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Biomedical subjects

B Iványi

Publications and source records attributed to B Iványi.

At least 19 recordsLinked to original sources
PubMed2005

Peritubular capillary damage in acute humoral rejection: an ultrastructural study on human renal allografts.

The ultrastructural features of peritubular capillary (PC) damage was studied in 12 kidney allografts with acute humoral rejection (AHR). AHR manifested in diffuse linear PC staining for C4d, and histology consistent with Banff grade III in 7 recipients and Banff grade II in 5. Allografts with acute tubular necrosis served as controls. First biopsies (post-transplantation day 16.2 +/- 2.2): The intra-capillary exudate comprised monocytes (59%), polymorphonuclears (14%), lymphocytes (12%) and not otherwise specified mononuclears (15%). Three patterns of focal PC endothelial injury were observed: lysis, an increased rate of apoptosis and fragmentation. No correlation was found between the respective damage types and the inflammatory cell types or the Banff grades. Controls revealed endothelial swelling, detachment from basement membrane and fragmentation. Follow-up biopsies: Monocytes transformed into macrophages intra-luminally. The reparative changes comprised endothelial cytoplasmic protrusions, binucleated endothelial cells and capillary sprouts. Early transplant capillaropathy and transplant glomerulopathy were noted in 2 recipients. Literature data indicate that lysis is mediated by anti-HLA alloantibodies; apoptosis, demonstrated first in the present study, may be induced by non-HLA-type anti-endothelial antibodies. Fragmentation is caused by ischemia. Ongoing endothelial injury leads to transplant capillaropathy and transplant glomerulopathy, the characteristic lesions of chronic rejection.

Acute Disease↗
PubMed2002

Induction of heat shock proteins fails to produce protection against trypsin-induced acute pancreatitis in rats.

Heat shock proteins (HSPs) are necessary in the synthesis, degradation, folding, transport, and translocation of different proteins. It is well known that the increased expression of HSPs may have a protective effect against cerulein-induced pancreatitis in rats or against choline-deficient ethionine-supplemented diet model pancreatitis in mice. The aim of this study was to investigate the potential effects of HSP preinduction by cold or hot water immersion on trypsin-induced acute pancreatitis in rats. Trypsin was injected into the interlobular tissue of the duodenal part of the pancreas at the peak level of HSP synthesis, as determined by Western blot analysis. The rats were sacrificed by exsanguination through the abdominal aorta 6 h after the trypsin injection. The serum amylase activity, the tumor necrosis factor-alpha, interleukin-1, and interleukin-6 levels, the pancreatic weight/body weight ratio, and the pancreatic contents of DNA, protein, amylase, lipase, and trypsinogen were measured. A biopsy for histology was taken. Hot water immersion significantly elevated the HSP72 expression, while cold water immersion significantly increased the HSP60 expression. Cold water immersion pretreatment ameliorated the pancreatic edema in trypsin-induced pancreatitis, however this was not due to the HSP60. Hot water immersion pretreatment did not have any effect on the measured parameters in trypsin-induced pancreatitis. The findings suggest that the induction of HSP60 or HSP72 are not enough to protect rats against the early phase of this localized necrohemorrhagic pancreatitis model.

Amylases↗
PubMed2001

[The role of autopsy in verifying diagnostic accuracy at the intensive care unit].

The accuracy of the clinical diagnoses compared to the findings of an autopsy is a more relevant characteristic of the quality of care than the length of stay in the hospital or the daily costs of the stay. The aim of this retrospective study was: a) to compare the clinical and pathological diagnoses, b) to determine the amount of new information supplied by the autopsy and c) to determine wether the knowledge of correct clinical diagnosis would have resulted in a change of therapy. At the medical ICU 163 patients died during 1998, autopsy was performed in 110 cases. Agreement of clinical and pathological diagnoses and causes of death were retrospectively assessed by a board. Acute myocardial infarction accounted for 26% of deaths, pneumonia and respiratory insufficiency for 15%, cardiac failure for 14%, sepsis for 14%, stroke for 13%, pulmonary embolism for 5% and others for 13%. The accuracy of the clinical cause of death was proved in 81% of the cases. The main disease was diagnosed correctly in 86% of the cases. As a tool in quality control, the agreement of clinical and pathological diagnoses and causes of death proved to be good during the examined period of time.

Autopsy↗
PubMed2000

[Diffuse alveolar hemorrhage in systemic lupus erythematosus].

