Browsing by Author "Queirós, J."
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- Are we building too many arteriovenous fistulas? A single-center experiencePublication . Leal-Moreira, C.; Teixeira, V.; Bessa, L.; Queirós, J.; Silva, F.; Cabrita, A.Introduction: Arteriovenous fistula has been associated with improved morbimortality in hemodialysis patients. This has resulted in the “fistula First, catheter last” initiative. Nonetheless, the survival benefit of arteriovenous fistula has been questioned. Methods: We conducted a retrospective observational study of all patients with non-end stage renal disease referred for first vascular access building between January 2014 and December 2015 in our hospital center. Our main goal was to evaluate the clinical impact and burden of building fistula in predialysis patients. Results: During this period, of 178 first arteriovenous accesses placed, 87 patients remained in predialysis and 91 patients started a chronic hemodialysis program. Median follow-up time by a nephrologist was 3.9 (2.5, 9.7) years. The mean age was 65.8±14.7 years, with 50.6% (n=90) of male patients. A higher rate of thrombosis in the predialysis group (26% vs 13%, p=0.037) was observed, but vascular access survival did not differ significantly (55% vs 67%, p=0.12). Mean vascular access placing was higher in the predialysis group (1.4±0.7 vs 1.2±0.4, p=0.006) and less interventions were requested (0.2±0.5 vs 0.3±0.6, p=0.10). Median time from vascular access placement to hemodialysis start was 22 (13, 41) months. At hemodialysis initiation, 10 (10.9%) patients used a central venous catheter; 80 (87.9%) patients an arteriovenous fistula, and one patient a graft. A total of 227 vascular accesses were built; 121 (53.3%) in predialysis vs 106 (46.7%) in incident hemodialysis patients. In a multivariate model, the presence of a functional arteriovenous fistula at hemodialysis start was only associated with a trend to survival benefit (HR 0.38, 95% CI 0.14-1.00, p=0.05). Conclusions: Our results stress the need for an individual approach and for future tools to assess the risk of death and progression to end-stage renal disease, therefore helping reduce the number of unutilized vascular accesses and rising cost of interventions.
- Arterio-arterial graft – an option for hemodialysis patients with exhaustion of venous patrimonyPublication . Castro, A.; Almeida, P.; Silva, F.; Rego, D.; Tavares, J.; Santos, J.; Silva, F.; Queirós, J.; Cabrita, A.; Almeida, R.Introduction: Vascular access (VA) for hemodialysis (HD) is the lifeline for End Stage Renal Disease (ESRD) patients. Long-term HD patients often have exhaustion of their venous patrimony for an autologous VA construction and, sometimes, even for a central venous catheter (CVC) placement. Case report: We describe the case of a 43-year-old woman with ESRD due to lupus nephritis, on maintenance HD since 2009. She also had secondary antiphospholipid syndrome and was chronically anticoagulated. Nevertheless, the patient had multiorgan thrombotic events (without sequelae) and several episodes of irreversible thrombosis of arteriovenous fistulas. Her HD course was also marked by multiple severe CVC infections, at diferente locations; a hemoperitoneum during cholecystectomy, and an immediate thrombosis of the renal artery of a kidney transplant. She was admitted to our hospital after an irreversible dysfunction of a right jugular CVC, with documentation of thrombosis of the superior and inferior vena cava. Exhaustion of the venous patrimony for HD was assumed and it was decided to make an arterio-arterial graft (AAG) of early cannulation. The first cannulation of the AAG was performed two days after surgical intervention, with no complications. The patient performed a twelve hour per week HD treatment with good efficiency. Conclusion: AAG is an alternative for HD patients who have exhausted all their venous patrimony and it can be considered prior to the placement of a CVC as their sole remaining vascular access.
