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Biomedical subjects

F Mallamaci

Publications and source records attributed to F Mallamaci.

59 records · Page 4Linked to original sources

Pentosidine, carotid atherosclerosis and alterations in left ventricular geometry in hemodialysis patients.

OBJECTIVE: To assess the relationship between advanced glycation end products (AGE) and cardiovascular damage in end-stage renal diseases. METHODS: Ninety-one hemodialysis patients who had been on dialysis treatment for at least six months were recruited for the study. Each patient underwent echocardiography and an echo-color Doppler study of the carotid arteries. We measured plasma pentosidine and related it to intima media thickness, atherosclerotic plaques and parameters of left ventricular geometry. RESULTS: Pentosidine was higher in patients treated by low-flux dialysis (31.0+/-16.6 pmol/mg protein) than in those treated by high-flux dialysis (25.4+/-7.6 pmol/mg protein), but this difference was of marginal statistical significance (P=0.08). On multivariate analysis, plasma IgG (beta=0.24, P=0.02) was the only independent correlate of plasma pentosidine. Intima media thickness and the number of atherosclerotic plaques were unrelated to plasma pentosidine. Mean wall thickness (beta=0.18, P<0.05), relative wall thickness (beta=0.20, P<0.05) and left ventricular end-diastolic volume (beta= -0.23, P<0.01) were independently related to plasma pentosidine. CONCLUSIONS: Pentosidine, a reliable marker of "carbonyl stress", is unrelated to intima media thickness and to the number of atherosclerotic plaques, but it is related to alterations in heart geometry. These data suggest that the effect of carbonyl stress on the cardiovascular system is complex and that the effects of AGE on the heart may be dissociated from those on the arterial system.

Arginine↗

[Hyperaldosteronism and simultaneous pheocromocytoma: a puzzle case].

Pheochromocytoma and primary hyperaldosteronism are well-known causes of hypertension. It was recently reported that their frequency in the hypertensive population is 0.1-0.2% and 3-15%, respectively. We describe the case study of a patient with severe hypertension (200/100 mmHg) and the coexistence of pheochromocytoma and primary hyperaldosteronism attributable to adrenal hyperplasia. The originality of this clinical report is that the patient presented a pheochromocytoma in the left adrenal gland and hyperplasia of the contralateral adrenal gland. The simultaneous presence of pheochromocytoma and primary hyperaldosteronism in the same patient is probably due to either genetic predisposition or to specific environmental risk factors for these adrenal diseases.

Adrenal Gland Neoplasms↗

Management of hypertension in chronic kidney disease: the Italian multicentric study.

BACKGROUND: Guidelines have indicated the achievement of blood pressure target (BP <130/80 mmHg) as a priority in the conservative treatment of chronic kidney disease (CKD), but the current implementation of these recommendations in clinical practice is unknown. METHODS: We assessed control rates, treatment and clinical correlates of hypertension in 1201 adult non-dialyzed CKD patients followed up by a nephrologist for at least 6 months. RESULTS: Estimated glomerular filtration rate (GFR) was 32 (SD 15) mL/min/1.73 m2. BP target was not achieved in 88% of patients (95% confidence interval (95% CI): 86-90%). In 84% of patients, BP levels were also above the target at the first visit to the nephrology unit 4.5 yrs previously. The risk of not achieving BP target during the nephro-logy follow-up was associated with older age (odds ratio (OR): 1.24, 95% CI 1.06-1.45, p=0.008), diabetes (OR: 2.25, 95% CI 1.20-4.20, p=0.011), and the duration of hypertension (OR: 1.13, 95% CI 1.02-1.24, p=0.016). Among patients with uncontrolled BP, about 70% received multidrug antihypertensive therapy including renin-angiotensin system (RAS) inhibitors; conversely, diuretic treatment was prescribed in a minority of patients (37%), and at insufficient doses in half the cases, despite the insufficient implementation of a low salt diet (18%). CONCLUSIONS: BP target was not reached in most CKD patients routinely seen in the renal clinics. The main barrier to guideline implementation is possibly the inadequate treatment of extracellular volume expansion despite the large prevalence of factors, such as older age and diabetes, which further enhance the intrinsic BP salt sensitivity of CKD.

Aged↗

Leptin in end stage renal disease (ESRD): a link between fat mass, bone and the cardiovascular system.

Adipose tissue is now considered an important system operating strictly in concert with other systems. The adipocyte is the main producer of two pleiotropic compounds, leptin and adiponectin, modulating inflammation and having multiple effects in disparate organs including the cardiovascular and the central nervous system. Leptin has disparate influences on various physiologic and organ systems including glucose homeostasis, hematopoiesis and the reproductive and cardiovascular systems and is a crucial hormone for the regulation of food intake and body weight. Peripherally, leptin modulates insulin sensitivity and high leptin triggers insulin resistance and vice versa. Obesity, a situation where circulating leptin attains very high levels is accompanied by increased bone mass, a phenomenon which may depend on direct stimulation of osteoblasts by leptin. However in animal models the stimulating effect of leptin on the osteoblast is counterbalanced by a strong inhibitor effect on bone formation in the central nervous system. Two recent studies reported an inverse link between leptin, bone mass and PTH in dialysis patients suggesting that leptin may be implicated in low bone turnover in these patients, likely by a mechanism involving the central nervous system. Leptin induces vascular calcifications in vitro. In uremic man leptin is unrelated to valvular calcifications but predicts incident cardiovascular events in overweight and obese dialysis patients. Leptin seems to be a relevant player in the emerging connection between bone and cardiovascular alterations in patients with end stage renal disease.

Adipose Tissue↗