Of the 120 systemic lupus erythematosus (SLE) patients treated by the authors, two have developed diffuse alveolar haemorrhage. The authors' objective is to present this rare, but severe manifestation. Patients 1 and 2 were 66- and 22-year old women, respectively. Both had SLE with multi-organ involvements including diffuse proliferative lupus nephritis. Before the diagnosis of the disease, both patients had experienced pneumonitis that resolved on corticosteroid treatment. Soon after the diagnosis, respiratory failure, haemoptoea and acute anaemia developed, accompanied by a rapid deterioration in the general condition. Chest radiographs revealed bilateral, diffuse, alveolar infiltrates. The pulmonary haemorrhage temporarily ceased in response to corticosteroid treatment, but both patients later died in consequence of active SLE and mixed bacterial and fungal sepsis. Post mortem examination demonstrated fibrosing alveolitis and alveolar bleeding in Patient 1, and an immune complex deposition-induced alveolocapillary inflammation with alveolar haemorrhage in Patient 2. Diffuse alveolar haemorrhage is a life-threatening manifestation of SLE. Its onset may be preceded by episodes of pneumonitis resolving on corticosteroid treatment. An active diagnostic workup, intensive observation and aggressive immunosuppressive treatment are the cornerstones of the management. The early detection and the active treatment of secondary infections are obligatory. The authors consider the most difficult challenge to be the optimum coordination of the above treatment modalities.

Adult↗
PubMed2000

Lipoma of the liver: a differential-diagnostic problem.

BACKGROUND AND AIMS: Lipomatous tumors of the liver are extremely rare; most of them are found incidentally at autopsy. Appropriate methods of the diagnosis of these lesions are ultrasonography (US), computed tomography (CT) and biopsy. CASE REPORT: The case of a 65-year-old man who had undergone an upper-rectum resection because of exulcerated adenocarcinoma of the rectum is described. Six months later, routine control examination revealed a solid tumor in the left lobe of the liver. The tumor was not demonstrated by either sonography or CT before the operation. Repeated US, CT scan and fine-needle biopsy could not exclude the possibility of a metastatic tumor secondary to previous malignancy. The lesion was removed by wedge resection and was proven to be a lipoma. CONCLUSION: Despite adequate preoperative examination (CT, biopsy and US), an anamnestic adenocarcinoma of the rectum can lead to inappropriate therapy. The inadequate result of our therapeutic policy can be explained by the extremely rare incidence of lipoma of the liver.

Adenocarcinoma↗
PubMed2000

Peritubular capillaries in chronic renal allograft rejection: a quantitative ultrastructural study.

Peritubular capillaries (PCs) with a circumferentially multilayered basement membrane have been suggested as an ultrastructural indicator of chronic renal allograft rejection (CR). The authors validated this lesion as a marker for CR, by analyzing its quantitative features, specificity, and sensitivity in 169 renal biopsy specimens. The mean number of circumferential layers (PCcirc) and the incidences of the grades (mild: 2 to 4, moderate: 5 to 6, severe: 7 or more layers) were investigated in biopsy specimens involving CR (CR(Bx), n = 46), acute rejection (n = 11), normal kidneys (n = 20), psoriatics treated with cyclosporine (n = 13), renal transplants with chronic cyclosporine toxicity (n = 12), native kidney diseases (NKD, n = 56), and transplant nephrectomies attributable to CR (Cr(nephr), n = 11). CR was diagnosed with regard to the clinical features and the presence of intimal fibrosis in 41 biopsy specimens or transplant glomerulopathy in 35 biopsy specimens (cg; identified only by electron microscopy in 10 cases). NKD included chronic glomerulonephritis, chronic tubulointerstitial nephritis, benign nephrosclerosis, thrombotic microangiopathy, diabetic nephropathy, and renal disease in elderly patients (median age, 72 years). All PCs around glomeruli were sampled (median, 14 profiles per case). PCs with a moderate/ severe lesion appeared as serrated profiles with a thick, ribbon-like basement membrane layer in semithin plastic sections. The numbers of circumferentially multilayered PCs were significantly characteristic of CR (PCcirc in CR(Bx): 2.87+/-1.83 SD; range, 0 to 7.36; P < .001 v other groups). A severe lesion occurred exclusively in CR (in 12% of the PCs in CR(Bx), and in 38% in CRnephr). A moderate lesion was observed in 0.6% of the PCs in NKD, 16% in CR(Bx), and 21% in CRnephr. Three or more PCs with a moderate lesion were encountered only in CR. A mild lesion was not suggestive of CR at all. In CR(Bx), 27 cases showed a severe lesion or 3 or more PCs with a moderate lesion (cpc; sensitivity: 59%). Four of the 27 cases lacked cg. The cumulative incidence of cpc and cg was 85%. In transplants with cyclosporine toxicity, the presence of cpc verified the coexistence of CR in 7 specimens. In conclusion, cpc is a specific marker of CR. The incidence of cpc increases as CR progresses. The lesion may be caused by a low-grade rejection injury to the PCs. Careful analysis of semithin sections promotes the better sampling of cpc. An ultrastructural demonstration of cpc and cg defines CR more precisely than does light microscopic evaluation per se.

