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Arpád Czifra,
Alida Páll,
Julianna Kulcsár,
Kitti Barta,
Attila Kertész,
György Paragh,
István L Rincz,
Zoltán Jenei,
Anupam Agarwal,
Abolfazl Zarjou, József Balla,
Zoltán Szabó
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ABSTRACT: BACKGROUND: Renal replacement therapy may have a favorable effect on diastolic left ventricular function, but it is not clear whether hemodiafiltration is superior to hemodialysis in this field. Nitric oxide (NO) and asymmetric dimethylarginine (ADMA) may play a role in the changes of intracardiac hemodynamics, but it is not clear whether the different renal replacement methods have disparate influence on the metabolism of these materials. METHODS: Thirty patients on renal replacement therapy were investigated. First, data was analyzed while patients received hemodiafiltration over a period of three months. Then, the same patients were evaluated during treatment with hemodialysis for at least another three months. Echocardiography was performed before and after renal replacement therapy. RESULTS: No significant difference was found in the volume removals between hemodialysis and hemodiafiltration. The left atrial diameter and transmitral flow velocities (E/A) decreased significantly only during hemodiafiltration. A positive correlation was observed between the left atrial diameter and E/Ea representing the left ventricular pressure load during hemodiafiltration. Significant correlations between NO and A and E/A were observed only in the case of hemodiafiltration. CONCLUSION: Hemodiafiltration has a beneficial effect on echocardiographic markers representing left ventricular diastolic function. This could be attributed to the differences between the dynamics of volume removal and its distribution among liquid compartments.
BMC Nephrology 04/2013; 14(1):76. · 2.18 Impact Factor
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Tamás Emri,
Viktória Tóth,
Csilla Terézia Nagy,
Gábor Nagy,
Imre Pócsi,
Gyöngyi Gyémánt,
Károly Antal, József Balla,
György Balla,
Gyula Román,
István Kovács,
István Pócsi
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ABSTRACT: BACKGROUND: Fungal siderophores are likely to possess atheroprotective effects in humans, and therefore studies are needed to develop siderophore-rich food additives or functional foods to increase the siderophore uptake in people prone to cardiovascular diseases. In this study the siderophore contents of mould-ripened cheeses and meat products were analysed and the coprogen production by Penicillium nalgiovense was characterised. RESULTS: High concentrations of hexadentate fungal siderophores were detected in penicillia-ripened Camembert- and Roquefort-type cheeses and also in some sausages. In one sausage fermented by P. nalgiovense, the siderophore content was comparable to those found in cheeses. Penicillium nalgiovense produced high concentrations of coprogen in submerged cultures, which were affected predominantly by the available carbon and nitrogen sources under iron starvation. Considerable coprogen yields were still detectable in the presence of iron when the fermentation medium was supplemented with the iron chelator Na(2) -EDTA or when P. nalgiovense was co-cultivated with Saccharomyces cerevisiae. CONCLUSION: These data may be exploitable in the future development of high-siderophore-content foods and/or food additives. Nevertheless, the use of P. nalgiovense fermentation broths for these purposes may be limited by the instability of coprogen in fermentation media and by the β-lactam production by the fungus. © 2012 Society of Chemical Industry.
Journal of the Science of Food and Agriculture 12/2012; · 1.44 Impact Factor
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Katalin Judit Szabó,
Róza Adány, József Balla,
Zoltán Balogh,
Zoltán Boda,
István Edes,
István Fekete,
Miklós Káplár,
János Mátyus,
László Oláh,
Sándor Olvasztó,
György Paragh,
Dénes Páll,
György Pfliegler,
Gusztáv Vajda,
Margit Zeher,
László Csiba
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ABSTRACT: Atherosclerosis is a systemic disease affecting the coronary, carotid, intracerebral, renal and peripherial arteries. The early morphological and functional impairments could be detected in the second or third decades of life and their progression depend on the number and severity of risk factors and individual susceptility. Although the vascular risk factors (smoking, overweight, age, unhealthy diet, lack of physical exercise, hypertension, diabetes mellitus, chronic kidney disease and dyslipidemia) are the same and common in the different vascular diseases, the present clinical routine artificially classifies the diagnosis and therapy of different vascular diseases into different subfields of medicine with the negative impact of possible polypragmasia. Recently, worldwide health surveys (e.g. REACH registry) have proven the usefulness of a holistic approach in the diagnosis and therapy of multiorgan-affected vascular patients. This review summarizes the multidisciplinary advances and future perspective of vascular diseases.
