M Migliori

C-Reactive Protein and Interleukin-6 Levels Are Related to Renal Function in Predialytic Chronic Renal Failure

Background: Several studies have provided convincing evidence that in apparently healthy subjects elevated serum levels of plasma C-reactive protein (CRP) are associated with an increased risk of experiencing myocardial infarction and sudden cardiac death. It has been claimed that, in dialytic patients, the hepatic synthesis of this ‘acute phase response’ plasma protein is primarily induced by the macrophage-derived interleukin 6 (IL-6). Little information is available, however, regarding CRP and IL-6 plasma levels in pre-dialytic renal failure. Methods: Plasma CRP by a modification of the laser nephelometry technique, IL-6 and serum albumin were determined in 103 chronic pre-dialytic patients (mean age 50 ± 6.3 years; creatinine clearance (Cr.cl.) 36.3 ± 23.1 ml/min). Results: CRP was >5 mg/l (normal upper range) in 42% of the global population. CRP and IL-6 were significantly related (r = 0.35, p < 0.0004). CRP and IL-6 were related to renal function (CRP vs. Cr.cl., r = –0.56, p < 0.0001; IL-6 vs. Cr.cl., r = –0.55, p < 0.0001, Spearman correlation coefficient). When patients were divided in tertiles according to renal function, CRP median value resulted 7.9 mg/l (interquartile interval: 5–12) in the first tertile (Cr.cl. <18.5 ml/min), 4.0 mg/l (3–6) in the second tertile (Cr.cl. 18.5–45 ml/min) and 3.2 mg/l (2.7–4.0) in the last tertile (Cr.cl. >45 ml/min) (p < 0.0001). A negative correlation between CRP and S-albumin was also found (r = –0.52, p < 0.0001, Spearman correlation coefficient). Conclusions: IL-6 and CRP were increased and were inversely related to creatinine clearance in our population of 103 chronic predialytic patients. The possibility of a decreased renal clearance of CRP and/or cytokines as a cause of an activated acute-phase response is discussed. A negative correlation between CRP and S-albumin was found confirming the link between chronic inflammation and malnutrition in chronic renal patients.

Sucralfate modulates uPAR and EGFR expression in an experimental rat model of cervicitis.

Sucralfate is a drug used in the treatment of gastric and duodenal ulcer; it is cytoprotective and able to increase the bioavailability of several growth factors, modulating the wound healing process. In this study we tested the possible therapeutic effect of Sucralfate in the treatment of ulcerative lesion occurring in uterine cervix; to investigate such effect we used an experimental rat model of cervicitis in which the uPAR and EGFR expression were evaluated. Cervicitis was induced in wild and ovariectomized wistar female rats by an acetic acid-soaked tampon. The animals were divided into two main groups (4 and 7 days) and Sucralfate was administered topically until the day they were sacrificed. In order to distinguish physiological and drug-induced healing, quantitative and qualitative uPAR and EGFR expression were evaluated by using Western Blot and Immunohistochemistry techniques. Western Blot analysis demonstrated an increased expression of both receptors after 4 days from wounding in wild and ovariectomized animals. In particular in ovariectomized animals the expression of uPAR and EGFR increased after 4 days while it reduced following the administration of Sucralfate. In wild rats the same was observed for uPAR expression, while EGFR was different; in fact, its expression increased significantly at day 4 in the animals treated with the drug and only at day 7 in those untreated. Immunohistochemistry highlighted a noteworthy epithelial colocalization of EGFR and uPAR after 4 days in the animals treated with Sucralfate. We conclude that Sucralfate can promote the healing of ulcerative cervicitis and moreover, it reduces the normal healing time because of its modulatory property on uPAR and EGFR expression.

Steno-Thrombosis of Vascular access for Hemodialysis: The Surgical Point of View

From the beginning of the hemodialytic era, it was evident that maintaining an adequate vascular access (VA) plays a pivotal role in the final performance of dialytic treatment. As reviewed by Feldman et al (1), complications associated with hemodialysis (HD) VA represent one of the most important causes of morbidity and mortality among end-stage renal disease (ESRD) patients in the US today. VA-related failures represent 20-30% of all hospitalizations in these patients, and the costs exceed

L'emofiltrazione Come Test Diagnostico Dell'iperparatiroidismo Secondario

1 billion per year. The situation is probably slightly better in Europe due to the higher rates of VA performed with native vessels instead of synthetic grafts, as demonstrated by the DOPPS Study (2). The most important cause of VA failure is represented by thrombosis (80-85%) (3, 4). Clinically, VA thrombosis can be classified as early, sudden-unexpected and delayed. Early thrombosis occurs during the first week after VA construction: it can be due to technical errors, perioperative complications or anatomic characteristics of the vessels, prolonged vascular spasms and hypercoagulability. In this situation VA can be recovered only by surgery. The sudden-unexpected thrombosis occurs in a perfectly working VA without any signs of alarm, and it is caused by excessive dialytic dehydration, by extrinsic compression such as perivasal hematoma or vigorous compression of the puncture site after the dialysis sessions, by ineffective dialytic anticoagulation and by an uncorrected arm position during sleep. Coadjutant factors are represented by reduced cardiac output, low albumin level, diabetes, anticardiolipin antibodies, and high hematocrit levels due to erythropoietin supplementation. The sudden-unexpected thrombosis can be treated by both surgery and by interventional radiology. Delayed VA thrombosis generally occurs over 3 months from VA construction and it is the more important factor affecting VA survival. The more important coadjutant factor is represented by venous stenosis (>80% of VA thrombosis). VA stenosis and thrombosis are strictly related and they can be treated simultaneously. Two different medical approaches are possible: waiting for the development of the thrombosis or acting directly on the stenosis when detected during the VA follow-up. In both it is an important multidisciplinary approach, involving nephrologists, the vascular surgeon and the interventional radiologist. In our opinion, better results are obtained with vascular surgery: Maya and Allon (5) evaluated whether graft patency following thrombectomy is improved by the placement of a stent in the stenotic lesion. Primary and secondary graft patency rates were, respectively, 27 and 46 days after angioplasty, leading to 85 and 1215 days if a stent was placed at the venous anastomosis. Other studies have reported a primary and secondary patency rate at 1 yr of 20-30% and 40-45%, respectively, after interventional radiology (6). Better results were obtained by Turmel-Rodrigues et al (7) both in upper limb native fistulae and in prosthetic grafts, with primary and secondary patency rates at 1 yr of 50% and 80%, respectively. Interventional radiology was also significantly associated with restenosis (adjusted relative risk being 2.77-fold higher, p=0.009) than surgery (8). Instead, cumulative patency 1, 2 and 3 yrs after elective surgery was 75-87%, 60-79% and 46-74% (9, 10), and a meta-analysis of Green et al has found that the use of endovascular techniques is in-

Interleukin-6 is a stronger predictor of total and cardiovascular mortality than C-reactive protein in haemodialysis patients

II ca lc io tot al e e ioni zat o so no s ta ti det erminati con un calcio ionometro (Nova 7 Pabi sh ); in 40 contro ll i normali la media ± 2 deviazioni stand ard nel no str o laboratorio per il calcio ione e risultata 1.26 ± 0 .05 mmol/L. II PTH i e sta to determinato con un m e(PTHi ). procollageno I e III. osteocalcina (GLA) e 1-25 vitamina D. Dopo un ora ed a l termi ne della dialisi sono sta te determ inate nellultrafi ltrato Ie co ncentrazioni di calcio ionizzato e PTH i; il calcio ionizzato e stato ino ltre dosato nel liquido di reinfusione. 42