochemical parameters as well as instrumental, and psychocognitive assessments (by SF-36 survey and MMSE, HAM-D, BDI-II) were recorded in all the participants at baseline (T0), at three months (T1) and at six months (T2). A total of 41 patients were enrolled: 18 in the intervention group and 23 in the control group. At T2, in both groups, we observed a significant reduction of serum nitrogen and phosphorus (p ≤ 0.01) and serum uric acid (p ≤ 0.03), and an improvement in metabolic acidosis (bicarbonates, p ≤ 0.01; base excess, p ≤ 0.02). Moreover, at T2 the intervention group showed a reduction in serum insulin (p = 0.008) and fasting glucose levels (p = 0.022), HOMA-IR (p = 0.004), as well as lower total serum cholesterol (p = 0.012), triglycerides (p = 0.016), C-reactive protein (p = 0.044) and homocysteine (p = 0.044) and higher HDL (p < 0.001) with respect to baseline. We also observed a significant amelioration of some quality of life and functional status indices (SF-36 survey) among the intervention group compared to controls, without a significant improvement in the cognitive state (MMSE). On the other hand, an amelioration in mood (by HAM-D and BDI-II) was found in the intervention group and in controls (only by BID-II). In conclusion, LPD in association with oral inulin supplementation improved glycemic and lipid metabolism and ameliorated the systemic inflammatory state, likely reducing cardiovascular risk in CKD patients and this may represent a promising therapeutic option, also improving quality of life and mood.

Pitfalls in the diagnosis of enteroviral infection in young children.

BACKGROUND: Three infants with enteroviral infections were admitted to a neonatal intensive care unit (NICU). Investigation into the possible nosocomial spread of enterovirus identified 31 other infected infants. Only 1 of the 31 was truly positive; 30 were false-positive results. METHODS: This was a retrospective observational study. Investigational laboratory studies were conducted to identify problems in diagnostic procedures. RESULTS: Stool cultures were used to identify asymptomatic infections. Investigation identified several problems in the procedures in identification of enterovirus: (1) stool specimens were not properly filtered, (2) insufficient number of tissue culture cell types were used, (3) nonspecific toxicity due to stool and the presence of Clostridia difficile toxin was responsible for cytopathic effects in tissue culture, (4) the failure to block nonspecific fluorescent staining led to misidentification of enteroviruses. CONCLUSIONS: The use of stool cultures to identify asymptomatic enteroviral infections in infants in an NICU can be fraught with problems because of high frequency of C. difficile toxin and the nonspecific toxic effects of stool on tissue culture cells. These problems can be rectified when proper procedures are followed.

Outbreak of adenovirus type 30 in a neonatal intensive care unit.

OBJECTIVES: To describe an outbreak of adenovirus, type 30, in a neonatal intensive care unit (NICU). STUDY DESIGN: This was a retrospective, observational study. RESULTS: An outbreak of adenovirus infection occurred in an NICU. It lasted 6 months and involved 21 of 333 (6.3%) infants. The introduction of infection control measures controlled the outbreak; however, premature discontinuation of the measures resulted in a second wave of cases. The virus caused pneumonia in 7 infants, conjunctivitis in 7 infants, pneumonia and conjunctivitis in 1 infant, and upper respiratory tract illness in 1 infant. Infection was asymptomatic in 5 infants. Six infants died. Death was associated with the presence of pneumonia ( P = .0001), administration of steroids ( P = .003), and mechanical ventilation ( P = .02). Investigation into the origin of the outbreak suggested that the virus may have been introduced and spread during ophthalmologic procedures. CONCLUSIONS: Adenovirus type 30 can cause severe disease among premature infants in an NICU. Infants with severe bronchopulmonary dysplasia requiring mechanical ventilation are more likely to have development of adenovirus pneumonia and die. Standard infection control measures are effective in controlling an outbreak. Ophthalmologic procedures continue to be a potential source of adenovirus outbreaks.