Orvosi Hetilap 04/2012; 153(13):483-98.
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ABSTRACT: Osteoblastic differentiation of vascular smooth muscle cells (VSMCs) is involved in the pathogenesis of vascular calcification. Hydrogen sulfide (H(2)S) is a gas endogenously produced by cystathionine γ-lyase in VSMC. Here we determined whether H(2)S plays a role in phosphate-induced osteoblastic transformation and mineralization of VSMC. Hydrogen sulfide was found to inhibit calcium deposition in the extracellular matrix and to suppress the induction of the genes involved in osteoblastic transformation of VSMC: alkaline phosphatase, osteocalcin, and Cbfa1. Moreover, phosphate uptake and phosphate-triggered upregulation of the sodium-dependent phosphate cotransporter (Pit-1) were also prevented by H(2)S. Reduction of endogenous production of H(2)S by inhibition of cystathionine γ-lyase activity resulted in increased osteoblastic transformation and mineralization. Low plasma levels of H(2)S, associated with decreased cystathionine γ-lyase enzyme activity, were found in patients with chronic kidney disease receiving hemodialysis. Thus, H(2)S is a potent inhibitor of phosphate-induced calcification and osteoblastic differentiation of VSMC. This mechanism might contribute to accelerated vascular calcification in chronic kidney disease.
Kidney International 06/2011; 80(7):731-9. · 6.61 Impact Factor
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ABSTRACT: Renal transplantation (RTx) is the treatment of choice for end-stage renal failure, but these patients are increasingly older and have additional conditions leading to high mortality after RTx. The aim of our study was to validate a Spanish prognostic function that estimates survival in Hungarian renal transplant recipients.
We estimated the 5-year survival of 339 patients who received a cadaver kidney between 1 January 1991 and 15 September 2004 at the Center of Transplantation, Medical and Health Science Centre, University of Debrecen, and who were followed up until death or 15 September 2009. To assess the calibration, we used the Hosmer-Lemeshow test to compare the observed and expected numbers of deaths in the deciles of the predicted 5-year risk of death. Additionally, we applied a smoother to obtain a nonparametric estimate of the 5-year cumulative incidence of death by robust locally weighted regression. To describe the discriminative power of the function, we calculated the area under the receiver operating characteristic (ROC) curve.
The range of the estimated 5-year risk of death was 7%-100%. In the high-risk groups, the function severely overestimated the risk of death. The area under the ROC curve was 0.65 (95% confidence interval, 0.60-0.70).
The poor performance of the prognostic function studied limits its clinical applicability.
Journal of nephrology 05/2011; 24(5):619-24. · 1.65 Impact Factor
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ABSTRACT: Iron is essential for almost all living organisms. It participates in a wide variety of fundamental metabolic processes, including
oxygen transport, DNA synthesis, and electron transport. However, when present in excess, iron poses a threat to cells and
tissues. The toxicity of iron is largely based on its ability to catalyze the generation of free radicals, which attack and
damage cellular membranes, protein, and DNA. Under physiological circumstances this threat is reduced because meticulously
regulated mechanisms have evolved to move iron across biological membranes and to ensure that its distribution in multicellular
organisms is carefully orchestrated. These mechanisms are responsible to keep free iron concentrations at the lowest sufficient
level under healthy conditions. High tissue iron concentrations have been associated with the development and progression
of several pathological conditions, including certain cancers, liver and cardiovascular diseases, diabetes, hormonal derangements,
skeletal abnormalities, several neurodegenerative disorders, and immune system dysfunctions. In this chapter, we discuss oxidative
stress related to iron metabolism and provide an overview of several diseases that are linked to iron overload and toxicity.
