Background: The prevalence of inflammation is high among patients with chronic renal failure but the reason of inflammation is unclear. We test the hypothesis that inflammation in chronic renal failure could be the consequence of an increased left-ventricular wall tension related to ventricular dysfunction, hypervolemia or both. Methods: For assessing left-ventricular filling pressure, plasma level of N-terminal pro-B-type natriuretic peptide (N-BNP) was used, as B-type natriuretic peptide is secreted from the cardiac ventricles in response to increased wall tension. N-BNP levels and C-reactive protein (CRP) were measured on the same day in 75 pre-dialysis patients. A previous history of cardiomiopathy with systolic dysfunction was present in 27 (36%) of them. Results: The levels of N-BNP were not normally distributed (mean: 2,589 ± 4,514 pg/ml; median: 789 pg/ml). The distribution of CRP levels was also not normal (mean: 15 ± 27 mg/l; median: 5 mg/l). Both parameters correlated significantly (r: 0.41; p < 0.005). N-BNP was higher (p < 0.001) in patients with known ventricular dysfunction. Excluding these patients, the correlation between N-BNP and CRP was stronger (r: 0.88; p < 0.001). Univariate analysis in these patients without known cardiomyopathy showed that N-BNP levels also correlated with systolic and diastolic blood pressure (r: 0.54; p < 0.005) and inversely with creatinine clearance (r: –0.43; p < 0.01), serum albumin (r: 0.6; p < 0.001) and hemoglobin levels (r: 0.37; p < 0.05). CRP levels correlated significantly (p < 0.01) with the same parameters as N-BNP in univariate analysis. However, in multiple stepwise regression analysis in which CRP was the dependent variable, only the association with N-BNP remained significant (r: 0.87; p < 0.001). Conclusions: Our results suggest a link between left-ventricular filling pressure and inflammation in patients with advanced renal insufficiency. The importance of strict volume control in these patients, in order to reduce left-ventricular pressure and therefore inflammation, should be considered.
In the spinal animal, some sympathetic preganglionic neurones show background discharge and some can be reflexly excited or inhibited. Recent work has pointed out that while only a fraction of the total sympathetic outflow is involved, elements responsive to reflexes are present in each of many segments (Beacham & Perl, 1964a, b). The fact that only a limited number of the cells in each segment participate in a reflex could reflect differences either in the excitability of various preganglionic neurones or some other feature of organization. As a step toward further understanding of the role of the spinal cord in sympathetic mechanisms, the present study aims to establish effector organs controlled by preganglionic neurones active in the spinal preparation.Our attention was directed to the circulatory system because several investigators have described cardiovascular responses in spinal animals (Sherrington, 1906;Langley, 1924;Brooks, 1933;Alexander, 1945;Mukherjee, 1957). Difficulty in recording from sympathetic preganglionic and post-ganglionic cells simultaneously forced the use of an indirect approach. In most experiments the effects of nerve volleys or adequate stimuli known to initiate spinal preganglionic reflexes were tested on postganglionic neuronal activity, arterial pressure, blood flow or heart rate. Alternatively, preganglionic discharge and cardiovascular events were recorded in parallel. The results indicate that not all effector organs are influenced by sympathetic reflexes or autogenous activity in the spinal cat. In addition, cyclic or periodic changes in preganglionic discharge and in the systemic arterial pressure were noted which could be modified so as to suggest some form of sympathetic control of the circulation at the spinal level.
TAI is present in many type 1 diabetes patients at the time of diagnosis and is associated with a high prevalence of thyroid dysfunction. The clinical presentation of diabetes and the evolution of metabolic control and insulin-secretory reserves are not influenced by the presence of TAI. Patients with type 1 diabetes should be screened for TAI at diagnosis.
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