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- Familial amyloid polyneuropathy type I (Portuguese): distribution and characterization of renal amyloid deposits.Publication . Lobato, L.; Beirao, I.; Guimaraes, S.; Droz, D.; Guimaraes, S.; Grunfeld, J.; Noel, L.
- Sclerosing encapsulating peritonitis: a case successfully treated with immunosuppression.Publication . Martins, La Salete; RODRIGUES, A.; CABRITA, A.; GUIMARAES, S.Perit Dial Int. 1999 Sep-Oct;19(5):478-81. Sclerosing encapsulating peritonitis: a case successfully treated with immunosuppression. Martins LS, Rodrigues AS, Cabrita AN, Guimaraes S. SourceDepartment of Nephrology, Hospital de Santo António, Porto, Portugal.
- 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)
- Hyperhomocysteinemia in Renal Transplantation: Preliminary ResultsPublication . Fonseca, Isabel; Queirós, J; Santos, M.J.; Mendonça, D.; Henriques, A. C.; Sarmento, A.M.; Santos, A.C.; Guimarães, S.; Pereira, M.Cardiovascular disease (CVD) is a major cause of morbidity and mortality after renal transplantation (RT).[1] and [2] The excess risk of CVD in RT is due in part to a higher prevalence of established atherosclerotic risk factors, including hypertension, dyslipidemia, diabetes, obesity, and physical inactivity.[1] and [2] However, some renal-related risk factors like immunosuppressive medication and residual renal insufficiency also contribute to this excess CVD risk and may complicate the management of dyslipidemia and hypertension in this population.[1] and [2] Accordingly, there is a compelling need to identify and safely manage other putative CVD risk factors among RT patients. Elevated plasma homocysteine is emerging as an important risk factor for cardiovascular disease in general populations.[3] and 4 R Clarke, L Daly and K Robinson et al., N Engl J Med 324 (1991), p. 1149. View Record in Scopus | Cited By in Scopus (1372)[4] Some studies have demonstrated that hyperhomocysteinemia is present in patients with impaired renal function and is associated with CVD.[5], [6] and [7] Only a small number of studies are available on the prevalence and determinants of hyperhomocysteinemia in renal transplant recipients.[8], [9], [10], [11], [12], [13], [14] and [15] We undertook this study to 1. estimate the prevalence of hyperhomocysteinemia in renal transplant recipients; 2. examine the relationships between plasma total homocysteine (tHcy) and its metabolic determinants vitamin B6, vitamin B12, and folic acid; and 3. identify other determinants of tHcy.
- Peritoneal rest may successfully recoverultrafiltration in patients who develop peritoneal hyperpermeability with time on continuous ambulatory peritoneal dialysisPublication . Rodrigues, A.; Cabrita, A.; Maia, P.; Guimarães, S.Temporary transfer to hemodialysis, as a peritoneal rest, may be a rescue therapy to recover ultrafiltration (UF) in patients who develop peritoneal hyperpermeability as a complication of continuous ambulatory peritoneal dialysis (CAPD). However, peritoneal sclerosis has been reported after peritoneal pause. Since the beginning of our CAPD program in 1985, 12°elective peritoneal pauses have been performed in 11°patients who developed type°I ultrafiltration failure (D/P240 creatinine: 0.88°± 0.09) after 42°± 14°months on CAPD. Eight patients recovered UF and remained on CAPD with standard solutions for 10°± 9°months more (minimum: 5°months; maximum: 29°months). Only 3 of those patients were later switched to hemodialysis because of recurring UF failure. One patient remains on CAPD (62°months of follow-up). Four patients failed to respond and were permanently transferred to hemodialysis, without signs of developing encapsulating peritoneal sclerosis. The failed pauses were performed later after the detection of UF failure than were the successful ones (483°± 574°days vs. 54°± 52°days). In our study, 8 of 12 peritoneal pauses (66.6%) successfully treated type°I UF failure and prolonged CAPD retention. If a pause is initiated soon after diagnosis of UF failure, results may improve further. We urge prospective studies to better determine the best and timely therapeutic approach in patients with loss of ultrafiltration.