KeywordsDiabetic nephropathy-Proteinuria-Endocytosis-Albumin-Carbonic anhydrase type III
12/2010: pages 205-228;
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ABSTRACT: Multipotent mesenchymal stem cells (MSC) have become a popular and promising therapeutic approach in many clinical conditions. MSC are beneficial in animal models of acute kidney injury (AKI), by mediating differentiation-independent paracrine properties, and have prompted ongoing clinical trials to evaluate the safety and efficacy of MSC. Heme oxygenase-1 (HO-1) is induced in response to stress including AKI and has important anti-apoptotic, anti-inflammatory, and proangiogenic properties in these settings. We therefore examined whether HO-1 plays a role in the beneficial effects of MSC in AKI. We isolated MSC from bone marrow of age-matched HO-1+/+ and HO-1-/- mice. Our studies indicate that while differentiation of MSC into osteo- and adipocytic lineages did not differ between cells isolated from HO-1+/+ and HO-1-/- mice, MSC from HO-1-/- mice had significantly lower angiogenic potential. Moreover, HO-1-/- MSC demonstrated reduced expression and secretion of several important growth and proangiogenic factors (stromal cell-derived factor-1, vascular endothelial growth factor-A, and hepatocyte growth factor) compared with MSC derived from HO-1+/+ mice. In addition, conditioned medium of HO-1+/+ MSC rescued functional and morphological changes associated with cisplatin-induced AKI, while the HO-1-/--conditioned medium was ineffectual. Our studies indicate that HO-1 plays an important role in MSC-mediated protection. The results expand understanding of the renoprotective effects of MSC and may provide novel strategies to better utilize MSC in various disease models.
AJP Renal Physiology 11/2010; 300(1):F254-62. · 4.42 Impact Factor
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Emoke Nagy,
John W Eaton,
Viktória Jeney,
Miguel P Soares,
Zsuzsa Varga,
Zoltán Galajda,
József Szentmiklósi,
Gábor Méhes,
Tamás Csonka,
Ann Smith,
Gregory M Vercellotti,
György Balla, József Balla
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ABSTRACT: We investigated whether red cell infiltration of atheromatous lesions promotes the later stages of atherosclerosis.
We find that oxidation of ferro (FeII) hemoglobin in ruptured advanced lesions occurs generating ferri (FeIII) hemoglobin and via more extensive oxidation ferrylhemoglobin (FeIII/FeIV=O). The protein oxidation marker dityrosine accumulates in complicated lesions, accompanied by the formation of cross-linked hemoglobin, a hallmark of ferrylhemoglobin. Exposure of normal red cells to lipids derived from atheromatous lesions causes hemolysis and oxidation of liberated hemoglobin. In the interactions between hemoglobin and atheroma lipids, hemoglobin and heme promote further lipid oxidation and subsequently endothelial reactions such as upregulation of heme oxygenase-1 and cytotoxicity to endothelium. Oxidative scission of heme leads to release of iron and a feed-forward process of iron-driven plaque lipid oxidation. The inhibition of heme release from globin by haptoglobin and sequestration of heme by hemopexin suppress hemoglobin-mediated oxidation of lipids of atheromatous lesions and attenuate endothelial cytotoxicity.
The interior of advanced atheromatous lesions is a prooxidant environment in which erythrocytes lyse, hemoglobin is oxidized to ferri- and ferrylhemoglobin, and released heme and iron promote further oxidation of lipids. These events amplify the endothelial cell cytotoxicity of plaque components.
