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Biomedical subjects

Judit Nagy

Publications and source records attributed to Judit Nagy.

At least 19 recordsLinked to original sources
PubMed2006

Serum carboxymethyllysine predicts mortality in hemodialysis patients.

BACKGROUND: Hemodialysis patients show markedly elevated serum levels of advanced glycation end products (AGEs). AGEs have been implicated in the pathogenesis of vascular damage and are regarded as a class of uremic toxins. However, to date, serum AGE level could not be identified as an independent predictor of mortality. The aim of the present study is to test whether serum level of the AGE carboxymethyllysine (CML) predicts all-cause or cardiovascular mortality in hemodialysis patients. METHODS: Serum total CML concentration was measured by means of enzyme-linked immunosorbent assay in 154 patients receiving long-term hemodialysis. Patients were divided into groups with serum CML levels less and greater than the median (23.8 ng/mg protein). All-cause and cardiovascular mortality were registered during a follow-up of 51 months. The relationship between serum CML level and mortality was tested by using Kaplan-Meier and Cox regression analyses. RESULTS: In the group with low serum CML levels, 38% of patients died during the follow-up period; 23% had a cardiovascular cause of death. However, in the group with high CML levels, 58% died (P < 0.01) and 36% had a cardiovascular cause of death (P < 0.05). The following parameters proved to be independent risk factors of all-cause mortality: age (hazard ratio, 1.056; P < 0.001), preexisting vascular disease (hazard ratio, 2.53; P < 0.05), smoking (hazard ratio, 3.03; P < 0.005), high serum CML level (hazard ratio, 1.776; P < 0.05), and C-reactive protein level (hazard ratio, 1.017; P < 0.001). CONCLUSION: The AGE CML may contribute to increased mortality in patients with uremia.

Adult↗
PubMed2006

[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↗
PubMed2005

[Contrast medium induced nephropathy].

Contrast medium induced nephropathy. The wide-spread use of invasive diagnostic and therapeutic procedures makes the use of contrast media more common. Acute renal failure may develop following their intravascular administration, referred as contrast medium induced nephropathy or briefly contrast nephropathy. It develops especially in patients with diabetic nephropathy, in cases of volume depletion and in chronic renal insufficiency. Contrast nephropathy is the third most common cause of acute renal failure acquired in hospital. In their present work current literature, pathogenesis, clinical characteristics and potential ways of prevention are reviewed.

Acute Kidney Injury↗
PubMed2005

Prevention and treatment of diabetic nephropathy.

Increasing number of diabetic patients develop different stages of renal failure. However, often an inappropriate parameter, the serum creatinine is measured as a marker of glomerular function. Calculated glomerular filtration rate or endogenous creatinine clearance are suggested to be used for the estimation of the glomerular function. Important structures preventing proteinuria in the kidney are glomerular basement membrane, podocytes and proximal tubular cells. In diabetes mellitus loss of nephrin of podocytes can play a role in the development of microalbuminuria, and podocyte desquamation may result in the progression to proteinuria. In diabetes mellitus there is an increased formation of advanced glycation endproducts (AGE), of which the only elimination organ is the kidney. The AGE induce proteinuria and atherosclerosis. Therefore, in diabetes mellitus a vicious circle develops due to proteinuria, nephron loss and accumulation of AGE, which play a role in the initiation and progression of diabetic nephropathy and atherosclerosis. Angiotensin converting enzyme inhibitors and angiotensin receptor blockers having antiproteinuric effect may decrease the risk of diabetic nephropathy and atherosclerosis. Improvement of carbohydrate metabolism with a consequential decrease in the formation of AGE is an important contributor to the prevention and treatment of diabetic nephropathy and atherosclerosis.

Albuminuria↗
PubMed2005

[Early anemia in diabetic nephropathy].

The number of diabetic patients with renal disease increased significantly in the last years worldwide. Anemia is an important and frequent component of diabetic nephropathy that may begin early in the course of the chronic renal disease of diabetics, and is more severe in diabetic patients with renal disease than in non - diabetic renal patients controlled for the same level of renal function. The reason for the anemia is decreased erythropoietin level caused by diminished production and, in a lesser degree, by increased excretion of erythropoietin in the urine. There is a close connection between diabetic nephropathy, anemia and cardiovascular complications. On the basis of small studies correction of anemia may decrease the progression of diabetic nephropathy and cardiovascular complications. However, the result of ongoing large randomised controlled studies are required to get "evidence-based" data to prove that correction of anemia has beneficial effects on microvascular and macrovascular diabetic complications, particularly cardiac disease, and on progression of diabetic nephropathy.