- Compared to mycophenolate mofetil, rapamycin induces significant changes on growth factors and growth factor receptors in the early days post‐kidney transplantationPublication . OLIVEIRA, J.G.; XAVIER, P.; SAMPAIO, S.M.; HENRIQUES, C.; TAVARES, I.; MENDES, A.A.; PESTANA, M.We found 1 article: Transplantation. 2002 Mar 27;73(6):915-20. Compared to mycophenolate mofetil, rapamycin induces significant changes on growth factors and growth factor receptors in the early days post-kidney transplantation. Oliveira JG, Xavier P, Sampaio SM, Henriques C, Tavares I, Mendes AA, Pestana M. Renal Department, Hospital S. João, Porto, Portugal. Abstract BACKGROUND: The new immunosuppressive drug Rapamycin (Rapa) is endowed with a mechanism of action that is distinct from that of calcineurin inhibitors. It has been claimed that Rapa does not significantly modulate either the cytokine expression or the transcription of several growth factors in mitogen-activated T cells. Previously, we reported that fine-needle aspiration biopsy (FNAB) sample cultures synthesize a large array of cytokines, and some of them may be powerful predictors of acute rejection in renal transplants. We hypothesized that Rapa may induce significant changes on cytokine production by FNAB sample cultures and on serum cytokine receptors when compared to other immunosuppressive drugs. METHODS: Kidney transplants treated with CsA-Rapa-Pred (Rapa group) were compared with transplants treated with CsA-mycophenolate mofetil-Pred (MMF group). They were studied on day 7 posttransplantation, and they remained rejection free for at least the first 6 months. FNAB samples were cultured and the supernatants were collected at 48 hr of incubation and analyzed by ELISA for interleukin 1 receptor antagonist (IL-1ra), IL-2, IL-6, IL-10, IL-18, monocyte chemotactic protein 1 (MCP-1), soluble tumor necrosis factor I, and transforming growth factor (TGF)-beta(1). The soluble receptors for IL-1, IL-2, IL-6, and tumor necrosis factor alpha, together with IL-2 and IL-18 were also measured in serum. RESULTS: Significant differences were observed when comparing Rapa with the MMF group. IL-18 and TGF-beta(1) synthesis were up-regulated, whereas IL-6 and MCP-1 were down-regulated in FNAB sample cultures. The Rapa group showed a significant down-regulation of each cytokine receptor and of IL-2 in serum. CONCLUSIONS: Rapa was associated with a decreased synthesis of primarily monocyte-derived cytokines and enhanced production of TGF-beta(1), which in an appropriate cytokine milieu may promote allograft tolerance. The down-regulation of cytokine receptors and IL-2 may be associated with a depressed immune response towards the kidney allograft. PMID: 11923692 [PubMed - indexed for MEDLINE]
- Familial ATTR amyloidosis: microalbuminuria as a predictor of symptomatic disease and clinical nephropathyPublication . Lobato, L.; Beirao, I.; Silva, M.; Bravo, F.; Silvestre, F.; Guimaraes, S.; Sousa, A.; Noel, LH.; Sequeiros, J.Familial ATTR amyloidosis: microalbuminuria as a predictor of symptomatic disease and clinical nephropathy. Lobato L, Beirão I, Silva M, Bravo F, Silvestre F, Guimarães S, Sousa A, Noël LH, Sequeiros J. SourceDepartment of Nephrology and Centro de Estudos de Paramiloidose, Hospital Geral de Santo António and Institute for Molecular and Cell Biology, Porto, Portugal. llobato@netcabo.pt Abstract BACKGROUND: Portuguese type familial amyloid polyneuropathy (FAP) is a neuropathic amyloidosis caused by a mutant transthyretin (TTR). Varying degrees of renal involvement have been reported. Our aim was to assess the value of microalbuminuria (MA) for predicting clinical neurological disease and overt nephropathy in TTR-related amyloidosis. METHODS: All subjects had the TTR Val30Met mutation, and were recruited between 1993 and 1999. We have prospectively evaluated 22 asymptomatic gene carriers (7 male, 15 female; mean age 41.6+/-9.6 years) and 32 patients with neuropathy (14 male, 18 female; 36.8+/-8.8 years, on average, 33.0+/-9.3 years at the onset of neuropathy). We measured urinary albumin excretion every year, if asymptomatic, or every 6 months if already affected. Kidney biopsies were performed in patients with normal urinary albumin excretion, MA, and overt nephropathy, respectively. RESULTS: In asymptomatic carriers, persistent MA was detected in eight (36%) subjects. The presence of MA in asymptomatic gene carriers, compared with those having normal urinary albumin excretion, conferred a 4.8-fold risk of developing neuropathy, usually within the subsequent 3 years. Once neurological signs appeared, nephropathy, manifested as MA, progressed to overt nephropathy in one-half of subjects. In patients with neuropathy, 24 (75%) had MA during follow-up: evolution towards clinical renal disease occurred in 14 (58%) and renal failure occurred in five (21%), always after a course of MA. Proteinuria or renal failure without prior persistent MA were never observed in the present patient cohort. Histopathological evaluation did not reveal glomerular lesions other than amyloid deposits to explain abnormal urinary albumin excretion. The amount of mesangial and vascular-pole amyloid deposits was correlated with the degree of albuminuria. CONCLUSIONS: Microalbuminuria represents the first stage of clinical TTR amyloid nephropathy and is premonitory of neuropathy. Its presence identifies a subgroup of patients who are more prone to develop overt nephropathy. Screening of MA may be important to assess disease onset and to recommend liver transplantation in individuals at risk.
