[Renal cell cancer].
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Carcinoma, Renal Cell↗
Biomedical subjects
Béla Iványi
Publications and source records attributed to Béla Iványi.
Erdheim-Chester's disease of the heart: a diagnostic conundrum and collision with the same mass in the orbit.
Erdheim-Chester's disease is a rare multisystem xanthogranulomatosis, afflicting the skeletal system with the occasional involvement of soft tissues. We delineate an unusual case of a cardiac variant of Erdheim-Chester's disease presenting with pericardial effusion and as a collision with a synchronous orbital manifestation. We describe our diagnostic pathway and propose a novel treatment option involving nonsteroidal anti-inflammatory drugs. The role of cyclo-oxygenase in the disease process and inhibition thereof by NSAIDs is hypothesized and discussed.
Celecoxib↗
[Merkel cell carcinoma].
Merkel cell carcinoma (Mcc) is a very rare, malignant, neuroendocrine tumour. Mcc has an aggressive behavior, local recurrence, and regional or distant metastasis generally develop within a short period of time. At the Oral Medicine Department 158,056 patients were treated between 1970 and 2004. A single case of Mcc was diagnosed, in a 79-year-old woman. The tumour was localized to the upper lip. After successful cryosurgery and a 7-year tumour-free period, a new tumour developed in her palatine tonsil. It was an anaplastic carcinoma with neuroendocrine features, raising the possibility of a late haematogenous metastasis, a second field tumour, or a second primary tumour. The clinical, histological, immunohistochemical and genetic findings suggested that the tumour of the palatine tonsil is a second field tumour.
Aged↗
[Collagen type IV nephropathy: from thin basement membrane nephropathy to Alport syndrome].
INTRODUCTION: Collagen type IV nephropathy includes the Goodpasture syndrome, thin basement membrane nephropathy and the Alport syndrome. Mutations in the coding Col(IV)A3/A4 and Col(IV)A5 genes are probable causes of the latter two. Thin basement membrane nephropathy is mostly familial and has an autosomal dominant inheritance, at least 40% of the families have hematuria that co-segregates with the Col(IV)A3 and/or Col(IV)A4 loci. 85% of Alport syndrome cases are transmitted as an X-linked semidominant form due to Col(IV)A5 mutations. About 14% of Alport syndrome cases exhibit autosomal recessive, and 1% autosomal dominant inheritance, both caused by mutations in the Col(IV)A3 or Col(IV)A4 genes in boys and in girls. AIM: The co-segregation pattern of hematuria was examined in two families with thin basement membrane nephropathy and one family with the Alport syndrome, using short tandem repeat markers, spanning the Col(IV)A3/A4 and Col(IV)A5 loci to assess their linkage to the clinical symptoms and morphological alterations in the renal biopsy specimens. METHODS: Markers: Col(IV)A3: CAll and D2S401; Col(IV)A4: HaeIII/RFLP; and Col(IV)A5: DXS456, 2B6 and 2B20. RESULTS: The hematuria displayed autosomal dominant inheritance and co-segregated with Col(IV)A3 markers in one of the thin basement membrane nephropathy families. In the second, the hematuria did not segregate with the Col(IV)A3/A4 or Col(IV)A5 loci, suggesting the possibility of another genetic locus for the disease. The Alport syndrome exhibited autosomal recessive inheritance and did not link to Col(IV)A5 markers, and the Col(IV)A3/A4 markers were informative only in part. CONCLUSION: Knowledge of the inheritance and genetic background of collagen type IV nephropathy will be very important in the diagnostics and genetic counseling in the future.
Adolescent↗
[Adult renal neoplasms in the material of the Pathology Department of the Szeged University].
