Biomedical subjects

Maria Aparecida Dalboni

Publications and source records attributed to Maria Aparecida Dalboni.

8 recordsLinked to original sources

PubMed2006

Coronary artery calcification, systemic inflammation markers and mineral metabolism in a peritoneal dialysis population.

AIMS: To assess the prevalence of coronary artery calcification (CAC) in peritoneal dialysis (PD) patients and to determine whether comorbidities such as inflammation, dyslipidemia and mineral metabolism disorders correlate with its development. METHODS: Forty-nine PD patients (45% male; median age, 52 years) were submitted to multislice computed tomography. Inflammatory markers, anti-oxidized LDL antibody, calcium-phosphate balance and lipid profiles were assessed. RESULTS: Twenty-nine patients (59.2%) presented CAC (median calcium score, 234.7 Agatston units). Patients with CAC were older than those without, more frequently presented a history of coronary artery disease or hypertension and had lower HDL cholesterol levels, as well as presenting higher levels of osteoprotegerin and LDL oxidation. The logistic regression revealed that the independent determinants of CAC were age (odds ratio = 1.12; p = 0.006) and number of prescribed anti-hypertensive drugs (odds ratio = 2.38; p = 0.048). When the population was stratified by calcium score quartile, soluble Fas levels were significantly higher in patients with severe calcification. In patients younger than 45, CAC correlated positively with phosphorus levels (r = 0.52; p = 0.04). CONCLUSION: In PD patients, CAC is highly prevalent. Our results indicate that conditions such as inflammation and mineral disturbances are associated with its development.

Adult↗

PubMed2006

Effect of microcystin on leukocyte viability and function.

Microcystin (MC) has been found in several areas of the world. In addition to its hepatotoxicity, microcystin may have an immunomodulatory effect. Considering that patients receiving hemodialysis may be chronically exposed to variable concentrations of MC, and that they present important changes in this immune response, we have assessed the effect of MC on the function of leukocytes. Polymorphonuclear leukocytes isolated from healthy volunteers (HV) and patients receiving hemodialysis (HD) were incubated with microcystin (10 microg/L) for 24h and evaluated for reactive oxygen species production (ROS), phagocytosis and apoptosis. Monocytes incubated with and without LPS (100 ng/mL) and microcystin for 24h were assessed for TNFalpha and IL-10 production. Leukocytes of HV presented an increase in apoptosis rates and leukocytes from HD exhibited a lower production of oxygen-reactive species, both spontaneously and after stimulus with S. aureus, when compared with leukocytes incubated without toxin. Monocytes presented an increase in cytokine production after stimulation by LPS in both groups, but there was no difference between the groups with and without MC that were incubated with or without LPS. Low concentrations of microcystin can induce mild changes in leukocyte function of HV and HDP, particularly in the ability to produce ROS.

Apoptosis↗

PubMed2005

Effects of uraemia and dialysis modality on polymorphonuclear cell apoptosis and function.

BACKGROUND: Previous studies have reported that incubation of polymorphonuclear cells (PMN) in uraemic plasma or with different haemodialysis membranes and peritoneal dialysis solutions increases apoptosis in this cell type. In addition, PMN harvested from uraemic patients show a reduced ability to generate superoxide in response to stimuli as well as impaired phagocytosis, chemotaxis and degranulation. The aim of the current study was to investigate the effect of uraemia and dialysis modality on apoptosis and function in freshly harvested non-incubated PMN. METHODS: Polymorphonuclear cells were harvested from 14 chronic haemodialysis (HD) patients, from 14 continuous peritoneal dialysis patients (CAPD), 28 chronic kidney disease (CKD), pre-dialysis patients and from 14 healthy subjects (Controls). In these in vivo experiments, PMN apoptosis was studied by means of flow cytometric analysis of annexin V binding to freshly isolated cells. Polymorphonuclear cell phagocytosis and production of reactive oxygen species by unstimulated or stimulated (S.aureus, fMLP, PMA) cells were also studied by flow cytometry using whole blood. RESULTS: We observed increased PMN apoptosis in CKD patients. CAPD and HD patients displayed PMN apoptosis rates similar to controls. In the HD group, PMN exhibited decreased phagocytosis rates. In contrast, phagocytosis rates in PMN from CAPD were not significantly different from controls. In the CKD and HD groups, apoptosis was inversely correlated with respiratory burst activity and phagocytosis. CONCLUSION: Our results suggest that both uraemia and treatment modality may interfere with PMN apoptosis and function. Dialysis appears to normalize the increased PMN apoptosis rates observed in CKD patients.

