Renal Allograft Rupture: A Clinicopathologic Review

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

Pulmonary alveolar proteinosis: a rare pulmonary toxicity of sirolimus.

Transpl Int. 2007 Mar;20(3):291-6. Pulmonary alveolar proteinosis: a rare pulmonary toxicity of sirolimus. Pedroso SL, Martins LS, Sousa S, Reis A, Dias L, Henriques AC, Sarmento AM, Cabrita A. Nephrology Department, Hospital Geral de Santo António, Porto, Portugal. [email protected] Abstract The aim of our paper is to describe an unusual pulmonary toxicity of sirolimus (SRL) in a kidney transplant recipient. We present a 34-year-old woman with a second renal transplantation, complicated with steroid-resistant acute rejection and chronic allograft dysfunction. Two years after initiating SRL, she presented complaints of progressive dyspnoea, nonproductive cough, chest pain and low-grade fever of 1 month duration. She had chronic allograft nephropathy and slight elevation of lactic dehydrogenase levels. After exclusion of common reasons of this condition, a computed tomography (CT) of the thorax and bronchoscopy was performed, revealing ground-glass opacification with polygonal shapes on CT and an opaque appearance with numerous macrophages on bronchoalveolar lavage. The alveolar macrophages stained positive by Periodic acid-Schiff. Diagnosis of pulmonary alveolar proteinosis (PAP) was made and drug-induced toxicity was suspected. SRL was withdrawn with marked improvement in the patients' clinical and radiological status. PAP resolved within 3 months without further therapy. PAP is a very rare complication of SRL therapy with only a few cases described. Withdrawal of SRL with conversion to another immunosuppressant seems to be an appropriate procedure in this condition. PMID: 17291222 [PubMed - indexed for MEDLIN

Homocysteine levels in pediatric renal transplant recipients.

Transplant Proc. 2003 May;35(3):1093-5. Homocysteine levels in pediatric renal transplant recipients. Mota C, Fonseca I, Santos MJ, Costa T, Faria MS, Henriques AC, Sarmento AM, Pereira E, Pereira M. Department of Paediatric Nephrology, Maria Pia Children's Hospital, R. da Boavista, 827, 4050-111, Porto, Portugal. [email protected] PMID: 12947872 [PubMed - indexed for MEDLIN

End-Stage Renal Disease in Familial Amyloidosis ATTR Val30Met: A

Transplant Proc. 2003 May;35(3):1116-20. End-stage renal disease in familial amyloidosis ATTR Val30Met: a definitive indication to combined liver-kidney transplantation. Lobato L, Ventura A, Beirão I, Miranda HP, Seca R, Henriques AC, Teixeira M, Sarmento AM, Pereira MC. Department of Nephrology, and Liver Transplantation Program, Hospital Geral de Santo António, Largo Professor Abel Salazar, 4050, Porto, Portugal. [email protected] PMID: 12947881 [PubMed - indexed for MEDLINE

Hyperhomocysteinemia in Renal Transplantation: Preliminary Results

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