AIMS: The authors investigated the frequencies of the various histological types of adult renal tumours. METHODS: The slides of 469 nephrectomies performed in the Department of Urology, Szeged University between 1990 and 2003 were revised according to the 1997 Heidelberg and 2004 WHO classification schemes. RESULTS: 86.7% of all the tumours (n = 407) were malignant. Among the malignant tumours, the frequency of renal cell carcinomas was 91.1% (n = 371). 88.4% of the renal cell carcinomas (n = 328) were of conventional type, 5.6% (n = 21) were papillary and 4% (n = 15) were chromophobe. The authors observed 3 Bellini duct, 1 mucinous tubular and 3 non-classifiable carcinomas, with a combined incidence of 1.8%. 84.5% of the conventional carcinomas were clear cell (n = 277), 8.8% were eosinophilic granular (n = 29), 3.9% were multilocular cystic (n = 13) and 2.7% were sarcomatoid carcinomas (n = 9). The median age of the patients with conventional carcinoma was 60 (median, range: 25-84), in the papillary group it was 62 (43-78), and in the chromophobe group was 59 (17-77). The median age of patients affected by transitional cell carcinoma was 64 (range: 45-81). As far as benign tumours are concerned (13.2%, n = 62), oncocytomas (n = 37, 7.8% of all the tumours) affected mainly females, whereas angiomyolipomas (n = 21, 4.4% of all the tumours) occurred in females only. In 13 oncocytoma cases, the tumours were initially diagnosed as malignant. CONCLUSIONS: Adult malignant renal tumours affect mainly patients around the age of 60. The commonest diagnosis was clear cell carcinoma of conventional type. The incidence of clear cell carcinoma was 5% higher than that reported in the literature (84.5% vs 70-80%) whereas that of papillary carcinoma was 5% lower (5% vs 10-15%). In comparison with the literature data, oncocytomas were relatively common (8% instead of 3%), and not rarely, it was difficult to distinguish them from renal cell carcinomas.
Adenocarcinoma, Clear Cell↗
A second field metachronous Merkel cell carcinoma of the lip and the palatine tonsil confirmed by microarray-based comparative genomic hybridisation.
Merkel cell carcinoma was diagnosed in a 79-year-old Caucasian woman. The tumour was localised to the upper lip and was in stage T2. After successful cryosurgery and a 7-year tumour-free period, a new tumour developed in her palatine tonsil. Histologically and immunohistochemically, this resembled the tumour in the lip. The regional lymph nodes were devoid of metastasis. The paraffin-embedded material of the two tumours and the unaffected lymphatic tissue were analysed with DNA microarrays for comparative genomic hybridisation to assess the genetic relationship of the tumours. In both tumours, regions on 2p and 10p were commonly over-represented, while 41 regions on chromosomes 1-4, 6, 8-9, 11 and 14-22 were commonly under-represented. Chromosomes 1, 3, 4, 16-18 and X were most frequently involved in the DNA losses. In gene copy numbers in the two tumours, 31 chromosome locations were found to be differently affected. The partly similar and partly different molecular patterns indicated a genetic relationship between the tumours and excluded the possibility that the tonsillar tumour was a metastasis. The findings suggest that a genetically altered field was the reason for the development of the tonsillar cancer; thus, it can be regarded pathogenetically as a second field tumour.
Aged↗
Ultrastructural analysis of the Fisher to Lewis rat model of chronic allograft nephropathy.
Chronic allograft nephropathy (CAN) is the leading cause of graft loss following kidney transplantation. One factor contributing to CAN is chronic alloimmune injury. However, the involvement of alloantigen-dependent and -independent factors in CAN is unclear. The pathomechanism of CAN has been extensively studied by utilizing the Fischer-to-Lewis (F344-to-LEW) rat model. Transplant capillaropathy (circumferential multiplication of the peritubular capillary basement membrane) and transplant glomerulopathy (reduplication of the glomerular basement membrane) have recently been validated clinicopathologically as ultrastructural indicators of chronic alloimmune injury. To investigate the presence of these markers, F344-to-LEW kidneys were examined by electron and light microscopy 32, 40 and 52 weeks after implantation. F344 rats with or without 30-min ischemia of the left kidney following right nephrectomy served as controls. All transplanted rats displayed marked proteinuria. On electron microscopy, transplant capillaropathy, transplant glomerulopathy, and T-cell cytotoxicity (indicator of ongoing cellular rejection) were absent. On light microscopy, the arteries were devoid of intimal fibrosis. Focal-segmental glomerulopathy resembling hyperfiltration injury was encountered, with mild interstitial infiltration, fibrosis, and tubular atrophy. The proteinuria and kidney pathology were more severe in transplanted than in ischemic or uninephrectomized rats. Because chronic-active rejection could not be detected between weeks 32 and 52, we propose that the alloantigen-dependent initial graft injury subsides, but induces the late events: glomerular hyperfiltration, proteinuria, and glomerulosclerosis. Accordingly, the model - in the late phase - is suitable to investigate alloantigen-independent factors of CAN and lacks markers of alloantigen-dependent processes.
Animals↗
[The incidence of renal diseases as diagnosed by biopsy in Hungary].