Adult↗

PubMed2004

Decreased resting energy expenditure in non-dialysed chronic kidney disease patients.

BACKGROUND: Non-dialysed chronic kidney disease (CKD) patients may have altered resting energy expenditure (REE) because of the important metabolic functions of the kidneys. The aim of the present study was to evaluate whether REE in clinically stable, non-diabetic and non-dialysed CKD patients with no clinical signs of inflammation, was different from that of gender and age pair-matched healthy controls. Subjects and methods. REE in 45 patients (20 male and 25 female; age 44.9 +/- 11.7 years; mean +/- SD) and 45 healthy individuals (20 male and 25 female; age 44.6 +/- 11.5 years) was measured by indirect calorimetry after a 12-h fast. In both groups, body composition was assessed by bioelectrical impedance. Glomerular filtration rate was assessed by creatinine clearance only in the CKD patients. RESULTS: The mean creatinine clearance and serum creatinine of the CKD patients were 29.1 +/- 14.6 ml/min/1.73 m(2) and 3.48 +/- 2.48 mg/dl, respectively. Body fat (BF) and lean body mass (LBM) were similar between the two groups (CKD patients: BF 28.6 +/- 11.3%, LBM 46.9+/-10.0 kg; and healthy individuals: BF 28.1 +/- 7.54%, LBM 49.5 +/- 10.5 kg). REE of CKD patients was significantly lower than that of healthy individuals (1325 +/- 206 vs 1448 +/- 258 kcal/day; P = 0.01, respectively) even after adjusting for LBM by multiple regression analysis. In fact, the presence of chronic renal insufficiency reduced REE by 103.2 kcal/day (P = 0.02; 95% confidence interval (-15.9; 190.5)). CONCLUSION: REE of clinically stable non-dialysed, non-diabetic patients in stages 2-5 of CKD was lower than that of age and gender pair-matched healthy individuals. Although the cause of reduced REE was unclear, it may be related to decreased food intake and to metabolic disturbances inherent with deterioration of renal function. Further studies will be necessary to clarify this issue.

Adult↗

PubMed2004

Balance between cytokine production by peripheral blood mononuclear cells and reactive oxygen species production by monocytes in patients with chronic kidney disease.

Hemodialysis (HD) and peritoneal dialysis are associated with inflammatory events and immunological incompetence. The purpose of this study was to evaluate the effect of both uremia and dialysis modality on the production of cytokines and reactive oxygen species (ROS) by monocytes. four groups of subjects were studied: 28 chronic kidney disease (CKD) patients, 14 chronic HD patients, 14 patients on continuous ambulatory peritoneal dialysis (CAPD) patients, and 14 healthy volunteers, peripheral blood mononuclear cells (PBMC) were isolated from blood samples and incubated for 24 hr with or without lipopolysaccharide (LPS). TNF-alpha and IL-10 production by PBMC and serum levels of these cytokines were quantified by ELISA. Aliquots of whole blood were incubated in vitro and ROS production and phagocytosis were quantified by flow cytometry. Compared to the control group, Staphylococcus aureus-stimulated ROS production by monocytes was significantly lower in the HD group. The highest levels of unstimulated TNF-alpha production in vitro were observed in the HD group. In the CKD group, as well as in the whole population, there were a negative correlation between TNF-alpha production by unstimulated PBMC and ROS production by S. aureus-stimulated monocytes and a positive correlation between PMA-stimulated ROS production by monocytes and unstimulated and LPS-stimulated IL-10 production by PBMC suggesting that the pro-inflammatory state in CKD patients is associated with decreased response to infectious challenges.

