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Biomedical subjects

J Chudek

Publications and source records attributed to J Chudek.

At least 19 recordsLinked to original sources
PubMed2004

Plasma leptin concentration in patients with acute renal failure.

BACKGROUND: Acute renal failure (ARF) is characterized by impaired excretory, endocrine, homeostatic and metabolic function of the kidneys. It is well-known that leptin is an adipose-derived polypeptide hormone which is predominantly biodegraded by the kidneys. Therefore, plasma leptin concentration is increased in chronic renal failure (CRF). However, its' concentrations in patients with ARF were not investigated until now. The aim of the present study was to evaluate plasma leptin concentration in patients with ARF. PATIENTS AND METHODS: 27 patients with ARF (age 44 +/- 4 years, BMI 26.0 +/- 0.9 kg/m2, means +/- SEM, 17 patients 15 M, 2 F recovered kidney function and 10 patients 7 M, 3 F died during the anuric phase), 27 hemodialysis patients (22 M, 5 F; age 45 +/- 2 years; BMI 26.2 +/- 0.8 kg/m2) with chronic renal failure (CRF) and 27 healthy subjects (HS) (22 M, 5 F; age 42 +/- 3 years; BMI 25.9 +/- 0.6 kg/m2) were examined. In patients with ARF, blood samples for plasma leptin and routinely assessed biochemical parameters were withdrawn before the first HD session (I), and in patients who survived a second time 5 days later during the anuric/oliguric phase (II), and a third one during the polyuric phase before discharge of the patient from hospital (III). In patients with CRF all examined parameters were estimated only once before a subsequent HD session. RESULTS: Patients with ARF (before the first HD session) and CRF did not differ significantly with respect to BMI, serum creatinine and blood hydrogen ion concentrations. Plasma leptin level in patients with ARF before the first HD session was similar to values obtained in HS, but significantly lower (p < 0.01) than in patients with CRF (2.5 (1.9 - 8.2) vs. 3.4 (2.5 - 8.3) vs. 8.4 (2.9 - 16.9) ng/ml in ARF, HS and CRF, respectively). There was no significant difference in leptinemia between patients with ARF who survived and who died. In patients with ARF who survived, improvement ofrenal function was accompanied by a slightly (not significant) declining tendency in plasma leptin concentration (5.6 +/- 2.2 vs. 4.8 +/- 1.7 vs. 4.5 +/- 1.3 ng/ml; I, II, III phases of ARF, respectively). CONCLUSIONS: In contrast to hemodialysis patients with chronic renal failure, patients with acute renal failure are characterized by normal plasma leptin concentration. Thus, difference in leptinemia between patients with chronic and acute renal failure seems to be due to preservation of large amounts of active renal parenchyma in ARF patients.

Acute Kidney Injury↗
PubMed2003

Plasma adiponectin concentration before and after successful kidney transplantation.

BACKGROUND: Adiponectin, a protein secreted exclusively by adipocytes, is presumed to be involved in the pathogenesis of atherosclerosis and insulin resistance. An elevated plasma adiponectin concentration was found in ESRD patients on hemodialysis (HD). However, the role of kidneys in adiponectin biodegradation/elimination is unknown. Therefore, we assessed plasma adiponectin concentrations in ESRD patients before and after successful kidney transplantation. METHODS: Among 44 hemodialyzed patients (29 men, 15 women; mean age 39 +/- 11 years; mean body mass index [BMI] 23.6 +/- 3.5 kg/m(2); mean duration of HD treatment before kidney transplantation 27 +/- 26 months), plasma adiponectin concentrations and insulin resistance indices (HOMA-R) were measured twice: immediately before kidney transplantation (Tx) and 1-2 days before patient discharge from the hospital with stable kidney transplant function (mean serum creatinine level 191 +/- 105 micromol/L). The control group consisted of 22 normotensive healthy subjects (12 men, 10 women). RESULTS: Among uremic patients, before Tx, plasma adiponectin concentrations were significantly higher than in healthy subjects (20.8 +/- 8.3 vs 8.7 +/- 4.8 microg/mL; P <.001) After successful Tx, plasma adiponectin concentrations decreased significantly (20.8 +/- 8.3 vs 15.7 +/- 7.0 microg/mL before and after Tx, respectively; P <.001). Simultaneously, after successful kidney transplantation, an increase in HOMA-R was observed (1.01 +/- 0.61 vs 1.43 +/- 0.83; P =.002). However, changes in adiponectinemia did not significantly correlate with serum creatinine or HOMA-R. CONCLUSION: The kidneys seem to play an important role in adiponectin biodegradation and/or elimination.

Adiponectin↗
PubMed2003

Relationship between plasma level of parathyroid hormone and carboxymethyllysine in hemodialyzed patients--does it exist?