AIM AND METHODS: The authors analysed the incidence of renal diseases as diagnosed by biopsy in the population living on the southern Great Hungarian Plain. 798 biopsy specimens were examined between 1990 and 2002. RESULTS: The most common diseases in decreasing order of frequency were IgA nephropathy (15%), membranous nephropathy (12%), thin-basement-membrane nephropathy (8%), minimal change nephropathy (7%), lupus glomerulonephritis (7%), focal sclerosis (6%), hypertensive kidney disease and arteriolosclerosis (5%), diabetic nephropathy (5%), and crescentic glomerulonephritis (4%). The most frequent diseases in decreasing order of frequency in children were minimal change nephropathy, thin-basement-membrane nephropathy, Henoch-Schönlein nephropathy and IgA nephropathy; in adults were IgA nephropathy, membranous nephropathy, lupus glomerulonephritis and thin-basement-membrane nephropathy; and in the elderly were membranous nephropathy, amyloidosis, crescentic glomerulonephritis and diabetic nephropathy. The incidence of the diseases differed significantly between the genders in IgA nephropathy, thin-basement-membrane nephropathy, lupus glomerulonephritis, chronic sclerosing nephropathy and Alport nephropathy. At the time of the biopsy, 69 patients were suffering from diabetes mellitus. 37 patients were diagnosed as having diabetic nephropathy, and 32 as having non-diabetic nephropathy. In 6 cases, the diabetic nephropathy was accompanied by other glomerular disorders. In more than half of the diabetic patients with non-diabetic nephropathy, membranous nephropathy or focal sclerosis was diagnosed. Crescentic glomerulonephritis was diagnosed on 30 occasions, which was due to vasculitis in 20 cases, proliferative glomerulonephritis in 7 cases and anti-glomerular-basement-membrane nephritis in 3 cases. In the middle-aged and the elderly, the renal disease was relatively often a consequence of systemic disease. CONCLUSION: The incidence and the gender distribution of renal diseases diagnosed by biopsy were similar to those reported by other European kidney biopsy centres. IgA nephropathy was the most frequent disease in the biopsy registry of the authors. The high incidence of thin-basement-membrane nephropathy seems to be related to consequent biopsy examinations of glomerular haematuria. In diabetics and the elderly, the diagnosis of the renal disease may be challenging.
Adolescent↗
Long-term effects of levamisole treatment in childhood nephrotic syndrome.
The effects of levamisole treatment on long-term outcome were evaluated in a retrospective study of frequently-relapsing (FRNS, n=15), steroid-dependent (SDNS, n=13), and steroid-resistant (SRNS, n=6) nephrotic syndrome in 34 children (21 boys, 13 girls, mean age 5.0+/-3.4 years) during a 60-month follow-up period. The definition of frequent relapses was > or = 4 relapses per year. The current relapse was treated with prednisolone 60 mg/m2 per day for 4 weeks, then with 40 mg/m2 every other day for 4 weeks, after which the dose was tapered by 10 mg weekly. From the beginning of the 5th week, levamisole was introduced at a dose of 2 mg/kg per day. The duration of levamisole treatment was 17+/-7 months. Before starting levamisole treatment the mean level of proteinuria was 2.17+/-1.34 g/day and the relapse rate was 4.41/year. By the end of levamisole therapy, proteinuria had fallen to 0.142+/-0.211 g/day and the relapse rate to 0.41/year. No relapse occurred in 23 of the 34 patients during levamisole treatment. In the 24-month follow-up period after the discontinuation of levamisole, 28 children remained in total remission, while 6 had relapses. The cumulative steroid dose before levamisole therapy was 7,564.4+/-3,497.1 mg/year and following the introduction of levamisole 1,472.9+/-1,729.9 mg/year (P<0.0001). We observed reversible neutropenia in 5 patients, but no other side effects were seen. Our findings suggest that in FRNS and SDNS levamisole significantly reduces both the relapse rate and the cumulative steroid dose; therefore, it could be recommended for these patients. In SRNS patients it has also some benefit because proteinuria and the cumulative steroid dose could be reduced significantly.
Adjuvants, Immunologic↗
The anti-inflammatory effect of methylprednisolone occurs down-stream of nuclear factor-kappaB DNA binding in acute pancreatitis.