Adolescent↗
PubMed1998

[The role of ultrasonography and biopsy following kidney transplantation].

Several complications can occur during both the early and late postoperative periods after kidney transplantation. The methods used to follow up 575 kidney transplanted patients, (transplantations performed between October 1979 and November 1997) in the early (within 6 weeks) and late postoperative periods have been assessed. The diagnostic value of core biopsies and ultrasound examinations, the prevalence of complications, and the applicability of the diagnostic tools in the evaluation of the graft status and viability were analyzed. In the early postoperative period, graft rupture occurred more frequently after biopsy than in the late period (7.4% vs 0.82%), this leading graft loss in 18 of 20 cases. The sonographically diagnosed morphologic and functional changes were also analyzed. Sonography proved a very accurate method for the detection of perirenal fluid collections and masses and severe vascular complications. The data demonstrated that biopsy is indicated in the early postoperative period when the result of sonography is doubtful. In the late postoperative period, biopsy should be performed in every case.

Biopsy↗
PubMed1998

Childhood membranous nephropathy, circulating antibodies to the 58-kD TIN antigen, and anti-tubular basement membrane nephritis: an 11-year follow-up.

Childhood membranous nephropathy (MNP) with anti-tubular basement membrane (anti-TBM) nephritis is a rare disorder that may have extrarenal manifestations. This article describes a new case to be added to the 10 previously reported. A renal biopsy specimen from a 1-year-old white boy with nephrotic syndrome, microhematuria, and hypertension showed MNP (granular global IgG, IgA and C3, and segmental IgM and C1q) associated with hypercellularity and granular deposits of IgM and C1q in the mesangium, arteriolar IgA, and linear TBM IgG, IgA, and C3. A biopsy at age 4 years showed MNP (IgG and C3) and linear IgG and C3 along the TBM. Six months later, temporary glucosuria suggested a mild tubular dysfunction. Biopsy at age 8 years showed sclerosing MNP (IgG and C3), linear TBM IgG and C3, and chronic active tubulointerstitial nephritis (TIN). Indirect immunofluorescence showed circulating anti-TBM antibodies, and the enzyme-linked immunosorbent assay (ELISA) approach verified strong reactivity with the 58-kd TIN antigen. Despite trials with steroids, chlorambucil, azathioprine, and cyclosporine, end-stage renal disease developed by the age of 9 years. At age 10 years, the patient received a cadaveric kidney transplant. With the patient now aged 12 years, the graft is still functioning well, without any clinical evidence of disease recurrence. Neurological, ocular, and abdominal symptoms, including nonbacterial diarrhea, were observed during the follow-up period. The pathophysiology of these extrarenal symptoms remains unclear. Serotyping and genotyping of HLA antigens (A2, A10, B12, B41, DR5 [1101, 1103-4, 1106 or 1108-1113], DR6 [1303, 1312, or 1413], DRB3 [*0101 and 0201-2 or 0301], DQA1 [*0501 homozygous], and DQB1 [*0301 homozygous]) did not indicate any HLA association similar to those described previously in childhood MNP with anti-TBM nephritis (HLA-B7 in four patients, HLA-DR8 in two patients). The presented case is the fifth in the literature that displays reactivity with the 58-kd TIN antigen, and for which data on HLA antigens are reported.

Antibodies↗
PubMed1997

Mitochondrial mutation as a probable causative factor in familial progressive tubulointerstitial nephritis.

Renal biopsy of two children and a maternal relative, diagnosed with severe progressive tubulointerstitial nephritis, has shown the presence of distorted mitochondria. Mitochondrial DNA from the blood of these patients was analysed. No major deletions were found, but an A to G mutation was detected in position 5656. It is proposed that this mutation might play a causative role in the renal disease of the patients.

Adult↗
PubMed1996

Acute tubulointerstitial nephritis: phenotype of infiltrating cells and prognostic impact of tubulitis.

