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Biomedical subjects

A Sofia

Publications and source records attributed to A Sofia.

At least 19 recordsLinked to original sources
PubMed2006

Peripheral tissue release of interleukin-6 in patients with chronic kidney diseases: effects of end-stage renal disease and microinflammatory state.

To examine if uremia influences muscle interleukin-6 (IL-6) metabolism we studied the exchange of IL-6 across the forearm in 16 patients with chronic kidney disease (CKD) (stages 3 and 4), in 15 hemodialysis (HD)-treated end-stage renal disease (ESRD) patients (n=15), and in six healthy controls. In addition, we performed an analysis of both IL-6 protein and IL-6 mRNA expression in muscle of CKD (stage 4) patients showing evidence of inflammation and in controls. A release of IL-6 from the forearm was observed in patients with elevated IL-6 plasma levels. Arterial IL-6 was directly related to released IL-6 (r=0.69; P<0.004) in HD patients. Both IL-6 protein and IL-6 mRNA expression were increased in muscle of inflamed CKD patients vs controls (P<0.05). Although muscle net protein balance was similar in all patients, it was significantly more negative in HD patients with high than in those with low IL-6 plasma levels (P<0.05). In addition, net protein balance was related to the forearm release of IL-6 in HD patients only (r=0.47; P<0.038). These data demonstrate that IL-6 expression is upregulated in muscle, and that muscle tissue, by releasing this cytokine, may contribute to the inflammatory response in HD patients. The release of IL-6 from peripheral tissues is associated with an increase in muscle protein loss in HD patients, suggesting that muscle release of IL-6 is linked to protein catabolism in these patients. The release of IL-6 from peripheral tissues may act as a signal for the inflammatory response and contribute to functional dysregulation in uremia.

Aged↗
PubMed2004

In-situ characterization of microbial community in an A/O submerged membrane bioreactor with nitrogen removal.

The bacterial community involved in removing nitrogen from sewage and their preferred DO environment within an anoxic/oxic membrane bioreactor (A/O MBR) was investigated. A continuously operated laboratory-scale A/O MBR was maintained for 360 d. At a sludge age of 150 d and a C/N ratio of 3.5, the system was capable of removing 88% of the influent nitrogen from raw wastewater through typical nitrogen removal transformations (i.e. aerobic ammonia oxidation and anoxic nitrate reduction). Characterization of the A/O MBR bacterial community was carried out using fluorescence in situ hybridization (FISH) techniques. FISH results further showed that Nitrosospira spp. and Nitrospira spp. were the predominant groups of ammonia and nitrite oxidizing group, respectively. They constituted up to 11% and 6% of eubacteria at DO below 0.05 mg/l (low DO), respectively, and about 14% and 9% of eubacteria at DO between 2-5 mg/l (sufficient DO), respectively, indicating preference of nitrifiers for a higher DO environment. Generally low counts of the genus Paracoccus were detected while negative results were observed for Paracoccus denitrificans, Alcaligenes spp, and Pseudomonas stutzeri under the low and sufficient DO environments. The overall results indicate that Nitrosospira spp., Nitrospira spp. and members of Paracoccus spp. can be metabolically functional in nitrogen removal in the laboratory-scale A/O MBR system.

Alcaligenes↗
PubMed1998

Inter-organ leptin exchange in humans.

To assess the individual role of splanchnic organs, kidney, and peripheral tissues on leptin metabolism, leptin exchange across the splanchnic bed, kidney, and leg has been evaluated by the arterio-venous technique in post-absorptive non-obese subjects. Leptin levels in the hepatic and renal veins were significantly lower (p < 0.001), while femoral vein levels were consistently greater (p < 0.05) than in the artery. The fractional extraction of leptin, namely the percentage of arterial leptin extracted, was greater in splanchnic organs (16%) than in the kidney (9.5%). Urinary excretion of leptin was undetectable in most subjects, indicating that leptin is degraded within the kidney. There was no correlation between fractional extraction of leptin and glomerular filtration rate, whereas leptin fractional extraction was directly related to renal plasma flow (p = 0.017). Renal leptin clearance was about 50% of the glomerular filtration rate. Our data demonstrate that both splanchnic organs and the kidney cooperate in the disposal of leptin, while peripheral tissues add significant amounts of leptin to the circulation. In non-obese subjects the contribution of the kidney to whole body clearance is no more than 50%. The removal of leptin by the kidney depends on renal plasma flow but not on glomerular filtration rate or filtered leptin.