Glucocorticoids are potent anti-inflammatory drugs. The molecular mechanisms underlying these effects have not yet been fully revealed. The aim of the present study was to establish whether methylprednisolone pretreatment is beneficial and if it can block the pancreatic DNA binding of the transcription factor nuclear factor-kappaB (NF-kappaB) and proinflammatory cytokine synthesis during cholecystokinin-octapeptide (CCK)-induced acute pancreatitis in rats. Additionally, we set out to investigate the potential effects of methylprednisolone and CCK on pancreatic heat shock protein (HSP) synthesis. The dose-response (5-40 mg/kg) and time-course (6-72 h) curves of methylprednisolone on pancreatic HSP60 and HSP72 synthesis were evaluated following methylprednisolone treatment. We demonstrated that methylprednisolone specifically and dose-dependently induced HSP72 in the pancreas of rats, while it did not have a significant effect on HSP60 expression. The pancreatitis was induced near the peak level of HSP72 synthesis (2 x 30 mg/kg body weight [b.w.] methylprednisolone i.m. at an interval of 12 h, followed by a 12-h recovery period after the second injection of methylprednisolone) by administering 2 x 100 microg/kg CCK subcutaneously at an interval of 1 h. The injections of CCK in the vehicle-pretreated group significantly elevated the levels of pancreatic HSP60 and HSP72 2-4 h after the second CCK injection. Methylprednisolone pretreatment ameliorated many of the examined laboratory (the pancreatic weight/body weight [p.w./b.w.] ratio, the serum amylase activity, the plasma trypsinogen activation peptide concentration, the pancreatic levels of tumor necrosis factor-alpha and interleukin-6, the degree of lipid peroxidation, protein oxidation, nonprotein sulfhydryl group content and the pancreatic myeloperoxidase activity) and morphological parameters of the disease. Methylprednisolone pretreatment did not influence pancreatic NF-kappaB DNA binding, but decreased proinflammatory cytokine synthesis in this acute pancreatitis model. The findings suggest that the anti-inflammatory effect of large doses of methylprednisolone in secretagogue-induced pancreatitis occurs downstream of NF-kappaB DNA binding, and that increased pancreatic HSP72 synthesis may play a role in the protective effect of the drug.
Acute Disease↗
Nontoxic heat shock protein coinducer BRX-220 protects against acute pancreatitis in rats.
BACKGROUND: Nontoxic heat shock protein (HSP) inducer compounds open up promising therapeutic possibilities by activating one of the natural and highly conserved defense mechanisms of the organism. AIMS: In the present experiments, we examined the effects of a HSP coinducer drug-candidate, BRX-220, on the cholecystokinin-octapeptide (CCK)-induced acute pancreatitis in rats. METHODS: Male Wistar rats weighing 240 to 270 g were divided into two groups. In group B, 20 mg/kg BRX-220 was administered orally, followed by 75 microg/kg CCK subcutaneously three times, after 1, 3, and 5 h. This whole procedure was repeated for 5 d. The animals in group slashed circleB received physiological saline orally instead of BRX-220, but otherwise the protocol was the same as in group B. The rats were exsanguinated through the abdominal aorta 12 h after the last administration of CCK. We determined the serum amylase activity, the plasma trypsinogen activation peptide concentration, the pancreatic weight/body weight ratio, the DNA and total protein contents of the pancreas, the levels of pancreatic HSP60 and HSP72, the activities of pancreatic amylase, lipase, trypsinogen, and free radical scavenger enzymes (superoxide dismutase, catalase, and glutathione peroxidase), the degree of lipid peroxidation, protein oxidation, and the reduced glutathione level. Histopathological investigation of the pancreas was also performed in all cases. RESULTS: Repeated CCK treatment resulted in the typical laboratory and morphological changes of experimentally induced pancreatitis. The pancreatic levels of HSP60 and HSP72 were significantly increased in the animals treated with BRX-220. In group B, the pancreatic total protein content and the amylase and trypsinogen activities were significantly higher vs. group slashed circleB. The plasma trypsinogen activation peptide concentration, and the pancreatic lipid peroxidation, protein oxidation, and the activity of Cu/Zn-superoxide dismutase were significantly decreased in group B vs. group slashed circleB, whereas the glutathione peroxidase activity was increased. The morphological damage in group B was significantly lower than that in group slashed circleB. CONCLUSION: The HSP coinducer BRX-220, administered for 5 d, has a protective effect against CCK-induced acute pancreatitis.
Acute Disease↗
Induction of HSP72 by sodium arsenite fails to protect against cholecystokinin-octapeptide-induced acute pancreatitis in rats.