The prognostic impact of tubulitis and the phenotype of the infiltrating cells in the tubules were studied in ten percutaneous renal biopsies from six patients with acute tubulointerstitial nephritis (ATIN). The inflammatory cell subsets in the tubules and interstitium (CD3+, CD4+, CD8+, CD20+, CD45RO+, CD56+, CD57+, CD68+ and TIA-1+ cells), the expression of vimentin and the proliferation-associated antigen Ki-67 by cortical tubular cells, and the grade of tubulitis, interstitial infiltration and fibrosis were analysed. Cytotoxic injury to tubular cells in the vicinity of tubular-wall-localized lymphocytes was studied ultrastructurally. ATIN was drug-induced in three patients, related to Legionella infection in two and idiopathic in one patient. Four patients recovered, one with reduced renal function. Two patients developed end-stage renal disease. CD8+ and CD4+ lymphocytes, and a smaller number of macrophages, infiltrated the tubules. The predominant lymphocyte subset in the tubules was the same as in the interstitium. Cytotoxic injury to tubular cells was not seen electron microscopically. The tubular cells exhibited increased proliferative activity and expressed vimentin, indicating non-specific tubular damage. The cell subset, the severity of tubulitis, and the tubular expression of vimentin were not related to outcome. The main prognostic factor was the severity of the interstitial fibrosis. Tubulitis in ATIN may be a harmless non-immune reaction, mediated by tubular expression of cytokines, together with adhesion and other molecules.

Adult↗
PubMed1996

Quantitative ultrastructural study of afferent and efferent arterioles in IgA glomerulonephritis and benign nephrosclerosis.

Arteriolosclerosis frequently occurs in IgA nephritis (IgAN), and it is the hallmark of benign nephrosclerosis (BNS). The quantitative ultrastructure of juxtaglomerular arterioles is not known in these disorders. We examined afferent and efferent arterioles in renal biopsies from 25 adult patients with IgAN (hypertension at biopsy: 14 patients) and 9 patients with BNS. Six age-matched living renal transplant donors acted as controls. A systematic independent sample of profiles was obtained in thin sections taken at predetermined levels. The thickness of the media (myomedial cells plus the matrix) and the thickness of the medial matrix were estimated stereologically. From these estimates, the matrix/myomedia ratio was calculated. In IgAN with normotension or hypertension, the afferent media and its compartments did not exhibit significant thickening compared with the controls, whereas in BNS the afferent media and its layers were markedly and significantly thickened. The efferent media in IgAN and BNS displayed mild and significant thickening, with significant thickening of the matrix in BNS and IgAN with normotension. The matrix/myomedia ratio was not altered significantly in any group. The results indicate that the afferent arterioles are not the main sites of IgAN-related arteriolosclerosis, that arteriolosclerosis in IgAN and arteriolosclerosis in BNS are different lesions, and that increased efferent arteriolar thickness, demonstrated here for the first time in IgAN and BNS, might be a manifestation of angiotensin II-mediated autoregulatory efferent vasoconstriction exerted to maintain the glomerular filtration pressure.

Adolescent↗
PubMed1995

Tubulitis in primary vascular and glomerular renal disease.

A semiquantitative light microscopic study of 274 renal biopsy and 12 nephrectomy specimens was carried out to assess the frequency and severity of tubulitis (mononuclear leukocytes in the renal tubular wall) in all common glomerular diseases, diabetic nephropathy, renal amyloidosis and renal artery stenosis. The extent of interstitial inflammatory infiltrates and severity of interstitial fibrosis were also graded. Tubulitis was 1) frequent in crescentic glomerulonephritis (GN) with pauci-immune, linear and granular immune deposits, renal artery stenosis, diabetic nephropathy, lupus GN of WHO type IV, and IgA GN; 2) rare in minimal change and idiopathic membranous nephropathy; 3) usually severe in crescentic GN and renal artery stenosis; and 4) predominantly located in atrophic tubules in renal artery stenosis, diabetic nephropathy and IgA GN. The most important parameter for the grading of tubulitis was interstitial infiltration. However, no correlation was found between the grades of tubulitis, interstitial infiltrates and interstitial fibrosis in crescentic and lupus GN. It is suggested that renal ischemic injury, by eliciting expression of proinflammatory cytokines and neo-antigens in the tubulointerstitial space, might play a role in the development of tubulitis in vascular and glomerular renal diseases.

Diabetic Nephropathies↗
PubMed1994

[Comparative analysis of ultrasonic studies, histopathological data and clinical parameters in dysfunctioning renal transplantation].