- Combined Pancreas-Kidney Transplantation: A New Program in Portugal, Results From the First 12 CasesPublication . Martins, L.; Henriques, A.; Dias, L.; Ventura, A.; Seca, R.; Almeida, R.; Dores, J.; Bacelar, C.; Oliveira, F.; Lhamas, A.; Amil, M.; Rua, F.; Coelho, T.; Esteves, S.; Ribeiro, A.; Pereira, R.; Sarmento, A.; Teixeira, M.; Pereira, M.Transplant Proc. 2003 May;35(3):1107-8. Combined pancreas-kidney transplantation: a new program in Portugal, results from the first 12 cases. Martins L, Henriques A, Dias L, Ventura A, Seca R, Almeida R, Dores J, Bacelar C, Oliveira F, Lhamas A, Amil M, Rua F, Coelho T, Esteves S, Ribeiro A, Pereira R, Sarmento A, Teixeira M, Pereira M. Transplantation Department, Hospital Santo António, 4050, Porto, Portugal. lasalete@clix.pt PMID: 12947877 [PubMed - indexed for MEDLINE]
- "Very urgent" kidney transplantation: results from one center.Publication . Costa, S.; Ventura, A.; Costa, T.; Martins, L.; Henriques, A.; Sarmento, A.Transplant Proc. 2003 May;35(3):1066. "Very urgent" kidney transplantation: results from one center. Costa S, Ventura A, Costa T, Martins L, Henriques A, Sarmento A. Nephrology Department, Hospital de Santo António, 4050 Porto, Portugal. PMID: 12947858 [PubMed - indexed for MEDLINE]
- Portuguese‐type amyloidosis (transthyretin amyloidosis, ATTR V30M).Publication . Lobato, L.J Nephrol. 2003 May-Jun;16(3):438-42. Portuguese-type amyloidosis (transthyretin amyloidosis, ATTR V30M). Lobato L. SourceDepartment of Nephrology, Santo António General Hospital, Porto, Portugal. llobato@netcabo.pt Abstract Portuguese-type amyloidosis (transthyretin amyloidosis, ATTR V30M) is the most common form of systemic hereditary amyloidosis, inherited in autosomal dominant mode. The disease, also called familial amyloid polyneuropathy type I (FAP-I), is caused by a mutant transthyretin (TTR) protein, which is synthesized by the liver. A single amino acid substitution of methionine for valine at position 30 of the TTR molecule (TTR V30M) was found in Portuguese patients. The clinical disease usually manifests as a peripheral sensory, motor and autonomic neuropathy starting in the 3rd or 4th decade of life. Renal manifestations of ATTR V30M, like other amyloidoses, are different levels of proteinuria and renal insufficiency. In ATTR V30M a large amyloid deposition in the medullary zone of the kidney and tubules is characteristic. A more extensive glomerular and vascular involvement is present only in patients with renal manifestations. A prospective survey in the north of Portugal showed that a stage of microalbuminuria (MA) could precede nephropathy and neurological disease. Nephropathy in FAP-I is present in one-third of affected patients and tends to aggregate in families. The progression towards end-stage renal disease (ESRD) affects 10% of the patients, and the survival after initiation of dialysis is a mean of 21 months. Patients who progress to ESRD have a late onset of neuropathy and lower prevalence of clinical disease in their families. Liver transplantation is a widely accepted treatment for FAP-I, and combined liver-kidney transplantation is also an option for selected patients with FAP-I and ESRD.