Adult↗
PubMed1998

Microalbuminuria is an early marker of target organ damage in essential hypertension.

Microalbuminuria has been associated with a cluster of metabolic and nonmetabolic risk factors, suggesting that it might indicate the presence of generalized microvascular damage in patients with essential hypertension. To explore whether microalbuminuria is associated with early target organ damage, two groups of essential hypertensive patients, with (n = 17) (HtAlb+) and without (n = 16) (HtAlb-) microalbuminuria, and a control group (C) of healthy normotensive subjects (n = 20) were studied. The study groups, selected among participants of a large epidemiologic trial, were carefully matched for several potentially confounding variables such as gender, age, duration of hypertension, and body mass index. Albumin excretion rate was evaluated by radioimmunoassay in three nonconsecutive timed overnight collections after 3 weeks of pharmacologic wash-out. Left ventricular mass was assessed by M-B-mode echocardiography, carotid wall thickness by a high resolution ultrasound scan, and renal vascular impedance by Doppler scan. Office as well as 24-h ambulatory pressure monitoring (Takeda TM-2420) were also evaluated. There was no difference between the two hypertensive groups for office and 24-h blood pressure levels except for a lower daytime/nighttime systolic blood pressure ratio in the group with microalbuminuria. Microalbuminuric patients showed signs of early organ damage as compared to normoalbuminuric patients and normal subjects, namely greater left ventricular mass indices (LVMI 167+/-7 g/m2 in HtAlb+; 139+/-9 g/m2 in HtAlb-; 118+/-5 g/m2 in C, P < .001) and increased wall thickness of common carotid arteries (intima plus media thickness 12.5+/-0.2 mm in HtAlb+; 11.7+/-0.3 mm in HtAlb-; 11.2+/-0.2 mm in C, P < .001) as well as higher intrarenal vascular resistance (mean resistive index 0.62+/-0.01 in HtAlb+; 0.59+/-0.01 in HtAlb-; 0.59+/-0.01 in C, P < .05). In conclusion, microalbuminuria is an early marker of diffuse target organ damage in essential hypertension and therefore can be useful to identify patients for whom more aggressive preventive strategies or additional treatment measures are advisable.

Albuminuria↗
PubMed1998

[Adverse drug reactions in childhood. A drug surveillance study in Sicily].

The aim of the present study was to investigate the spontaneous reports of suspected adverse drug reactions, observed in paediatric patients in Sicily during the period between the 1st January 1995 and the 31st August 1997. The ADRs were classified according to the "WHO Programme for International Monitoring of Adverse Reactions to Drugs". On 1020 reports, the paediatric suspected ADRs were 130 (12.7%); 23% of these was serious, and 29.2% involved children aged 3 years or less. The antimicrobial and the musculoskeletal drugs were responsible of 74.6% of the whole suspected paediatric ADRs. Cutaneous and gastrointestinal apparatus were involved in 70% of reports and were the most frequently targets of ADRs. On 57 different molecules ceftriaxone and co-amoxiclav were the most common drugs causing ADRs with a percentage of 13%. In 45.4% of ADRs the suspension of the treatment occurred, in 34.6% therapy was needed besides the suspension of the drug, whilst in 11.5% patients needed an hospital visit. In 59.2% spontaneous reports were sent by hospitals, in 32.3% by primary health care and the remaining percentage by other sources. Our investigation should stimulate physicians to better evaluate the potential side effects of drugs and the cost/effectiveness profile of paediatric therapies.

Adolescent↗
PubMed1997

Effects of recombinant human growth hormone on muscle protein turnover in malnourished hemodialysis patients.

