[Superior vena cava syndrome unrelated to central venous catheter in a patient on chronic hemodialysis]. / Sindrome cavale superiore in un paziente in dialisi cronica: non e' sempre colpa del catetere venoso centrale!

A 67-year-old woman with end-stage renal disease (polycystic kidney disease) who had been on dialysis for 10 years came to our department for a second opinion about upper left arm edema homolateral to the arteriovenous fistula (AVF). Because of the suspicion of venous stenosis she had already been submitted to angiographic examination of the AVF which, however, did not show any occlusive process. In addition to the kidney problem, the clinical history included dilated cardiomyopathy, and 2 years earlier a biventricular implantable cardioverter defibrillator (ICD) had been placed. The patient had never had a central venous catheter (CVC). She presented a typical superior vena cava syndrome picture with arm, neck and hemifacial edema and superficial cutaneous venous reticulum. The venous pressure during extracoroporeal circulation was high and blood recirculation was documented. Angio-CT was performed to look for a compressive process in the chest, but this was excluded. We then performed a new trans-AVF angiography to study extensively the axillary-subclavian-superior vena cava district. At first, no stenosis or thrombosis was observed, but the presence of ICD and its leads (left-sided implanted) in the anonymous vein created obstacles to diagnosis. Repeated injections of contrast medium and focusing imaging on the leads route allowed us to highlight a venous stenosis in the anonymous vein. Transluminal angioplasty was successfully carried out during the same procedure. 1) In hemodialysis patients the appearance of signs of intrathoracic vein drainage obstacles is not always associated with previous CVC implantation; 2) in the hemodialysis patient, any device (PM, ICD) should be implanted contralaterally to the fistula arm in order to avoid the risk that a venous stenosis may cause AVF dysfunction.

Determinants of thromboxane biosynthesis in patients with moderate to severe chronic kidney disease.

BACKGROUND: Mechanisms of accelerated atherothrombosis in patients with chronic kidney disease (CKD) are only partly characterized. The aims of this study were to evaluate the extent of thromboxane (TX)-dependent platelet activation in patients with CKD, and to characterize the determinants of altered TX biosynthesis in this setting, with particular reference to enhanced lipid peroxidation, low grade inflammation and CKD-related anemia. PATIENTS AND METHODS: A cross sectional comparison between urinary 8-iso-PGF2α and 11-dehydro-TXB2, in vivo markers of oxidative stress and platelet activation, respectively, was performed in 115 patients with stage 1-4 CKD. RESULTS: Levels of both urinary 11-dehydro-TXB2 and 8-iso-PGF2α increased sequentially across the four CKD stages (P<0.0001, Kruskal-Wallis test). Both urinary prostanoids were inversely associated with either estimated glomerular filtration rate (eGFR, P<0.0001) or hemoglobin levels (P<0.0001). A significant direct correlation was also observed between urinary 11-dehydro-TXB2 and 8-iso-PGF2α (Rho=0.620, P<0.0001). On multivariate analysis, urinary 8-iso-PGF2α (ß=0.459, P<0.0001), hemoglobin levels (ß=- 0.261, P=0.002) and eGFR (ß=-0.172, P=0.032) were independent predictors of urinary 11-dehydro-TXB2 (adjusted R(2)=0.488). CONCLUSIONS: This study provides biochemical evidence of persistent platelet activation in patients with CKD. This condition occurs early in the natural history of the disease and is related to kidney function and oxidative stress. Moreover, we found an independent inverse relationship between hemoglobin levels and TX-dependent platelet activation. This finding may provide a mechanistic link between CKD-related anemia and increased cardiovascular risk.

Effects of a pulsatile electrostatic field on ischemic injury to the diabetic foot: evaluation of refractory ulcers.

AIMS: The macro- and microcirculation disease, in patients with type 2 diabetes mellitus (T2DM), induces ischemic wounds of the lower limbs. We have tried to reduce the aggregation of red blood cells and to improve the O2 supply to the tissues and speed the healing of ulcers in T2DM patients. METHODS: We enrolled 25 obese subjects without glucose intolerance (group A; BMI greater than 30 kg/m2), 20 obese adults intolerant to glucose (group B) and two subgroups, groups C and D, with T2DM and with leg ulcers. The groups A, B and C were treated with PESF. Body weight, O2 extraction, the capillary pulse, blood pressure and the surface of the ulcers were monitored. RESULTS: The technique PESF shows to have positive effects on the metabolism, on the reduction of body weight in the groups A and B, increasing extraction of O2 in group C and increase the speed of healing of wounds in group C compared to group D. In group A, there was a significant reduction in systolic and diastolic blood pressure. CONCLUSIONS: The technique PESF has affected the metabolic processes and the speed of wound healing ulcer in patients with T2DM.

Lamin B-receptor mutations in Pelger-Huët anomaly.

Pelger-Huët anomaly is an inherited abnormality of neutrophils, characterized by reduced nuclear segmentation and an apparently looser chromatin structure. Following linkage studies in two families, the lamin B-receptor (LBR) was sequenced and mutations found: CCG-->CTG causing proline-->leucine in codon 119 of exon 3, and IVS11-9 A-->G, disrupting the splice acceptor site. The LBR gene (LBR) was also sequenced from a single English man with Pelger-Huët anomaly and a heterozygous C-->G mutation was found in codon 569 of exon 14, predicted to cause a proline-->arginine. Our results confirm recently published findings that LBR mutations cause Pelger-Huët.