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Brachial artery transposition (BAT) is not a well known method for obtaining vascular access (VA) for maintenance haemodialysis. This study evaluated the outcomes of BAT. This multicentre retrospective cohort study included 233 consecutive patients who underwent BAT between January 2012 and December 2013. The indications were inadequate vessels for obtaining VA, severe heart failure, hand ischaemia, central vein stenosis/occlusion, or a history of catheter/graft infection. The transposed brachial artery was used only for arterial inflow and other routes were used for outflow. BAT was successful in 227 patients, and adequate blood flow was achieved during dialysis sessions. The first successful cannulation was after a median of 18 days. BAT was performed using superficial veins as the return route in 127 patients and arteriovenous fistula (AVF) creation in 63 patients to prevent maturation failure. In 41 patients with central venous catheterisation, the transposed brachial artery was used for arterial inflow. The complications of BAT were impaired wound healing in 14 patients, including skin necrosis in two; large aneurysms in six, including a mycotic pseudo-aneurysm in one; arterial thrombosis in five; hand ischaemia in five; lymphorrhoea in four; and haematoma/bleeding in three. The transposed brachial artery was abandoned in four, three, three, and one case of arterial thrombosis/stenosis, haematoma/bleeding, skin necrosis, and large aneurysm, respectively. Access to the return routes failed in 48 cases because of vein damage caused by cannulation in 22, AVF thrombosis/stenosis in 14, catheter infection in six, and catheter occlusion in six. At two years, the primary patency rates of the transposed brachial artery and access circuit were 88% and 54%, respectively. BAT is a safe and effective technique. The patency was high for the transposed brachial artery but adequate for the access circuit. BAT can be considered for patients with an unobtainable standard arteriovenous access. [ABSTRACT FROM AUTHOR]

Atrial natriuretic polypeptide (ANP) is a hormone secreted by the atrial tissue of the heart as a result of an increase in blood pressure. This hormone regulates blood pressure, blood volume, and cardiac output, or the amount of blood pumped by the ventricles per minute. ANP also stimulates the elimination of salt in the urine, and these actions contribute to a reduction in the workload on the heart. The expression and distribution of ANP in the ventricles was assessed in tissue obtained at autopsies of 27 children with Kawasaki disease, an acute fever-associated illness. This disease affects children under five years of age and may be associated with the development of aneurysms in the coronary arteries, which supply the heart. Patients with Kawasaki disease often die of myocarditis, or inflammation of the heart muscle; coronary thrombosis, the formation of blood clots; rupture of coronary aneurysms; or coronary heart disease. In this study, 14 children died in the acute stage of the disease, including 3 of myocarditis and 11 of coronary heart disease. Evidence of a heart attack was detected in three of the children who died of coronary heart disease. Seven of the 14 children with acute-stage deaths developed heart failure 2 to 22 days before death. The remaining 13 children developed coronary artery aneurysms and died during the recovery period. Three children with granulations, or granular tissue, and congestive heart failure had detectable amounts of ANP in the heart cells surrounding the granulations. These three patients died within eight days after a heart attack. ANP was detected near sites of fiber-like tissue formation in 10 patients with a previous heart attack, including four with a history of congestive heart failure. These findings suggest that ANP was secreted into the ventricle more than a week after a heart attack in children with Kawasaki disease who died during recovery. In addition, a history of congestive heart failure was associated with an increase in the expression of ANP in patients with Kawasaki disease and a previous heart attack. (Consumer Summary produced by Reliance Medical Information, Inc.)

Atrial natriuretic peptide (ANP) is a protein hormone released by the atria of the heart in response to an increase in blood pressure. ANP affects blood pressure and volume and cardiac output, the amount of blood emptied from the ventricle per minute, and increases the elimination of salt from the body; these actions serve to decrease the workload on the heart. Although ANP is normally produced, stored and released from the atria, the upper receiving chambers of the heart, studies have shown that it is also present in the enlarged or failing ventricle, a pumping chamber. ANP levels were shown to be increased in the blood and ventricular tissues of patients with myocardial infarction, the deterioration of heart tissue due to cessation of blood supply. An antibody, or protein factor, that specifically binds to human ANP was used to detect ANP in the ventricles of five patients with myocardial infarction and five normal subjects. ANP was present in the ventricular tissue of patients with myocardial infarction. When infarction had affected both ventricles, ANP was detected in both ventricles. In a case of ventricular aneurysm, in which a portion of the ventricle wall is abnormally dilated, ANP was found in the affected area. The hormone was not observed in the ventricles of normal subjects. The presence of ANP in the ventricle in disease conditions such as myocardial infarction may serve as one of the body's compensatory mechanisms, or methods for coping with decreased heart function under abnormal conditions. (Consumer Summary produced by Reliance Medical Information, Inc.)

Investigates the role of adrenomedullin (AM) in cultured endothelial and mesangial cells. Description about AM; Secretion of AM by endothelial cells (EC); Modulation of EC and mesangial cells.

