Cases reported "Recurrence"

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21/242. Renal relapse in bilateral synchronous testicular lymphoma.

    Bilateral synchronous testicular lymphoma is an uncommon presentation of non-Hodgkin's lymphoma. A young man with non-Hodgkin's lymphoma of both testes synchronously is described here. He underwent bilateral orchiectomy, received chemotherapy, and was in complete remission when there was a relapse in the kidneys. Salvage chemotherapy was given. The patient developed progression of the residual lesion subsequently and was started on palliation with chlorambucil and prednisolone. He was alive at 34 months after diagnosis with disease.
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22/242. Evidence of recurrent type I diabetes following HLA-mismatched pancreas transplantation.

    Type 1 diabetes mellitus is considered as an autoimmune disease against beta cells. Diabetes recurrence after pancreas transplantation is well known in HLA-identical twins while it is rarely reported in recipients of cadaveric pancreatic grafts. In the present case report, diabetes recurrence occurred in a recipient who underwent cadaveric combined pancreas kidney transplantation. Seven years after transplantation the patient exhibited progressive hyperglycemia needing insulin therapy while the renal graft was well functioning. The diagnosis of recurrent disease was obtained on the histological features such as selective loss of beta cells without clear signs of insulitis and on the presence of markers (GAD 65 and IA-2) for humoral autoimmunity. It is intriguing that, at the time of recurrence of type 1 diabetes, the patient had stopped steroids and azathioprine, while only cyclosporine was maintained as immunosuppressive treatment. Our case report underlines the relevance of studying the humoral autoimmune response directed to islet autoantigens in cadaveric pancreas allograft recipients. Furthermore, it suggests that an efficient immunosuppressive treatment after transplantation may be able to reduce the autoimmune response against the pancreatic allograft.
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23/242. role of lipids in the progression of renal disease in systemic lupus erythematosus patients.

    Systemic lupus erythematosus (SLE) is an autoimmune connective tissue disease marked by immune-complex mediated lesions in small blood vessels of various organs, especially the kidneys, although other factors may also be implicated in the pathogenesis of the disease. This article focuses on the role of lipids in the progression of glomerular, vascular and tubulo-interstitial lesions in two patients with lupus nephritis associated with pronounced hyper- and dyslipidemia. The pathogenesis of progressive glomerulosclerosis in both patients appears to be multifactorial. In addition to immune complex mediated lupus glomerulonephritis, progressively active in the first patient, severe nephrotic-range persistent proteinuria, arterial hypertension associated with hyperfiltration and hyperperfusion injuries and, to a minor extent, hyper- and dyslipidemia were observed. Immunological and non-immunological factors were shown to contribute to the development of tubulo-interstitial lesions. In both patients, in addition to local immune deposits, prominent tubulo-interstitial lipid deposits were probably causally related to both hyperlipidemia and the increased permeability of the glomerular filtration barrier. Tubular lesions were highlighted by intracytoplasmic lipid droplets as well as small cleft-like spaces found to be impacted in the tubular lumina. They were seen to penetrate tubular epithelial cells and eventually lodge in the interstitium, surrounded by mononuclear cell infiltrates and foam cells. In both patients, hypertensive angiopathy and extraglomerular vascular immune deposits were demonstrated. In addition, in the second patient, arteriolar and small arterial hyaline was found at the age of 28 years to be full of lipids and calcium precipitates, suggesting a peripheral atherosclerosis-like process which never occurs as a natural age-related condition. In conclusion, all parts of the nephron may be involved in the pathogenetic process causally related or influenced by hyper- or dyslipidemia. Associated either with endothelial cell injury and consequent insudation of lipids in the vascular walls, glomerular filtration barrier injury with hyperfiltration, or tubulo-interstitial lipid deposition, the mechanism of tissue damage by lipids in all parts of the nephron shares similarities with the pathogenesis of systemic atherosclerosis.
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24/242. A case of relapse of C-ANCA-associated glomerulonephritis in post-transplant patients.

    We experienced a case of relapse of proteinase 3-specific antineutrophil cytoplasmic autoantibody (C-ANCA)-associated rapid progressive glomerulonephritis (RPGN) in a patient after renal transplantation. A 19-yr-old man, who underwent a living donor kidney transplantation, presented a rapid renal function deterioration along with a sign of infection. Initially he was treated as acute rejection, but renal function did not improve. Renal biopsy revealed crescentic glomerulonephritis, and C-ANCA titer was 12 EU/mL, resulting in the diagnosis of C-ANCA-associated RPGN. He was treated with three consecutive methylprednisolone pulses twice in addition to the basal immunosuppressive medications (cyclosporine A and mizoribine), then his renal function improved to normal. Bearing the possibility of recurrence of glomerulonephritis in mind, we re-evaluated the nature and disease course of renal failure of original kidney. He experienced a rapid deterioration of renal function in 1992, and eventually CAPD was started in 1992. His serum in 1992 revealed high titer of C-ANCA (24 EU/mL), and renal biopsy performed in 1992 showed a crescentic glomerulonephritis. Taken together, we diagnosed this event as a relapse of C-ANCA-associated GN. Lessons from our experience are: 1) steroid pulse and high-dose corticosteroid therapy may be useful for the treatment of relapse of C-ANCA-associated GN patients after renal transplantation; 2) the possibility of a relapse of C-ANCA-associated GN following renal transplantation has to be kept in mind, especially when infection precedes the deterioration of allograft kidney function.
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25/242. adenine phosphoribosyltransferase deficiency and renal allograft dysfunction.

    adenine phosphoribosyltransferase (APRT) deficiency is a rarely diagnosed cause of renal allograft dysfunction. We report the case of a 42-year-old man who presented in 1996 with idiopathic renal failure. Native kidney biopsy showed extensive microcrystalline interstitial nephritis. The patient subsequently underwent a living-related kidney transplant with excellent early graft function. During the next year, however, he had worsening allograft function, and allograft biopsy showed recurrent interstitial nephritis. Further chemical and spectroscopic analysis showed this lesion to be an annular microcrystalline nephritis consistent with APRT deficiency. This diagnosis was confirmed on erythrocyte assay. Treatment with allopurinol and a low-purine diet led to improvement and stabilization of renal function. APRT is a rare cause of renal allograft dysfunction requiring a high index of suspicion for early diagnosis and treatment. Increased physician awareness in the united states may hasten diagnosis and limit the morbidity associated with this disease.
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26/242. An unusually aggressive case of endometriosis showing p53 expression.