Arteriosclerosis Thrombosis and Vascular Biology 04/2010; 30(7):1347-53. · 6.37 Impact Factor
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ABSTRACT: Hemochromatosis is a known cause of osteoporosis, and iron overload has deleterious effects on bone. Although iron overload and its association with osteoporosis has long been recognized, the pathogenesis and exact role of iron have been undefined. Bone is an active tissue with constant remodeling capacity. Osteoblast (OB) development and maturation are under the influence of core binding factor alpha-1 (CBF-alpha1), which induces expression of OB-specific genes, including alkaline phosphatase, an important enzyme in early osteogenesis, and osteocalcin, a noncollagenous protein deposited within the osteoid. This study investigates the mechanism by which iron inhibits human OB activity, which in vivo may lead to decreased mineralization, osteopenia, and osteoporosis. We demonstrate that iron-provoked inhibition of OB activity is mediated by ferritin and its ferroxidase activity. We confirm this notion by using purified ferritin H-chain and ceruloplasmin, both known to possess ferroxidase activity that inhibited calcification, whereas a site-directed mutant of ferritin H-chain lacking ferroxidase activity failed to provide any inhibition. Furthermore, we are reporting that such suppression is not restricted to inhibition of calcification, but OB-specific genes such as alkaline phosphatase, osteocalcin, and CBF-alpha1 are all downregulated by ferritin in a dose-responsive manner. This study corroborates that iron decreases mineralization and demonstrates that this suppression is provided by iron-induced upregulation of ferritin. In addition, we conclude that inhibition of OB activity, mineralization, and specific gene expression is attributed to the ferroxidase activity of ferritin.
Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research 10/2009; 25(1):164-72. · 6.04 Impact Factor
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ABSTRACT: Vascular calcification plays a role in the pathogenesis of atherosclerosis, diabetes, and chronic kidney disease. Human aortic smooth muscle cells (HSMCs) undergo mineralization in response to elevated levels of inorganic phosphate (Pi) in an active and well-regulated process. This process involves increased activity of alkaline phosphatase and increased expression of core binding factor alpha-1, a bone-specific transcription factor, with the subsequent induction of osteocalcin. Mounting evidence suggests an essential role for the heme oxygenase 1 (HO-1)/ferritin system to maintain homeostasis of vascular function. We examined whether induction of HO-1 and ferritin alters mineralization of HSMCs provoked by high Pi. Upregulation of the HO-1/ferritin system inhibited HSMC calcification and osteoblastic differentiation. Of the products of the system, only ferritin and, to a lesser extent, biliverdin were responsible for the inhibition. Ferritin heavy chain and ceruloplasmin, which both possess ferroxidase activity, inhibited calcification; a site-directed mutant of ferritin heavy chain, which lacked ferroxidase activity, failed to inhibit calcification. In addition, osteoblastic transformation of HSMCs provoked by elevated Pi (assessed by upregulation of core binding factor alpha-1, osteocalcin, and alkaline phosphatase activity) was diminished by ferritin/ferroxidase activity. We conclude that induction of the HO-1/ferritin system prevents Pi-mediated calcification and osteoblastic differentiation of human smooth muscle cells mainly via the ferroxidase activity of ferritin.
Journal of the American Society of Nephrology 06/2009; 20(6):1254-63. · 9.66 Impact Factor
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ABSTRACT: The concentrations of essential metal ions in various compartments of the human body are accurately regulated (homeostasis). Irregularities in the accumulation or depletion of the trace elements may lead to well characterized diseases. This review covers the metabolism of zinc regulations by which the intracellular and extracellular levels are kept in physiological range, biological functions, as well as pathological states that develop in its altered metabolism. The focus is on the molecular mechanisms of zinc ion traffic between compartments of the body and cells and their sequestration, gene regulations that regulate the ion fluxes via biological membranes and their storage, zinc-mediated cell and tissue damages, and development of symptoms in zinc deficiency is also discussed.
Orvosi Hetilap 05/2009; 150(15):681-7.
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ABSTRACT: Heme-mediated oxidative modification of low-density lipoprotein (LDL) plays a crucial role in early atherogenesis. It has been shown that hydrogen sulfide (H(2)S) produced by vascular smooth muscle cells is present in plasma at a concentration of about 50 micromol/L. H(2)S is a strong reductant which can react with reactive oxygen species like superoxide anion and hydrogen peroxide. The current study investigated the effect of H(2)S on hemin-mediated oxidation of LDL and oxidized LDL (oxLDL)-induced endothelial reactions. H(2)S dose dependently delayed the accumulation of lipid peroxidation products-conjugated dienes, lipid hydroperoxides (LOOH), and thiobarbituric acid reactive substances-during hemin-mediated oxidation. Moreover, H(2)S decreased the LOOH content of both oxidized LDL and lipid extracts derived from soft atherosclerotic plaque, which was accompanied by reduced cytotoxicity. OxLDL-mediated induction of the oxidative stress responsive gene, heme oxygenase-1, was also abolished by H(2)S. Finally we have shown that H(2)S can directly protect endothelium against hydrogen peroxide and oxLDL-mediated endothelial cytotoxicity. These results demonstrate novel functions of H(2)S in preventing hemin-mediated oxidative modification of LDL, and consequent deleterious effects, suggesting a possible antiatherogenic action of H(2)S.