Anemia, Hypochromic↗
PubMed2005

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↗
PubMed2005

Proteomic analysis of cell surface proteins from Clostridium difficile.

Clostridium difficile is a bacterium that causes disease of the large intestine, particularly after treatment with antibiotics. The bacterium produces two toxins (A and B) that are responsible for the pathology of the disease. In addition, a number of bacterial virulence factors associated with adhesion to the gut have previously been identified, including the cell wall protein Cwp66, the high-molecular weight surface layer protein (HMW-SLP) and the flagella. As the genome sequence predicts many other cell wall associated proteins, we have investigated the diversity of proteins in cell wall extracts, with the aim of identifying further virulence factors. We have used a number of methods to remove the proteins associated with the cell wall of C. difficile. Two of the resulting extracts, obtained using low pH glycine treatment and lysozyme digestion of the cell wall, have been analysed in detail by two-dimensional electrophoresis and mass spectrometry. One hundred and nineteen spots, comprising 49 different proteins, have been identified. The two surface layer proteins (SLPs) are the most abundant proteins, and we have also found components of the flagellum. Interestingly, we have also determined that a number of paralogs of the HMW-SLP are expressed, and these could represent targets for further investigation as virulence factors.

Bacterial Proteins↗
PubMed2005

A history of diabetes mellitus or how a disease of the kidneys evolved into a kidney disease.

Diabetes mellitus has a long history during which it was considered to be a disease of the kidneys well into the middle of the 19th century. Recognized in antiquity from its excessive urine output and described as a disease of the urinary tract, its clinical features and fatal outcome were quite accurately recorded by the 1st century ad . Galen (129-200) described it as a disease specific to the kidneys because of a weakness in their retentive faculties. The sweet taste of diabetic urine, which is described in ancient Indian texts and noted by Avicenna (980-1037) and Morgagni (1635-1683), was attributed to the passage of absorbed water and nutrients unchanged into the urine. In 1674, Thomas Willis (1621-1675) first differentiated diabetes from other causes of polyuria by the sweet taste (quasi melle) of diabetic urine and suggested that the sweetness first appears in the blood. A century later, Matthew Dobson (1732-1784) showed that the urine sweetness was because of sugar and was preceded and accompanied by sugar in the blood. Although diabetes then came to be ascribed to increased sugar in the blood, the presence of sugar in the urine continued to be attributed to the decreased retentive properties of the kidneys. The experimental production of diabetes in pancreatectomized dogs that could be reversed by subcutaneous pancreatic transplantation in 1889, and ultimate isolation of insulin in 1922 clearly established diabetes as an endocrine disease. The stage of diabetes as a disease of the kidneys was now over but that of diabetes as a cause of kidney disease was yet to come. Diabetes as a cause of end stage kidney disease was first described in 1936 and extensively documented shortly thereafter, whereas the evidence of its increasing prevalence as a cause of chronic kidney disease continues to accrue.

Diabetes Mellitus↗
PubMed2005

Urinary ortho-tyrosine excretion in diabetes mellitus and renal failure: evidence for hydroxyl radical production.

BACKGROUND: Phenylalanine is converted to para- and ortho-tyrosine by hydroxyl free radical, or to para-tyrosine by the phenylalanine hydroxylase enzyme. The aim of this study was to measure para- and ortho-tyrosine in the urine and plasma of patients with chronic renal disease and/or diabetes, to obtain information on the renal handling of the different tyrosine isomers and, furthermore, to measure urinary levels of 8-epi-prostaglandin-F(2alpha), a marker of lipid peroxidation. METHODS: In our cross-sectional study we measured para-, ortho-tyrosine, and phenylalanine levels, using high performance liquid chromatography and 8-epi-prostaglandin-F(2alpha) with enzyme-linked immunosorbent assay (ELISA). We compared 4 groups: (1) controls (CONTR, N = 14), (2) patients with chronic kidney disease (CKD, N = 12), (3) patients with type 2 diabetes mellitus (DIAB, N = 17), (4) patients with chronic kidney disease and type 2 diabetes (DIAB-CKD, N = 19). RESULTS: We found a decreased plasma para-tyrosine level and decreased urinary para-tyrosine excretion in CKD patients, while the fractional excretion of para-tyrosine was similar in all 4 groups, approximately 1%. There was no difference in the plasma ortho-tyrosine levels between the groups. However, urinary ortho-tyrosine excretion was higher in all 3 groups of patients than in the CONTR group, and higher in DIAB and in DIAB-CKD patients than in CKD patients. The fractional excretion of ortho-tyrosine was significantly higher in DIAB and in DIAB-CKD patients than in the CONTR group. The fractional excretion of ortho-tyrosine exceeded 100% in the 2 diabetic groups. Urinary 8-epi-prostaglandin-F(2alpha)/creatinine ratio did not correlate with urinary ortho-tyrosine excretion. CONCLUSION: The difference between para-tyrosine levels of the groups is probably due to renal impairment, while there is indirect evidence for an increased tubular secretion or production of ortho-tyrosine in the kidney in diabetic patients with or without CKD.