    A 43 year old woman who underwent a hysterectomy and bilateral salpingo-oophorectomy for secondary dysmenorrhoea was found to have bilateral ovarian endometriosis. During the following four years she developed a series of tumour-like vaginal masses, which were locally excised, a pelvic mass causing acute large bowel obstruction, which necessitated an emergency Hartmann's procedure, and a further pelvic mass causing hydronephrosis with a non-functioning kidney. Pathological examination of all the resected specimens showed endometriosis with abundant stromal and glandular elements. Immunoreactivity for p53 protein was detected within endometriotic foci from the initial oophorectomy as well as the latest resection specimens. Immunostaining for p53 may help identify potentially aggressive cases of endometriosis for proactive treatment.
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27/242. Symptomatic type 1 protein c deficiency caused by a de novo Ser270Leu mutation in the catalytic domain.

    Heterozygosity for a C8524T transition in the protein C gene converting Ser270(TCG) to Leu(TTG) in the protease domain was identified in a family with venous thrombosis. The mutation was associated with parallel reduction in plasma levels of protein C anticoagulant activity and protein C antigen, which is consistent with a type 1 deficiency. Transient expression of mutant protein C cDNA in human kidney 293 cells and analysis of protein C antigen in culture media and cell lysates showed that the secretion of mutant protein compared with wild-type protein was reduced by at least 97% while the intracellular content of mutant and wild-type protein was similar. Northern blot analysis of total mRNA from transfected cells showed no reduction of the mutant protein C mRNA compared with wild-type protein C mRNA. Collectively, these results indicate that the Ser270Leu mutation in the affected family caused the plasma protein c deficiency and are consistent with a disease mechanism that involves synthesis of mutant protein followed by intracellular degradation before its secretion into the extracellular space. The mutation was not present in the parents of the proband, suggesting a de novo mutation. Non-paternity was excluded after the analysis of three intragenic protein C polymorphisms and six dinucleotide repeat allele sets located in five different chromosomes.
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28/242. Acute promyelocytic leukemia with additional chromosome abnormalities in a renal transplant case.

    Some cases of acute myeloid leukemia following organ transplant (PT-AML) have been published in the literature. We report the second case of acute promyelocytic leukemia (APL), which developed post-transplant and immunosuppressive treatment, in a 50-year-old male who had undergone a renal transplant. At diagnosis he presented typical t(15;17)(q12;q13) with additional abnormalities, including 8,t(13;22)(q12;q13) and an abnormal chromosome 1 which was better characterized by fluorescence in situ hybridization (FISH). He obtained cytological, karyotypic and molecular complete remission (CR) with induction treatment according to the all-trans retinoic acid idarubican (AIDA) protocol; after 12 months, he relapsed (molecular relapse) and achieved molecular remission with all-trans retinoic acid (ATRA) plus mitoxantrone and cytosine arabinoside. After a further 14 months, he was treated with arsenic trioxide for cytological relapse and obtained a third CR; at the cytological relapse the karyotype showed 47,XY, 8, t(15;17)(q22;q21),t(13;22)(q12;q13),der(22)t(1;22)(p22;q13). He is alive 3.3 years after diagnosis of APL. Cyclosporin A (CsA) was given during all cycles of chemotherapy. We did not observe any severe infections or kidney failure during treatments. The use of conventional cytogenetic analysis plus FISH may identify complex karyotype also in transplanted patients receiving immunotherapy, and may also contribute to a better assessment of PT-AL.
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29/242. recurrence of light chain nephropathy in a renal allograft. A case report and review of the literature.

    Myeloma and monoclonal gammopathies can affect the kidney in many ways with cast nephropathy and light chain deposition disease being the most commonly recognised histological entities. Renal transplantation in these patients remains controversial both because of the risk of recurrent disease affecting the graft and also because of concerns around the possibility of disease relapse within the patient. We suggest that the histological pattern of disease within the native kidneys is crucial in the overall assessment of these patients for renal transplantation. Those patients in whom renal deposition of light chains is associated with a proliferative glomerulonephritis have a considerably worse graft survival than those presenting with cast nephropathy.
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30/242. Rapid recurrence of ANCA-negative pauci-immune vasculitis after cadaveric renal transplantation.

    We report a patient with renal failure secondary to antineutrophil cytoplasmic autoantibody (ANCA)-negative pauci-immune systemic vasculitis who developed rapid recurrence of vasculitis involving skin, eye, and kidney allograft 1 month after cadaveric renal transplant while being maintained on cyclosporine, mycophenolate mofetil, and prednisolone. Despite early institution of aggressive treatment with plasma exchange, the disease remained uncontrolled and resulted in substantial morbidity and subsequent graft failure within 1 year post-transplantation. This case confirms that ANCA-negative vasculitides may recur in transplanted patients taking mycophenolate mofetil. Transplantation is contraindicated when active disease is evident.
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