Free radical biology & medicine 01/2009; 46(5):616-23. · 5.42 Impact Factor
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ABSTRACT: Iron-mediated oxidation of low-density lipoprotein has been implicated in the pathogenesis of vascular disorders such as atherosclerosis. The present investigations were performed to test whether hydrophobic fungal siderophores - hexadentate trihydroxamates desferricoprogen, desferrichrome, desferrirubin, and desferrichrysin - might suppress heme-catalyzed LDL oxidation and the toxic effects of heme-treated LDL on vascular endothelium. Indeed, two of these - desferricoprogen and desferrichrome - markedly increased the resistance of LDL to heme-catalyzed oxidation. In similar dose-response fashion, these siderophores also inhibited the generation of LDL products cytotoxic to human vascular endothelium. When iron-free fungal siderophores were added to LDL/heme oxidation reactions, the product failed to induce heme oxygenase-1, a surrogate marker for the noncytocidal effects of oxidized LDL (not in the case of desferrichrysin). Desferricoprogen also hindered the iron-mediated peroxidation of lipids from human atherosclerotic soft plaques in vitro, and was taken up in the gastrointestinal tract of rat. The absorbed siderophore was accumulated in the liver and was secreted in its iron-complexed form in the feces and urine. The consumption of mold-ripened food products such as aged cheeses and the introduction of functional foods and food additives rich in fungal iron chelators in diets may lower the risk of cardiovascular diseases.
Molecular Nutrition & Food Research 12/2008; 52(12):1434-47. · 4.30 Impact Factor
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ABSTRACT: Malaria, the disease caused by Plasmodium infection, is endemic to poverty in so-called underdeveloped countries. Plasmodium falciparum, the main infectious Plasmodium species in sub-Saharan countries, can trigger the development of severe malaria, including cerebral malaria, a neurological syndrome that claims the lives of more than one million children (<5 years old) per year. Attempts to eradicate Plasmodium infection, and in particular its lethal outcomes, have so far been unsuccessful. Using well-established rodent models of malaria infection, we found that survival of a Plasmodium-infected host is strictly dependent on the host's ability to up-regulate the expression of heme oxygenase-1 (HO-1 encoded by the gene Hmox1). HO-1 is a stress-responsive enzyme that catabolizes free heme into biliverdin, via a reaction that releases Fe and generates the gas carbon monoxide (CO). Generation of CO through heme catabolism by HO-1 prevents the onset of cerebral malaria. The protective effect of CO is mediated via its binding to cell-free hemoglobin (Hb) released from infected red blood cells during the blood stage of Plasmodium infection. Binding of CO to cell-free Hb prevents heme release and thus generation of free heme, which we found to play a central role in the pathogenesis of cerebral malaria. We will address hereby how defense mechanisms that prevent the deleterious effects of free heme, including the expression of HO-1, impact on the pathologic outcome of Plasmodium infection and how these may be used therapeutically to suppress its lethal outcomes.
Journal of Molecular Medicine 10/2008; 86(10):1097-111. · 4.67 Impact Factor
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ABSTRACT: Nowadays chronic kidney disease has become a major public health problem due to the great increase in atherogenic nephropathies. In the absence of classic renal symptoms, chronic kidney disease is mostly diagnosed when renal failure is already advanced, although it can be revealed by laboratory tests in the earlier stages. When diagnosis is late, the progression to end-stage renal failure is unavoidable and renal replacement therapy is needed. Even early-moderate renal failure significantly increases the risks for atherosclerosis, thereby leading to the deaths of patients from cardiovascular disease before initiation of dialysis. Therefore screening for asymptomatic chronic kidney disease is urgently needed. Estimated glomerular filtration rate has the greatest importance in the screening and in the timely intervention to slow down the progression of renal failure and cardiovascular disease. In 2005, the Hungarian Society of Nephrologists and the Hungarian Society of Laboratory Medicine suggested the automatic estimation and reporting of glomerular filtration rate, each time serum creatinine measurements were made. This practice is used more frequently by laboratories in Hungary. This article aims to help facilitate the utilization and evaluation of estimated glomerular filtration rate.