- Atypical Cogan’s SyndromePublication . Queirós, J.; Maia, S.; Seca, M.; Friande, A.; Araújo, M.; Meireles, A.Background. Cogan's syndrome is a rare clinical entity whose etiopathology is still unknown, and the treatment strategies are not clearly defined. Case. A 23-year-old male presented with symptoms of headache, peripheral facial palsy, persistent right hearing loss and bilateral papillitis. Workup excluded all infectious, granulomatous, neoplastic, and immune causes. The diagnosis of atypical Cogan's syndrome was established, and the patient was treated with systemic corticosteroids and later on with cyclophosphamide and methotrexate. There were improvement of visual symptoms and stabilisation of left hearing. Conclusion. Cogan's syndrome is a very rare disease with no specific biological tests for the diagnosis. The diagnostic exams are mostly important to exclude other etiologies. The atypical ocular and audiovestibular manifestations make the diagnosis difficult, delaying the institution of appropriate therapy which may result in profound bilateral deafness.
- Impact of Homocysteinemia on Long-Term Renal Transplant SurvivalPublication . Fonseca, Isabel; Martins, La Salete; Queirós, J.; Mendonça, D.; Dias, L.; Sarmento, A.M.; Henriques, A.C.; Cabrita, A.Impact of Homocysteinemia on Long-Term Renal Transplant Survival I. Fonseca, L. Martins, J. Queirós, D. Mendonça, L. Dias, A.M. Sarmento, A.C. Henriques, and A. Cabrita ABSTRACT Aim. We prospectively followed cohort of 202 renal transplant recipients for years to examine the impact of fasting homocysteinemia on long-term patient and renal allograft survival. Methods. Cox proportional hazards regression analysis was used to identify independent predictors of all-cause mortality and graft loss. Results. Hyperhomocysteinemia (tHcy 15 mol/L) was present in 48.7% of the 202 patients, predominantly among men (55.8%as opposed to women (37.1%)At the end of the follow-up period, 13 (6.4%patients had died including 10 from cardiovascular disease, and 23 had (11.4%had lost their grafts. Patient death with functioning allograft was the most prevalent cause of graft loss (13 recipients)Levels of tHcy were higher among patients who died than among survivors (median 23.9 vs 14.3 mol/L; .005)Median tHcy concentration was also higher among the patients who had lost their allografts than those who did not (median 19.0 vs 14.1 mol/L; .001)In Cox regression model including gender, serum creatinine concentration, transplant duration, traditional cardio- vascular risk factors, and associated conditions, such as past cardiovascular disease, only tHcy concentration (ln) (HR 5.50; 95% CI, 1.56 to 19.36; .008) and age at transplantation (HR 1.07; 95% CI, 1.02 to 1.13; .01) were independent predictors of patient survival. After censoring data for patient death, tHcy concentration was not risk factor for graft loss. Conclusions. This prospective study shows that tHcy concentration is significant predictor of mortality, but not of graft loss, after censoring data for patient death.
- Renal Allograft Rupture: A Clinicopathologic ReviewPublication . Ramos, M.; Martins, L.; Dias, L.; Henriques, A.C.; Soares, J.; Queirós, J.; Sarmento, A.M.Transplantation Proceedings Volume 32, Issue 8, December 2000, Pages 2597-2598 -------------------------------------------------------------------------------- doi:10.1016/S0041-1345(00)01801-7 | How to Cite or Link Using DOI Copyright © 2000 Elsevier Science Inc. All rights reserved. Cited By in Scopus (4) Permissions & Reprints Renal allograft rupture: a clinicopathologic review M Ramosa, , L Martinsa, L Diasa, A.C Henriquesa, J Soaresa, J Queirósa and A.M Sarmentoa aDepartments of Urology and Nefrology, Hospital Geral de Santo António, Oporto, Portugal Available online 19 December 2000. Article Outline Patients and methods Results Discussion References Renal allograft rupture (RAR) is a rare but very serious complication of renal transplantation, requiring emergency surgery. The most common cause is acute allograft rejection, but other causes such as renal vein thrombosis (RVT), acute tubular necrosis (ATN), renal biopsy, and lymphatic obstruction have been reported.