Stenting of transplant renal artery stenosis: outcome in a single center study.

AIM: Transplant renal artery stenosis (TRAS) is the most frequent vascular complication following transplantation and is a potential curable cause of resistant hypertension, allograft dysfunction, and graft loss. Percutaneous angioplasty (PTA) is the treatment of choice, but the incidence of restenosis may be as high as 35%. Alternative treatment option combines the angioplastic procedure with the placement of a stent. The aim of this study was to evaluate retrospectively the clinical outcome of 30 patients with TRAS or post-PTA recurrent TRAS between 1991 and 2006 treated by endoluminal stenting. Primary outcomes of this study were survival rate, percentage of restenosis and lost of the graft. Secondary outcomes were: reduction of blood pressure, creatinine levels and number of antihypertensive medications. METHODS: From May 1991 to May 2006 a retrospective review of stent placement procedures for TRAS was performed. Reviewed parameters included: technical success, arterial blood pressure and number of antihypertension medications, serum creatinine level before and after intervention. Thirty-two interventions in 30 allografts were carried out. Allograft survival rate was estimated using the Kaplan-Meier RESULTS: The technical success rate of stenting was 100% with a single major complication event (a puncture site pseudoaneurysm). Mean follow-up time was 7.1 years; of the 30 allograft that underwent stent placement, all were patent at the last follow-up, with five restenosis (15.6%) of which only one needed to be retreated endoluminally. A reduction of the mean serum creatinine levels and of the number of blood pressure medications was observed. There was no difference in the survival curve of the grafts without TRAS compared to those with stenting treated TRAS. CONCLUSION: The treatment of the TRAS with selective or primary stenting is safe with a long-term patency rate. The efficacy of the stenting in this retrospective study is suggested by a decrease in mean systolic and diastolic blood pressure, serum creatinine levels and number of blood pressure medications.

Should we consider gestational diabetes a vascular risk factor?

Few and contrasting data have reported vascular endothelial dysfunction and increased serum levels of endothelial dysfunction and inflammatory markers in women with previous gestational diabetes mellitus (pGDM). We aimed at evaluating 6.5 years after delivery: intimal medial thickness (IMT), and C-reactive protein (CRP), interleukin-6 (IL-6), E-selectin, intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1) levels in 82 non-pregnant pGDM and 113 control women without pGDM. A subgroup of 21 women, taken from the pGDM group, showing current normal BMI, and no metabolic abnormalities, was separately analysed. All the subjects were free of medication and non-smokers. Women with pGDM, independently by their current BMI and presence of metabolic abnormalities, showed significantly higher E-selectin, ICAM-1 and IMT values than controls. IMT proved to be significantly associated with pGDM in a regression model, after adjustments for BMI, waist circumference, blood pressure, and glucose values (beta=0.046; 95% CI 0.028-0.064). In all pGDM women, E-selectin, ICAM-1, IL-6 and hs-CRP values were significantly associated with IMT in the same model. Post-GDM women, despite being currently free from metabolic abnormalities, showed higher values of markers of endothelial dysfunction and IMT than controls, consistent with an increased future cardiovascular risk.

Worsening of hypertension in a pregnant woman with renal arteriovenous malformation: a successful superselective embolization after delivery.

A 30-year-old female presented with uncontrolled hypertension due to arteriovenous malformation in the upper third of the right kidney, which worsened during pregnancy. The arteriovenous malformation was detected by color-coded Doppler sonography, confirmed by angiography, and the fistula was sealed by superselective arterial embolization with metallic coils. Superselective embolization is the most effective and safe treatment for this rare and complex pathology.

Duplex scan sonography of renal artery stenosis.

Renal artery stenosis is the most common cause of potentially remediable secondary hypertension. The most common causes include atherosclerosis and fibromuscular dysplasia. Particularly the atherosclerotic form is a progressive disease that may lead to gradual and silent loss of renal functional tissue. Thus, early diagnosis of renal artery stenosis is an important clinical objective since interventional therapy may improve or cure hypertension and preserve renal function. Screening for renal artery stenosis is indicated in the suspicion of renovascular hypertension or ischemic nephropathy in order to identify patients in which an endoluminal or a surgical revascularization is advisable. In the recent years many noninvasive tests have been proposed and evaluated in the clinical practice, in alternative to arteriography. These include nuclear scan, color Doppler sonography, CT angiography and MR angiography. Sonography is usually the first diagnostic modality for the non invasive evaluation of renal vascular disease with 95% sensitivity and 90% specificity when performed in dedicated laboratories. Despite sonography is highly affected by operator dependence, and it takes a lot of time to train good operators, actually is the best screening test because it is not expensive, non invasive and accurate. When a discrepancy exists between the clinical data and the results of US, other tests are mandatory.

G1/S transition in normal human T-lymphocytes requires the nuclear protein encoded by c-myb.

Exposure of peripheral blood mononuclear cells (PBMC) to an 18-base c-myb antisense oligomer before mitogen or antigen stimulation resulted in almost complete inhibition of c-myb messenger RNA and protein synthesis and blockade of T lymphocyte proliferation. Expression of early and late activation markers, interleukin-2 receptor and transferrin receptor, respectively, by PBMC was unaffected by antisense oligomer exposure as was the expression of c-myc messenger RNA. In contrast, histone H3 messenger RNA levels and DNA content were selectively decreased. These results suggest that c-myb protein deprivation does not perturb T lymphocyte activation or early molecular events that may prepare the cell for subsequent proliferation. Rather, it appears to specifically block cells in late G1 or early S phase of the cell cycle.

Identification of serum-responsive elements in the promoter of human calcyclin, a growth-regulated gene.

The calcyclin gene is growth regulated in a number of cell types from different animal species. We have identified in the promoter region of the human calcyclin gene the sequences responsible for its growth regulation by serum. A number of deletion mutants and synthetic nucleotides, all driving the chloroamphenicol transferase (CAT) gene, were constructed for this purpose. Serum-responsive elements can be localized in the last 42 bp immediately upstream from the CAP site.

Regulation of c-myc mRNA levels by insulin or platelet-poor plasma.

Cell lines have been permanently established from BALB/c3T3 cells that constitutively express either the murine p53, the human IGF-1 gene, or both (Gai et al., 1988). The derivative cell lines grow well in platelet-poor plasma or in serum-free medium supplemented with the appropriate growth factors, while BALB/c3T3 cells do not grow in platelet-poor plasma, nor do they grow in serum-free medium unless supplemented with both platelet-derived growth factor and insulin (or IGF-1). In BALB/c3T3 cells, steady-state levels of c-myc mRNA decrease promptly and sharply once the cells are transferred to platelet-poor plasma. In the derivative cell lines, constitutively expressing p53, IGF-1, or both, c-myc mRNA levels remain elevated and actually increase when the cells are transferred to platelet-poor plasma. In serum-free medium, the c-myc mRNA levels decreased in BALB/c3T3 cells, as well as in the derivative cell lines. However, in the latter cell lines, but not in BALB/c3T3, the addition of platelet-poor plasma or insulin again increased the expression of c-myc. The increase in c-myc mRNA levels could be partially explained by an increase in transcription. These results indicate that in certain cell lines the expression of c-myc mRNA can be induced by insulin or platelet-poor plasma.