To assess the effect of recombinant human growth hormone (rhGH) on muscle protein metabolism in uremic patients with malnutrition, forearm [3H]phenylalanine kinetics were evaluated in six chronically wasted (body weight 79% of ideal weight) hemodialysis (HD) patients in a self-controlled, crossover study. Forearm protein dynamics were evaluated before, after a 6-wk course of rhGH (5 mg thrice weekly) and after a 6-wk washout period. After rhGH: (a) forearm phenylalanine net balance--the difference between phenylalanine incorporation into and phenylalanine release from muscle proteins--decreased by 46% (-8+/-2 vs. -15+/-2 nmol/min x 100 ml at the baseline and -11+/-2 after washout, P < 0.02); (b) phenylalanine rate of disposal, an index of protein synthesis, increased by 25% (25+/-5 vs. 20+/-5 at the baseline and 20+/-4 after washout, P < 0.03); (c) phenylalanine rate of appearance, an index of protein degradation, was unchanged (33+/-5 vs. 35+/-5 at the baseline and 31+/-4 after washout); (d) forearm potassium release declined (0.24+/-0.13 vs. 0.60+/-0.15 microeq/min at the baseline, and 0.42+/-0.20 microeq/min after washout P < 0.03); (e) changes in the insulin-like growth factor binding protein (IGFBP)-1 levels and insulin-like growth factor-I (IGF-I)/IGFBP-3 ratios accounted for 15.1% and 47.1% of the percent variations in forearm net phenylalanine balance, respectively. Together, these two factors accounted for 62.2% of variations in forearm net phenylalanine balance during and after rhGH administration. These data indicate: (a) that rhGH administration in malnourished hemodialysis patients is followed by an increase in muscle protein synthesis and by a decrease in the negative muscle protein balance observed in the postabsorptive state; and (b) that the reduction in net protein catabolism obtained with rhGH can be accounted for by the associated changes in circulating free, but not total, IGF-I levels.

Adult↗
PubMed1997

Prevalence and clinical correlates of microalbuminuria in essential hypertension: the MAGIC Study. Microalbuminuria: A Genoa Investigation on Complications.

The prevalence of microalbuminuria and its relationship with several cardiovascular risk factors and target organ damage were evaluated in a cohort of 787 untreated patients with essential hypertension. Albuminuria was measured as the albumin-to-creatinine ratio in three nonconsecutive, first morning urine samples. The prevalence of microalbuminuria was 6.7%. Albuminuric patients were more likely to be men and to be characterized by higher blood pressure, body mass index, and uric acid levels and lower HDL cholesterol and HDL cholesterol-to-LDL cholesterol ratio. Piecewise linear regression analysis demonstrated that uric acid and diastolic blood pressure significantly influence albuminuria and together account for a large part of its variations. K-means cluster analysis performed on the entire cohort of patients confirmed that microalbuminuria is associated with a worse cardiovascular risk profile. Furthermore, microalbuminuria was associated with the presence of target organ damage (eg, electrocardiographic [ECG] abnormalities and retinal vascular changes). Age and the presence of microalbuminuria act as independent risk factors for the development of ECG abnormalities and retinal vascular changes. Cluster analysis allowed us to identify three subgroups of patients who differed in the presence or absence of microalbuminuria, retinopathy, and ECG abnormalities. We conclude that the prevalence of microalbuminuria in essential hypertension is lower than previously reported. Increased urinary albumin excretion is associated with a worse cardiovascular risk profile and is a concomitant indicator of early target organ damage.

Adolescent↗
PubMed1997

Protein and amino acid metabolism in splanchnic organs in metabolic acidosis.

Metabolic acidosis causes a cooperative participation of different organs such as the liver, kidney, and muscle in restoring acid-base balance. In splanchnic organs, metabolic acidosis has repercussions on several nitrogen metabolism pathways. The decrease in urea synthesis due to reduced activity of urea cycle enzymes, ammonia uptake and amino acid transport, and changes in glutamine metabolism support renal ammoniagenesis thus offering a response to rid the body of excess protons. While some of the mechanisms are adaptive others may be harmful for the body. Metabolic acidosis may have effects on splanchnic protein turnover. In severe acidosis, synthesis of secreted liver proteins may be reduced. Acidosis may also modulate the response of the liver to growth hormone (GH) for insulin-like growth factor-I synthesis, thus inducing a state of GH resistance. Splanchnic abnormalities in acidosis might contribute to the malnutrition observed in uremia.

Acidosis↗
PubMed1997

Microalbuminuria: a marker of cardiovascular risk and organ damage in essential hypertension.

Microalbuminuria (Mi) is thought to reflect diffuse vascular damage and to predict cardiovascular morbidity and mortality in essential hypertension, although its pathogenesis remains to be fully elucidated. The relationship between microalbuminuria and several cardiovascular risk factors and target organ damage was evaluated in a large cohort of untreated essential hypertensive patients. Albuminuria was measured as the albumin to creatinine ratio in three non consecutive first morning urine samples. Cardiac damage was evaluated by ECG and retinal vascular changes by direct ophtalmoscopy. In a subgroup of 23 patients with Mi and in a control group of 22 normoalbuminurics, selected from the entire cohort of patients and carefully matched for age, gender, body mass index (BMI) and duration of disease, we also measured left ventricular mass index by M-B mode echocardiography, common carotid wall thickness by high resolution US-scan, and renal vascular resistances by US-doppler of interlobar arteries. K-means cluster analysis performed on the entire cohort of patients showed that microalbuminuria is associated with the presence of an unfavorable risk profile and target organ damage. Furthermore, microalbuminuric hypertensive patients have a larger left ventricular mass index, increased intima media thickness of carotid arteries and higher intrarenal vascular resistances as compared to a well matched group of normoalbuminuric patients. We conclude that in essential hypertension increased urinary albumin excretion can be useful to identify patients for whom more aggressive preventive strategies and/or additional treatment measures are advisable.