Immunosuppressants and inhibitors of the renin angiotensin system are major reagents to treat nephrotic syndrome but their clinical effects are not necessarily satisfactory. Injection of doxorubicin in several strains of mice causes nephrotic syndrome-like disorder. Zhou et al. report that PPAR-α expression is downregulated in murine doxorubicin nephropathy and a PPAR-α agonist, fenofibrate, partially ameliorates the disorder induced likely through stabilization of nephrin expression and suppression of apoptosis in podocytes, providing a new preventive strategy. [ABSTRACT FROM AUTHOR]

Urinary neutrophil gelatinase-associated lipocalin (Ngal or lipocalin 2) is a very early and sensitive biomarker of kidney injury. Here we determined the origin and time course of Ngal appearance in several experimental and clinically relevant renal diseases. Urinary Ngal levels were found to be markedly increased in lipoatrophic- and streptozotocin-induced mouse models of diabetic nephropathy. In the latter mice, the angiotensin receptor blocker candesartan dramatically decreased urinary Ngal excretion. The reabsorption of Ngal by the proximal tubule was severely reduced in streptozotocin-induced diabetic mice, but upregulation of its mRNA and protein in the kidney was negligible, compared to those of control mice, suggesting that increased urinary Ngal was mainly due to impaired renal reabsorption. In the mouse model of unilateral ureteral obstruction, Ngal protein synthesis was dramatically increased in the dilated thick ascending limb of Henle and N was found in the urine present in the swollen pelvis of the ligated kidney. Five patients with nephrotic syndrome or interstitial nephritis had markedly elevated urinary Ngal levels at presentation, but these decreased in response to treatment. Our study shows that the urinary Ngal level may be useful for monitoring the status and treatment of diverse renal diseases reflecting defects in glomerular filtration barrier, proximal tubule reabsorption, and distal nephrons.Kidney International (2009) 75, 285–294. doi:10.1038/ki.2008.499 [ABSTRACT FROM AUTHOR]

Long-term peritoneal dialysis induces peritoneal fibrosis with submesothelial fibrotic tissue. Although angiogenesis and inflammatory mediators are involved in peritoneal fibrosis, precise molecular mechanisms are undefined. To study this, we used microarray analysis and compared gene expression profiles of the peritoneum in control and chlorhexidine gluconate (CG)-induced peritoneal fibrosis mice. One of the 43 highly upregulated genes was pleiotrophin, a midkine family member, the expression of which was also upregulated by the solution used to treat mice by peritoneal dialysis. This growth factor was found in fibroblasts and mesothelial cells within the underlying submesothelial compact zones of mice, and in human peritoneal biopsy samples and peritoneal dialysate effluent. Recombinant pleiotrophin stimulated mitogenesis and migration of mouse mesothelial cells in culture. We found that in wild-type mice, CG treatment increased peritoneal permeability (measured by equilibration), increased mRNA expression of TGF-β1, connective tissue growth factor and fibronectin, TNF-α and IL-1β expression, and resulted in infiltration of CD3-positive T cells, and caused a high number of Ki-67-positive proliferating cells. All of these parameters were decreased in peritoneal tissues of CG-treated pleiotrophin-knockout mice. Thus, an upregulation of pleiotrophin appears to play a role in fibrosis and inflammation during peritoneal injury. [ABSTRACT FROM AUTHOR]

Background: High glucose reportedly stimulates prostaglandin (PG) E2 production and DNA synthesis in mesangial cells (MCs). However, the pathophysiological significance of PGE2 in MCs has remained unclear.Methods: The effects of prostanoids on [3H]-thymidine uptake and cAMP production in rat MCs cultured with 5.6 mM glucose, 25 mM glucose, or 5.6 mM glucose supplemented with 19.4 mM mannitol were examined. The gene expression of PGE2 receptor (EP) subtypes in MCs was analyzed with Northern blotting techniques.Results: Northern blotting indicated EP1 and EP4 gene expression in MCs. EP1 agonists and PGE2 stimulated [3H]-thymidine uptake in MCs. EP1 antagonists dose dependently attenuated high-glucose-induced [3H]-thymidine uptake, which suggests EP1 involvement, by an increase in intracellular Ca2+, in DNA synthesis of MCs. On the other hand, forskolin, db-cAMP, and 11-deoxy-PGE1, an EP4/EP3/EP2 agonist, significantly decreased DNA synthesis in MCs. These inhibitory effects are thought to be mediated via EP4 as a result of an increase in cAMP synthesis. The effects via EP4 seem to be particularly important because PGE2-induced cAMP synthesis was significantly attenuated in the high-glucose group compared with the mannitol group, in which [3H]-thymidine uptake did not increase in spite of augmented PGE2 production.Conclusion: The increase in DNA synthesis in MCs under high-glucose conditions can be explained, at least in part, by the high-glucose-induced inhibition of cAMP production via EP4, which augments EP1 function in conjunction with the overproduction of PGE2. [ABSTRACT FROM AUTHOR]