Orvosi Hetilap 02/2008; 149(2):77-82.
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ABSTRACT: Iron-derived reactive oxygen species are involved in the pathogenesis of numerous vascular disorders. One abundant source of redox active iron is heme, which is inherently dangerous when it escapes from its physiologic sites. Here, we present a review of the nature of heme-mediated cytotoxicity and of the strategies by which endothelium manages to protect itself from this clear and present danger. Of all sites in the body, the endothelium may be at greatest risk of exposure to heme. Heme greatly potentiates endothelial cell killing mediated by leukocytes and other sources of reactive oxygen. Heme also promotes the conversion of low-density lipoprotein to cytotoxic oxidized products. Hemoglobin in plasma, when oxidized, transfers heme to endothelium and lipoprotein, thereby enhancing susceptibility to oxidant-mediated injury. As a defense against such stress, endothelial cells upregulate heme oxygenase-1 and ferritin. Heme oxygenase opens the porphyrin ring, producing biliverdin, carbon monoxide, and a most dangerous product-redox active iron. The latter can be effectively controlled by ferritin via sequestration and ferroxidase activity. These homeostatic adjustments have been shown to be effective in the protection of endothelium against the damaging effects of heme and oxidants; lack of adaptation in an iron-rich environment led to extensive endothelial damage in humans.
Antioxidants and Redox Signaling 01/2008; 9(12):2119-37. · 8.46 Impact Factor
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Márton Mohás,
Nóra Szigeti,
Lajos Markó,
Gergo A Molnár,
Judit Cseh,
Boglárka Laczy,
Mónika Tamaskó, József Balla,
János Kappelmayer,
László Wagner,
Zoltán Wagner,
Botond Csiky,
Judit Nagy,
István Wittmann
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ABSTRACT: Proteinuria, hypoproteinaemia, hypoalbuminaemia and oedema are major characteristics of nephrotic syndrome. Aims of this study were to detect serum total LDH activity and its isozymes in nephrotic syndrome.
In a cross-sectional study, clinical parameters were compared in three cohorts, namely kidney patients with or without nephrotic syndrome and hypoalbuminaemic controls (NEPHR, NON-NEPHR, CONTR, respectively).
Serum total LDH activity in the NEPHR group was increased compared with the NON-NEPHR and CONTR groups (p < 0.001) and correlated with serum total protein (r = -0.549, p < 0.001), serum albumin (r = -0.596, p < 0.001), proteinuria (r = 0.456, p < 0.001) and serum total cholesterol (r = 0.523, p < 0.001). LDH isozyme pattern was analysed in three subgroups of the patients. Serum LDH-2 activity was higher in the NEPHR subgroup compared with the NON-NEPHR and CONTR subgroups (p < 0.001). Serum LDH-2 activity correlated with serum total protein (r = -0.665, p < 0.001), serum albumin (r = -0.615, p < 0.001), proteinuria (r = 0.694, p < 0.001), and serum total cholesterol (r = 0.723, p < 0.001). Linear regression analysis revealed that serum total protein proved to be an independent predictor of serum total LDH activity, while serum total protein and proteinuria were predictors of LDH-2.
These findings suggest that serum total LDH activity might be a marker of the activity of the nephrotic syndrome.