Albuminuria↗
PubMed1996

The deletion polymorphism of the angiotensin I-converting enzyme gene is associated with target organ damage in essential hypertension.

The activity of the renin-angiotensin-aldosterone system is thought to play a significant role in the development of target organ damage in essential hypertension. An insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene has recently been associated with increased risk for left ventricular hypertrophy and coronary heart disease in the general population. The D allele is associated with higher levels of circulating ACE and therefore may predispose to cardiovascular damage. The study presented here was performed to investigate the association between the ACE genotype, microalbuminuria, retinopathy, and left ventricular hypertrophy in 106 patients with essential hypertension. ACE gene polymorphism was determined by polymerase chain reaction technique. Microalbuminuria was evaluated as albumin-to-creatinine ratio (A/C) in three nonconsecutive first morning urine samples (negative urine culture) after a 4-wk washout period. Microalbuminuria was defined as A/C between 2.38 to 19 (men) and 2.96 to 20 (women). Hypertensive retinopathy was evaluated by direct funduscopic examination (keith-Wagener-Barker classification) and left ventricular hypertrophy by M-B mode echocardiography. The distribution of the DD, ID, and II genotypes was 27, 50, and 23%, respectively. The prevalence of microalbuminuria, retinopathy, and left ventricular hypertrophy was 19, 74, and 72% respectively. There were no differences among the three genotypes for age, known duration of disease, body mass index, blood pressure, serum glucose, uric acid, and lipid profile. DD and ID genotypes were significantly associated with the presence of microalbuminuria (odds ratio, 8.51; 95% confidence interval, 1.07 to 67.85; P = 0.019), retinopathy (odds ratio, 5.19; 95% confidence interval, 1.71 to 15.75; P = 0.005) and left ventricular hypertrophy (odds ratio, 5.22; 95% confidence interval, 1.52 to 17.94; P = 0.016). Furthermore, patients with DD and ID genotypes showed higher levels of A/C (3.6 +/- 0.9, DD; 2.6 +/- 0.7, ID; 0.9 +/- 0.2 mg/mmol, II; P = 0.0015 by analysis of variance) and increased left ventricular mass index (152 +/- 4.7, DD + ID versus 133 +/- 5.7 g/m2, II; P = 0.01) compared with II patients. The D allele was significantly more frequent in patients with microalbuminuria (odds ratio, 2.59; 95% confidence interval, 1.24 to 5.41; P = 0.013) and in those with retinopathy (odds ratio, 2.44; 95% confidence interval, 1.21 to 4.90; P = 0.015). Multiple regression analyses performed among the entire cohort of patients demonstrated that ACE genotype significantly and independently influences the presence of retinopathy, left ventricular hypertrophy, and microalbuminuria. In conclusion, the D allele of the ACE gene is associated with microalbuminuria as well as with retinopathy and left ventricular hypertrophy, and seems to be an independent risk factor for target organ damage in essential hypertension.

Adult↗
PubMed1996

Muscle protein turnover in chronic renal failure patients with metabolic acidosis or normal acid-base balance.

It is currently unknown if metabolic acidosis has any effect on muscle protein metabolism in patients with chronic renal failure (CRF). To address this question, muscle protein turnover was studied in patients with CRF and controls in the postabsorptive state by using the forearm perfusion method together with the 3H-phenylalanine kinetics. Nine patients were acidotic ([HCO-3]a = 20 +/- 0.5 mEq/l) whereas 4 patients had a normal acid-base balance ([HCO-3]a = 25 +/- 0.3 mEq/l). In patients with metabolic acidosis the rates of phenylalanine appearance and disposal from the forearm were increased as compared to controls. Phenylalanine net balance, i.e. net proteolysis, was only slightly higher than in controls. In patients under a normal acid-base balance both rates of appearance and disposal of phenylalanine as well as phenylalanine net balance were similar to controls. These preliminary data suggest that metabolic acidosis can enhance the rate of muscle protein degradation in patients with CRF.