[1] and [2] We reviewed our experience with the aim of identifying RAR predisposing conditions. Patients and methods In a consecutive series of 934 renal transplants performed between July 1983 and September 1999, 11 patients (1.2%) had RAR. In these cases we studied donor and recipient characteristics, preservation conditions, clinical signs and symptoms, treatment, and pathology findings. This group of patients was then compared with their paired cohort. Data analysis was computer-based. In the statistical analysis t test and Fisher’s exact test were used. Results All 11 kidneys that suffered RAR were from cadaver donors, nine male and two female. The mean age was 29.5 years with good terminal serum creatinine (mean 1.1 mg/dL). All organs were stored in Eurocollins solution and the mean cold ischemia time was 21 hours and 25 minutes (range, 10 hours to 29 hours and 20 minutes). Excluding one black patient, all recipients were Caucasian. Eight were female and 3 were male, with a mean age of 33.8 years. The mean HLA match was 1.7, and the mean peak panel reactive antibody (PRA) was 22% (range 0 to 93%) and current was 15% (range 0 to 67%). All patients had cyclosporine treatment, eight had delayed graft function requiring dialysis, and three underwent renal allograft biopsy. In two patients rupture occurred in the second allograft; the others were first transplants. The day of RAR was a mean of 5.3 (range 2 to 13). All patients had new onset of severe allograft pain, eight had a drop in daily hematocrit, and six had hypotension. The four patients with more precocious ruptures had sudden onset of bleeding through the drainage tube. Transplant nephrectomy was performed in 10 patients, and surgical conservative treatment with fibrin glue and collagen foam was performed in one. All patients survived RAR. Three had a second transplant and currently have functioning allografts. Pathology examination revealed RVT in three patients and some degree of rejection in the remaining eight. One patient had a rupture on the second day because of hyperacute rejection, and three had severe acute cellular rejection, but in four patients the dominant figure was ATN with minimal rejection. Excluding the patient with hyperacute rejection, the day of rupture was later for those with severe acute rejection, a mean of 9.6 days (range 6 to 13). In those with ATN, the day of RAR was a mean of 4.5 (range 3 to 6) and the patients with RVT had ruptures even sooner, on mean third day (range 2 to 4). Variables associated with RAR were: sex mismatch (P = .004), current PRA (P = .012), and a need for dialysis (P = .042). Age of the recipient, transplant number, cold ischemia time, total HLA match, and peak PRA were not associated with RAR. Discussion Higher current PRA and a need for dialysis are variables associated with rejection and ATN. Therefore they are expected to be related to rupture. The well-documented conditions that are associated with ATN and rejection3 must be the same, which in extreme conditions predispose to RAR. We find no explanation for the statistically significant association of sex mismatch and RAR, other than random error. Acute allograft rejection is the most frequent cause of graft rupture in the literature (60 to 80%),3 but ATN has received little note. In our series, ATN was responsible for 36% of the ruptures, as much as severe acute rejection. ATN alone can cause RAR,4 because of interstitial edema and rise in intrarenal pressure. But when associated with rejection, it seems that these two conditions can act synergistically to cause allograft rupture. Our data suggests that rupture occurs later when caused by rejection, rather than when RVT is responsible. To our knowledge this finding had never been reported in world literature. Perhaps the timing of RVT is related to technical problems, such as twisting and kinking of the vein or intima tear, although the thrombogenic effect of cyclosporine can also have a role in this process.5 All these patients were on cyclosporine therapy, which may explain the small number of RAR caused by rejection alone and the significant number of patients that had RVT (27%). It appears that cyclosporine therapy is changing the etiology of the graft rupture.6 References 1 T. Grochowiecki, J. Szmidt and K. Madej et al., Transplantation Proc 28 (1996), p. 3461. View Record in Scopus | Cited By in Scopus (2) 2 R.S. Lord, D.J. Effeney and J.M. Hayes et al., Ann Surg 177 (1973), p. 268. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (4) 3 G.J. Azar, A. Zarifian and G.D. Frentz et al., Clin Transplantation 10 (1996), p. 635. View Record in Scopus | Cited By in Scopus (12) 4 Y.H. Chan, K.M. Wong and K.C. Lee et al., Am J Kidney Dis 34 (1999), p. 355. Abstract | Article | PDF (86 K) 5 R.M. Jones, J.A. Murie and A. Ting et al., Clin Transplant 2 (1988), p. 122. 6 A.J. Richardson, R.M. Higgins and A.J. Jaskowski et al., Br J Surg 77 (1990), p. 558. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (19)