Aged↗
PubMed2004

[Decreased first-phase secretion of insulin may play a role in the development of insulin resistance].

Decreased first-phase secretion of insulin may play a role in the development of insulin resistance. In the development of type 2 diabetes an abnormal function of the beta-cells and insulin resistance of liver, fat cells and muscle play the main role. An early sign of beta-cell damage can be the loss of first-phase insulin response. This is supposed to precede the development of insulin resistance. Decrease of first-phase secretion of insulin can induce early postprandial hyperglycaemia and hypertriglyceridaemia damaging endothelium of precapillary arterioles of the nutritive capillaries. Insulin-induced endothelium-dependent dilation of these arterioles is inhibited by high glucose and triglyceride levels preventing metabolic effect of insulin on the parenchymal cells surrounded by nutritive capillaries and leading this way to insulin resistance. Second-phase hyperinsulinaemia develops in the impaired glucose tolerance. With the progression of the disease into the type 2 diabetes, insulin secretion decreases in the second-phase, as well. Because of decrease of first-phase insulin secretion in type 2 diabetic patients, early insulin therapy could be a choice of treatment in type 2 diabetes. Results of the UKPDS suggest that insulin-treated type 2 diabetic patients are longer in the near-euglycaemic state compared to those treated by oral hypoglycaemic agents. Recent data support that early insulin therapy of type 2 diabetic patients retains their own insulin secretion capacity and results in lower haemoglobin A1c. A comparison of before-meal rapid-acting insulin analogue and bedtime NPH insulin regimens verified that rapid-acting insulin analogue decreased haemoglobin A1c compared to NPH insulin treatment in type 2 diabetes. On the basis of these data arises the possibility of the change of the attitude "Oh no, not insulin in type 2 diabetes" to the "early rapid-acting insulin analogue treatment" of these patients.

Animals↗
PubMed2004

[Effect of ACE gene polymorphism on carbohydrate metabolism, on oxidative stress and on end-organ damage in type-2 diabetes mellitus].

ACE gene insertion/deletion (I/D) polymorphism is a well-known risk factor of hypertension, cardiovascular diseases and progression of diabetic nephropathy. In carriers of allele D, serum level of angiotensin-II is higher, which can be associated with increased oxidative stress and subsequent endothelial damage. Albuminuria is a sensitive marker of endothelial damage, while serum activity of the enzyme gamma-glutamyl transferase--that plays important role in the antioxidant defense--may refer to the level of oxidative stress. The present paper reports on a cross-sectional clinical study, where authors have examined on the relation between ACE gene insertion/deletion polymorphism and carbohydrate metabolism, hypertension as well as albuminuria in type 2 diabetics (n = 145). In patients carrying allele D, fructosamine levels were significantly higher (p = 0.007) than in carriers of allele I. Patients with II + ID genotypes and those who were treated with insulin took more antihypertensive drugs than the ones with II genotype or orally treated (p = 0.015). They found a significant association between genotype and fructosamine level (p = 0.023). Association between genotype or modality of treatment of diabetes (oral vs, insulin) and combined treatment of hypertension (number of antihypertensive drugs) was of borderline significance. They found that fructosamin level of patients receiving ACE inhibitor was lower than that of patients not receiving ACE inhibitors. In patients with allele D, they have also found higher activity of gamma-GT and higher albuminuria. From this results and data of the literature the authors conclude that because of insulin resistance (in connection with the presence of allele D), these patients tend to have a worse metabolic state, more advanced glycation products, due to which oxidative stress and endothelial cell damage may develop. As albuminuria and activity of gamma-GT were both found higher in patients with allele D, and our patients did not suffer of any hepatic disease, authors take the consequence that gamma-GT is a marker of the oxidative stress caused by allele D. Endothelial damage may explain that these patients take a higher number of antihypertensive combination. Based on this, D allele may contribute--via increased glycation and oxidative stress--to the target organ damage in type 2 diabetes.