Kidney and Blood Pressure Research 01/2008; 31(1):47-54. · 1.46 Impact Factor
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ABSTRACT: The authors review the case of their young patient, who underwent a lung transplantation in Vienna because of an end stage idiopathic pulmonary fibrosis. During the prolonged postoperative phase renal failure full of complications developed, which necessitated haemodialysis. As the pulmonological rehabilitation was complete, but the regular dialyses considerably raised the risk of opportunistic infections, and also significantly reduced the quality of life of the patient, renal transplantation was performed in Debrecen four years after the lung transplantation. This is the first lung transplanted patient in Hungary who also underwent renal transplantation. Now, more than two years after the renal transplantation the patient lives a compensated, rehabilitated life, the respiratory function values have improved and the renal function values are also acceptable. The number of transplanted patients has significantly increased in recent years worldwide, and also in Hungary. However, due to immunosuppressive medications, calcineurin inhibitors mainly, numerous complications must be reckoned with. An outstanding one among them is the secondary renal failure which may occur both in acute and chronic form and may even necessitate renal transplantation. Renal transplantation is an excellent treatment option for end stage renal failure patients, who had received another organ transplant earlier. Kidney transplantation improves quality of life and increases expected survival, too.
Orvosi Hetilap 12/2007; 148(45):2147-51.
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ABSTRACT: Iron is essential for all living organism, although in excess amount it is dangerous via catalyzing the formation of reactive oxygen species. Absorption of iron is strictly controlled resulting in a fine balance of iron-loss and iron-uptake. In countries where the ingestion of heme-iron is significant by meal, great part of iron content in the body originates from heme. Heme derived from food is absorbed by a receptor-mediated manner by enterocytes of small intestine then it is degraded in a reaction catalyzed by heme oxygenase. Iron released from the porphyrin ring leaves enterocytes as transferrin associated iron. Prosthetic group of several proteins contains heme, therefore, it is synthesized by all cells. One of the most significant heme proteins is hemoglobin which transports oxygen in the erythrocytes. Hemoglobin released from erythrocyte during intravascular hemolysis binds to haptoglobin and is taken up by cells of the monocyte-macrophage lineage. Oxidation of hemoglobin (ferro) to methemoglobin (ferri) is inhibited by the structure of hemoglobin although it is not hindered. Superoxide anion is also formed in the reaction that initiates further free radical reactions. In contrast to ferrohemoglobin, methemoglobin readily releases heme, therefore, oxidation of hemoglobin drives the formation of free heme in plasma. Heme binds to a plasma protein, hemopexin, and is internalized by cells of monocyte-macrophage lineage in a receptor-mediated manner, then degraded in reaction catalysed by heme oxygenase. Heme is also taken up by plasma lipoproteins and endothelial cells leading to oxidation of LDL and subsequent endothelial cell damage. The purpose of this work was to summarize the processes related to heme.
Orvosi Hetilap 10/2007; 148(36):1699-706.
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Andrea Fekete,
Tamás Emri,
Agnes Gyetvai,
Zoltán Gazdag,
Miklós Pesti,
Zsuzsa Varga, József Balla,
Csaba Cserháti,
Levente Emody,
Lajos Gergely,
István Pócsi
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ABSTRACT: We tested the hypothesis that adaptation of Candida albicans to chronic oxidative stress inhibits the formation of hyphae and reduces pathogenicity. Candida albicans cells were exposed to increasing concentrations of t-butylhydroperoxide (tBOOH), a lipid peroxidation-accelerating agent, and mutants with heritable tBOOH tolerance were isolated. Hypha formation by the mutants was negligible on Spider agar, indicating that the development of oxidative stress tolerance prevented Candida cells from undergoing dimorphic switches. One of the mutants, C. albicans AF06, was five times less pathogenic in mice than its parental strain, due to its reduced germ tube-, pseudohypha- and hypha-forming capability, and decreased phospholipase secretion. An increased oxidative stress tolerance may therefore be disadvantageous when this pathogen leaves blood vessels and invades deep organs. The AF06 mutant was characterized by high intracellular concentrations of endogenous oxidants, reduced monounsaturated and polyunsaturated fatty acid contents, the continuous induction of the antioxidative defense system, decreased cytochrome c-dependent respiration, and increased alternative respiration. The mutation did not influence growth rate, cell size, cell surface, cellular ultrastructures, including mitochondria, or recognition by human polymorphonuclear leukocytes. The selection of oxidative stress-tolerant respiratory Candida mutants may also occur in vivo, when reduced respiration helps the fungus to cope with antimycotic agents.
FEMS Yeast Research 10/2007; 7(6):834-47. · 2.40 Impact Factor