Acidosis↗
PubMed1995

Disposal of exogenous amino acids by muscle in patients with chronic renal failure.

Muscle exchange of amino acids (AAs) was evaluated by using the arteriovenous-difference technique across the leg in seven patients with chronic renal failure (CRF) and eight control subjects before and for 75 min after the ingestion of an AA mixture simulating an animal-protein meal. Total AAs increased in arterial blood much more in patients with CRF after AA ingestion than in control subjects, as a consequence of an exaggerated increase in nonessential AAs (NEAAs) (+127%). Moreover, total AAs were taken up by the leg in larger amounts than in control subjects (+71%, P < 0.0025) because of increased uptake of NEAAs (+156%, P < 0.005). Branched-chain AA uptake by the leg was, in absolute values, similar to that of control subjects; however, because of the increased uptake of total AAs, branched-chain AA uptake was only 30% of total AA extraction, compared with 46% in control subjects. Abnormalities in AA uptake by muscle paralleled those in arterial AAs. In fact the same AAs that increased abnormally in blood were taken up by the leg at higher rates than in control subjects. Variations in arterial concentrations and muscle uptake of AAs were inversely related to arterial bicarbonate concentration, suggesting a role for acid-base status in modifying both the arterial supply and muscle metabolism of AAs. Results indicate that in CRF patients the normal pattern of postprandial AA repletion is disrupted. Muscle tissue faces the increased and unbalanced postprandial supply of AAs with an augmented and unbalanced uptake. Data are consistent with an abnormal use of exogenous AAs in CRF patients, possibly induced by metabolic acidosis.

Adult↗
PubMed1995

Prevalence of micro- and macroalbuminuria and their relationship with other cardiovascular risk factors in essential hypertension.

A cohort of 227 untreated essential hypertensive patients from north-western Italy was studied in order to evaluate the prevalence of micro- and macroalbuminuria and their relationship with other cardiovascular risk factors. Albuminuria was evaluated as the albumin to creatinine ratio (Alb/Cr) in three non-consecutive first morning samples. The prevalence of microalbuminuria and macroalbuminuria was 10% and 2.2%, respectively. Albuminuric patients showed higher blood pressure, serum creatinine, triglycerides and uric acid as well as a greater prevalence of retinopathy. Stepwise multiple regression analysis demonstrated that only a small part of variations in albuminuria was explained by changes in blood pressure. Duration of disease did not seem to influence microalbuminuria. The presence of hypertensive retinopathy was associated with greater albuminuria, longer duration of hypertension, and higher prevalence of major ECG changes, but not with higher blood pressure levels. Microalbuminuria, rather than a consequence of elevated blood pressure levels, seems to be a marker of a syndrome featuring, among other characteristics, essential hypertension. Furthermore, microalbuminuria must be considered as an independent cardiovascular risk factor.

Adolescent↗
PubMed1994

Skeletal muscle protein synthesis and degradation in patients with chronic renal failure.

Muscle protein turnover and amino acid (AA) exchange across the forearm were studied in nine postabsorptive patients with chronic renal failure (CRF) under unrestricted calorie-protein diets and eight controls by using the arterio-venous difference technique associated with the 3H-phenylalanine kinetics. In patients with CRF: (1) the rate of appearance (Ra) of phenylalanine (Phe) from the forearm, reflecting proteolysis, was 27% increased in comparison with controls (P < 0.01). Also the rate of disposal (Rd) of Phe, reflecting protein synthesis, was increased in patients (P < 0.01). As a consequence of these counterbalanced alterations, net balance of Phe across the forearm, that is, net proteolysis, was not changed. (2) The release of total AA from the forearm was not different from controls. Valine and ketoisocaproate release was reduced (P < 0.05). Serine uptake was not detectable. (3) Net proteolysis and the Rd/Ra ratio were inversely and directly, respectively, related to arterial [HCO3-] (P < 0.02 and P < 0.03, respectively). (4) Moreover, net proteolysis and Phe Rd/Ra ratio were directly and inversely, respectively, correlated with plasma cortisol (P < 0.01 and < 0.005, respectively). Plasma cortisol was in the normal range and inversely related to arterial [HCO3-] (P < 0.02). (5) While in controls phenylalanine appearance from the forearm was inversely related to insulin levels, no correlation was found in patients. In conclusion, in patient with CRF, forearm Phe kinetics indicate the existence of an increased muscle protein turnover. Changes in protein synthesis and degradation are well balanced and net proteolysis is not augmented.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