Adult↗
PubMed2004

[Hypertension and 24-hours blood pressure monitoring in kidney diseases].

Hypertension is common in most types of kidney diseases and it may lead to end-stage renal failure. The pathogenesis of hypertension in kidney disease is multifactorial. High blood pressure may accelerate the progression of kidney diseases, and it has major contribution to the high cardiovascular risk of these patients. Twenty-four hour ambulatory blood pressure monitoring makes the diagnosis of hypertension faster and more accurate and enables the diagnosis of "white-coat hypertension". It makes possible to study the diurnal blood pressure rhythm and the effect of the antihypertensive medication. In the majority of kidney diseases the normal diurnal blood pressure rhythm is lost. Hypertension and abnormal circadian blood pressure rhythm accelerates the development of end-stage renal disease and they are major contributors of the high cardiovascular mortality of patients with renal disorders. Therefore, ambulatory blood pressure monitoring should be part of the routine evaluation of patients with renal disorders.

Blood Pressure↗
PubMed2004

Analgesic nephropathy in Hungary: the HANS study.

BACKGROUND: The diagnosis of analgesic nephropathy has improved significantly with modern imaging techniques. We reviewed a large portion of the Hungarian dialysis population to obtain additional insight into the problem. METHODS: Twenty-two participating dialysis units enrolled 1400 patients on renal replacement therapy between 1 January 1995 and 1 January 1998. Patients with no known aetiology (n = 284) were interviewed and studied with renal imaging. We assessed the presence of decreased renal mass combined with either bumpy contours, papillary calcification, or both. The subjects studied were interrogated extensively. RESULTS: Our survey suggested analgesic nephropathy in 47 of 1400 patients (3.3%), 3-fold higher than the EDTA database estimate for Hungary. The analgesics most commonly abused were phenacetin-containing mixtures. The driving symptoms were mainly headache and joint pain. Cardiovascular complications were more common than in the rest of the dialysis population, independent of smoking and lipid values (P<0.01). CONCLUSIONS: Phenacetin should be banned. Our study results support the need for longitudinal cohort and case-control studies in Hungary.

Analgesics, Non-Narcotic↗
PubMed2003

[Role of the renin-angiotensin system in the pathogenesis, clinical picture and treatment of diabetic nephropathy].

Prevalence of diabetic nephropathy is increasing. Understanding of pathogenesis and clinical picture helps to manage this disease. Recent data of the research of this disease support that the renin-angiotensin system plays a pivotal role in the pathogenesis. Hyperglycaemia activates the renin-angiotensin system and induces transforming growth factor-beta expression. These both lead to glomerulosclerosis and tubulointerstitial fibrosis. Diabetic nephropathy develops earlier and progress faster in patients with DD or ID genotypes of angiotensin-I-converting-enzyme gene. Angiotensinogen and type 1 angiotensin-II-receptor gene mutations may be also predisposing factors for diabetic nephropathy. All these factors can be responsible for the hyperfiltration, albuminuria, salt sensitivity, and hypertension, which are characteristic features of diabetic nephropathy. According to these, one can suppose that inhibitors of the renin-angiotensin system are effective in the prevention and treatment of this disease. Evidence of clinical studies suggests that angiotensin-I-converting-enzyme inhibitors in type 1 diabetes can prevent overt nephropathy, decrease proteinuria, inhibit the loss of the glomerular filtration and decelerate progression. Angiotensin-II-receptor blockers exert the same effect in type 2 diabetic patients, and presumably angiotensin-I-converting-enzyme inhibitors have similar activity in this group of patients. That is why, in the case of intolerance of one class of drugs, the other should be substituted. Combination therapy of angiotensin-I-converting-enzyme inhibitors with angiotensin-II-receptor blockers can be the choice of treatment in the future.

Albuminuria↗
PubMed2003

[Rapidly developing bone destruction in a patient with type 1 Gaucher disease].

The authors report on a 25 year-old male Gaucher patient who developed rapid bone deterioration. The patient was splenectomised at age 3 and had no signs and symptoms of bone involvement for more than 20 years. In addition to the infarction in the right tibia, severe bone necrosis was detected in components of the left hip. This report suggests that bone deterioration may develop insidiously at any time in Gaucher patients, and that long-term and regular follow up is warranted.

Adult↗