The correlation of B mode and Doppler sonographic parameters and diagnoses established by histological examination of graft biopsies, nephrectomies and clinical data are discussed. 48 histological samples from 36 patients were reevaluated. The maximum interval between sonography and histology was 36 hours. The Banff classification criteria were used during histological examinations. Doppler examination evaluation was based on the resistance index (RI). Reproducibility was controlled by means of intra- and interobserver variability in 10 patients. RI values higher than 75% were regarded as abnormal. On the basis of these observations and the literature data specific sonographic features can be detected in renal artery occlusion and renal vein thrombosis. In pyelonephritis, dilatation of the collecting system was frequent. No morphological changes were detected in cyclosporin-A nephrotoxicity and the Doppler signs were not characteristic for this disease. No differentiation was found between acute rejection and acute tubular necrosis. The noninvasive duplex sonographic examinations can provide very important information regarding the flow situation of a transplanted kidney. In some cases a definitive diagnosis can be achieved, but in other cases biopsy is the method of choice.

Biopsy, Needle↗
PubMed1993

Segmental localization and quantitative characteristics of tubulitis in kidney biopsies from patients undergoing acute rejection.

The term tubulitis denotes infiltration of the renal tubular epithelium by mononuclear cells. Tubulitis is one of the most reliable signs of acute renal allograft rejection. However, its segmental localization and quantitative characteristics are not precisely known. To investigate this question, formalin-fixed kidney biopsy specimens from 15 patients with transplanted allografts undergoing acute rejection were studied stereologically by identifying cortical tubules with segment-specific markers. The periodic acid-Schiff reaction, peanut lectin, and antibodies against Tamm-Horsfall protein and epidermal cytokeratins, all applied to the same section, were used to identify the profiles of proximal tubules (PTs), distal convoluted tubules (DCTs), distal straight tubules (DSTs), and the cortical collecting system (CCS, connecting tubules and cortical collecting ducts), respectively. Two parameters, the relative intrasegmental length and the average intensity of tubular damage, were determined to describe the degree of tubulitis quantitatively. Tubulitis was most prominent in the DCTs, followed by the CCS. The average intensity of tubulitis was lowest in the DSTs. The results indicate that the PTs are not the main site of tubulitis, despite the fact that they are regarded primary targets of the rejection response.

Adolescent↗
PubMed1993

Development of chronic renal failure in patients with multiple myeloma.

Glomerulotubular disconnections at the immediate postglomerular segment of the proximal tubules, accounting for an impaired renal function, were demonstrated recently in several chronic nonglomerular renal disorders. To analyze the glomerulotubular junctions in Bence Jones cast nephropathy, paraffin blocks from the kidneys of nine deceased patients with myeloma and chronic renal failure on whom autopsies were performed were studied in serial sections. Kidneys from seven deceased patients without renal disease on whom autopsies also were done served as controls. For stereological estimations, the percentages of patent and sclerosed glomerular profiles, the relative volume fractions, and the absolute volumes of the interstitium, tubules, and glomeruli were determined. In Bence Jones cast nephropathy, 96% of the glomerular profiles were patent, and the reconstruction of randomly chosen glomerulotubular junctions revealed that 84% of the patent glomeruli had normal tubular connections. There was an increased relative interstitial volume (fibrous tissue) and a decreased relative tubular volume. The absolute values indicated severe interstitial fibrosis, but not tubular atrophy. The results show that in contrast with other chronic nonglomerular nephropathies, chronic renal failure in Bence Jones cast nephropathy does not result from nephron disconnection at the immediate postglomerular segment of the proximal tubules. The main factor responsible for the decrease in renal function appears to be the progressive severe fibrosis of the interstitium.

Adult↗
PubMed1992

[Simultaneous occurrence of persistent hematuria (thin basement membrane nephropathy) and light-chain proteinuria (benign monoclonal gammopathy) in a middle-aged male].

IgG lambda type of monoclonal gammopathy and thin basement membrane nephropathy were established in a middle-aged man examined because of persistent haematuria, lambda light-chain proteinuria and moderately diminished renal function. A 10% level of plasmocytosis was verified by bone-marrow aspiration. The more than 6-year follow-up showed the gammopathy to be benign. The thin basement membrane nephropathy was verified by electronmicroscopic analysis of renal tissue obtained by percutaneous renal biopsy: lamina densa of the glomerular capillaries thinned to 30-100 nm. In spite of the usually good outcome of thin basement membrane nephropathy, in this case it was accompanied by glomerular sclerosis, subsequent destruction of nephrons, hypertensive vascular alterations and a clinical deterioration of the renal function after 4 years. A rebiopsy excluded the possible complications (amyloidosis, non-amyloid immunoglobulin nephropathy, cylinder nephropathy, etc) of light-chain proteinuria.

Adult↗