A number of investigators have demonstrated that the preinduction of heat-shock protein (HSP) expression (particularly HSP60 and HSP72) by hyper- or hypothermia may have a protective effect against cerulein-induced acute pancreatitis. The aim of the present study was to induce HSPs in the pancreas and lungs by thermal (hot-water immersion, HWI) and nonthermal methods (injection of sodium arsenite intraperitoneally) and to investigate the potential effects of HSP preinduction on cholecystokinin-octapeptide (CCK) induced acute pancreatitis and pancreatitis-associated lung injury in rats. The dose-response and time-effect curves observed following HWI and sodium arsenite treatments were evaluated. Animals were injected with 3 x 75 microg/kg CCK subcutaneously at intervals of 2 hr at the peak level of HSP synthesis, as determined by Western blot analysis. The rats were killed by exsanguination through the abdominal aorta 2 or 6 hr after the last CCK injection. HWI and the injection of sodium arsenite significantly elevated the expression of HSP72 in the pancreas and lungs, whereas they did not influence the levels of HSP60. Overall, HWI pretreatment had a protective effect against CCK-induced pancreatitis and pancreatitis-associated lung injury. In contrast, the nonthermal preinduction of HSP72 by sodium arsenite did not result in any beneficial effects on the measured parameters of the disease. The findings suggest that the preinduction of HSP72 is not sufficient to protect against CCK-induced acute pancreatitis and pancreatitis-associated lung injury or that the beneficial effect of hyperthermia may not be exclusively related to HSP72 expression.
Acute Disease↗
The effects of hypo- and hyperthermic pretreatment on sodium taurocholate-induced acute pancreatitis in rats.
INTRODUCTION: Heat shock proteins (HSPs) have indispensable functions in the synthesis, degradation, folding, transport, and translocation of intracellular proteins. HSPs are proteins that help cells to survive stress conditions by repairing damaged proteins. AIM: To investigate the potential effects of HSP preinduction by cold-water (CWI) or hot-water immersion (HWI) on sodium taurocholate (TC)-induced acute pancreatitis in rats. METHODOLOGY: TC was injected into the common biliopancreatic duct of the animals at the peak level of HSP synthesis, as determined by Western blot analysis. The rats were killed by exsanguination through the abdominal aorta 6 hours after the TC injection. The serum amylase activity, the IL-1, IL-6 and TNF-alpha levels, the pancreatic weight/body weight ratio, and the pancreatic contents of DNA, protein, amylase, lipase, and trypsinogen were measured, and a biopsy for histology was taken. RESULTS: HWI significantly elevated HSP72 expression, whereas CWI significantly increased HSP60 expression. It was demonstrated that CWI pretreatment ameliorated the pancreatic edema and the serum amylase level increase, whereas the morphologic damage was more severe in this form of acute pancreatitis. HWI pretreatment did not have any effects on the measured parameters in TC-induced pancreatitis. CONCLUSIONS: The findings suggest a possible role of HSP60, but not HSP72, in the slight protection in the early phase of this necrohemorrhagic pancreatitis model.
Amylases↗
Comparative effects of water immersion pretreatment on three different acute pancreatitis models in rats.
Cells respond to stress by upregulating the synthesis of cytoprotective heat shock proteins (HSPs) and antioxidant enzymes. The aim of this study was to compare the effects of cold (CWI) or hot water immersion (HWI) stress on three different acute pancreatitis models (cholecystokinin octapeptide (CCK), sodium taurocholate (TC), and L-arginine (Arg)). We examined the levels of pancreatic HSP60, HSP72, and antioxidants after the water immersion stress. Male Wistar rats were injected with CCK, TC, or Arg at the peak level of pancreatic HSP synthesis, as determined by Western blot analysis. HWI significantly elevated HSP72 expression and CWI significantly increased HSP60 expression in the pancreas. Water immersion stress decreased the levels of pancreatic antioxidants. CWI and-HWI pretreatment ameliorated most of the examined laboratory and morphological parameters of CCK-induced pancreatitis. CWI pretreatment decreased pancreatic edema and the serum amylase level; however, the morphological damage was more severe in TC-induced acute pancreatitis. Overall, CWI and HWI pretreatment only decreased the serum cytokine concentrations in Arg-induced pancreatitis. CWI and HWI resulted in differential induction of pancreatic HSP60 and HSP72 and the depletion of antioxidants. The findings suggest the possible roles of HSP60 and (or) HSP72 (but not that of the antioxidant enzymes) in the protection against CCK- and TC-induced acute pancreatitis. Unexpectedly, CWI pretreatment was detrimental to the morphological parameters of TC-induced pancreatitis. It was demonstrated that CWI and HWI pretreatment only influenced cytokine synthesis in Arg-induced pancreatitis.
Acute Disease↗