Adult↗

PubMed2003

Soluble Fas: a novel marker of inflammation in uremia.

BACKGROUND: Inflammation has been associated with atherosclerotic cardiovascular disease (CVD) and anemia in patients with end-stage renal disease (ESRD). Recent studies have shown that serum levels of soluble Fas (sFas), an antiapoptotic and proinflammatory molecule, are elevated in patients with cardiac disease and patients with ESRD. We therefore sought to investigate serum levels of sFas in uremic patients and its correlation with known markers of inflammation, anemia and CVD. METHODS: The study included 25 ESRD patients (14 on hemodialysis, 11 on CAPD), 27 patients with chronic kidney disease (CKD; creatinine clearance <50 ml/min/1.73 m2), and 14 normal control subjects. We measured serum levels of sFas, C-reactive protein (CRP), and albumin. We also investigated the association of serum sFas levels with the presence of CVD and with erythropoietin (EPO) dosage. RESULTS: Levels of sFas were elevated in CKD and ESRD patients compared to controls. sFas levels correlated negatively with creatinine clearance. In the dialysis patients, we observed that sFas levels were higher among those with CVD. Serum levels of sFas correlated with serum levels of CRP (r=0.31; P=0.03), serum levels of albumin (r=-0.35, P=0.02), and EPO dosage (r=0.51; P=0.009). CONCLUSION: These results suggest that sFas may be a marker of inflammation in CKD and ESRD patients.

Adult↗

PubMed2003

Upregulation of reactive oxygen species generation and phagocytosis, and increased apoptosis in human neutrophils during severe sepsis and septic shock.

We evaluated neutrophil activation by measuring its phagocytic ability and oxidative burst activity in 16 patients with sepsis and 16 healthy volunteers. We also focused on neutrophil apoptosis as a regulatory mechanism of the inflammatory response. Neutrophil phagocytosis was evaluated by the detection of propidium iodide (PI)-labeled Staphylococcus aureus added to whole blood. Reactive oxygen species (ROS) formation was quantified by measuring the oxidation of 2',7' dichlorofluorescein diacetate (DCFH-DA) at baseline and after cell stimulation with phorbol myristate acetate (PMA), and bacterial cells (killed S. aureus) or products (lipopolysaccharide [LPS] and N-formyl-methionyl-leucyl-phenylalanine [FMLP]). Apoptosis was assessed in neutrophils stained with annexin V and PI. Neutrophil phagocytic ability was increased in patients with sepsis compared with healthy controls (median geometric mean fluorescence intensity [GMFI] was 101.9 and 54.7, respectively; P = 0.05). ROS formation was enhanced in patients with sepsis compared with healthy volunteers at baseline (median GMFI 275.6 and 52.1, respectively; P < 0.001), and after stimulation with S. aureus (median GMFI 2395.8 and 454.9, respectively; P < 0.001), PMA (median GMFI 1120.6 and 307.5, respectively; P = 0.003), FMLP (median GMFI 792.4 and 123.2, respectively; P < 0.001), and LPS (median GMFI 624.8 and 144.8, respectively; P < 0.001). Early neutrophil apoptosis was increased in patients with sepsis compared with healthy volunteers (median 11.3% and 9.1%, respectively; P = 0.03). These data demonstrate that neutrophil function is enhanced in patients with sepsis. Additionally, circulating neutrophils from patients with sepsis presented with increased early apoptosis, which may be consequence of a regulatory mechanism of the inflammatory response.

Annexin A5↗

PubMed2003

A model for improving quality in nephrology settings.

Continuous quality improvement (CQI) programs have been instituted in many health care organizations over the last decade. PDCA, a tool composed of planning (P), doing (D), checking (C), and acting (A), has proved to be very useful in the CQI problem-solving process. The use of the PDCA tool described in this article resulted in the successful resolution of a hepatitis B outbreak in a Brazilian hemodialysis population and can serve as a model methodology for improving care in nephrology settings.

Brazil↗