AIMS: Both parathyroid hormone and advanced glycated end products (AGEs) are uremic toxins. The present study aimed to examine the likely interrelationship between these compounds. METHODS: Seventy-four hemodialyzed patients (41 female, 33 male; mean age 47 +/- 2 years, mean duration on hemodialysis 36 +/- 6 months) were enrolled in this study. In all subjects, the body mass index (BMI) was calculated and total lean mass (TLM) and total fat mass (TFM) were assessed by dual X-ray absorptiometry. Blood samples for estimation of plasma calcium, phosphorus, carboxymethyl lysine (as marker of AGEs) and PTH-1-84 were obtained after overnight fasting, before subsequent hemodialysis session. RESULTS: BMI, TFM and TLM were 23.6 +/- 0.5 kg/m2, 16.3 +/- 1.0 kg and 46.3 +/- 1.1 kg, respectively. PTH plasma level (223 +/- 32 pg/ml) and plasma CML (1,837 +/- 84 ng/ml) were markedly elevated as compared with reference values. A significant positive correlation was found between TLM and CML levels (tau = 0.225; p = 0.04) and between plasma PTH and CML levels (tau = 0.224; p = 0.04). CONCLUSION: It seems likely that PTH and AGEs are interrelated. The pathophysiological relevance of this finding in the pathogenesis of uremic toxicity remains to be elucidated.

Body Mass Index↗
PubMed2002

Relationship between body composition, sex hormones and leptinemia in hemodialyzed patients with chronic renal failure.

BACKGROUND: Females are characterized by significantly higher plasma leptin concentration than males. It seems likely that sex hormones influence leptinemia independently from differences in body composition. The aim of the present study was to analyze the contribution of plasma concentrations of testosterone and estradiol on leptinemia in hemodialyzed patients. METHODS: 110 hemodialyzed patients--HD (60 M, 50 F) and 70 healthy subjects (HS) (30 M, 40 F) were enrolled in this study. Plasma leptin, testosterone or estradiol and CRP concentrations and body composition by dual-energy X-ray absorptiometry (DEXA) were assessed. RESULTS: Total body fat was significantly higher in females than in males (27.5 +/- 1.5% vs. 17.2 +/- 1.0% of body weight in HD and 36.0 +/- 1.0% vs. 18.2 +/- 1.4% in HS, respectively). Plasma leptin concentrations were markedly higher in females than in males both in HD (27.9 +/- 5.4 ng/ml vs. 9.6 +/- 1.9 ng/ml) and HS (16.5 +/- 1.7 ng/ml vs.3.1 +/- 0.4 ng/ml). A highly significant, strong positive correlation was found between total fat mass (TFM) and leptinemia in all studied groups. No significant univaried correlation between plasma leptin and testosterone or estradiol concentrations respectively was found both in HD and HS. Multiple regression analyses showed that the main determinant of leptinemia is TFM (beta = 0.623 and 0.798 in HS females and males respectively, and beta = 1.058 and 0.797 in HD females and males respectively). Plasma concentration of testosterone (beta = -0.139 and beta = -0.075 in male HD and HS respectively) and estradiol (beta = 0.199 and beta = 0.046 in females HD and HS, respectively) contributed to leptinemia only in a minor degree. CONCLUSION: Both testosterone and estradiol are minor contributors to leptinemia both in HS and HD patients. The main determinant of leptinemia in these subjects is total body fat mass.

Absorptiometry, Photon↗
PubMed2001

Cloning a calcium channel alpha2delta-3 subunit gene from a putative tumor suppressor gene region at chromosome 3p21.1 in conventional renal cell carcinoma.

We have identified loss of heterozygosity (LOH) of approx. 1 cM region around locus D3S1289 at chromosome 3p21.1 in a conventional renal cell carcinoma (RCC). During construction of a YAC/BAC contig for this region and shotgun sequencing of BACs 277p5, 55m24 and 428i24, we detected four new microsatellites. We narrowed down the target region by analysing these new loci to less than 100 kb within the BAC 55m24 and subsequently cloned a human calcium channel alpha2delta-3 subunit gene. This gene is widely expressed in fetal tissues and different types of adult tumors. The exons of the alpha2delta-3 subunit gene are distributed along approx. 500 kb DNA sequences. As the LOH involved exclusively intronic sequences and sequencing the entire coding region did not reveal any mutation, the alpha2delta-3 subunit gene is probably not a tumor suppressor gene.

Alternative Splicing↗
PubMed2001

Accumulation of allelic changes at chromosomes 7p, 18q, and 2 in parathyroid lesions of uremic patients.

We examined by microsatellite allelotyping 69 hyperplastic lesions of the parathyroid glands from 23 patients with refractory, uremic hyperparathyroidism. Allelic changes, at least at one chromosomal arm, were found in 31 of the 69 lesions (43%). Alteration at a single chromosome was seen in 14 lesions and at two to four chromosomes in 11 lesions, and there were five to eight alterations in 5 nodules. Allelic imbalance occurred most frequently at chromosome 7p between the EGFR gene and locus D7S817 (16%), at 18q between loci D18S61 and D18S70 (14%), and at chromosome 2 between D2S380 and D2S1391 (9%). X-inactivation study showed a monoclonal growth in 18 of 29 nodules in females, and a loss of the Y chromosome was seen in 8 of the 39 nodules obtained from males. Our results suggest that the uremic "hyperplastic" nodules have a molecular pathway distinct from those known for sporadic primary parathyroid adenomas.

Adolescent↗
PubMed2001

Interrelationship between plasma leptin concentration and severity of metabolic acidosis in haemodialysed patients with chronical renal failure.

Patients with chronic renal failure are frequently characterized by malnutrition, hyperleptinaemia and metabolic acidosis. Both hyperleptinaemia and chronic metabolic acidosis are presumed to contribute to the pathogenesis of malnutrition observed in this group of patients. It has been reported, that in vitro adipocytes exposed to acidotic medium decrease leptin secretion. The aim of present study was to analyze the possible impact of uraemic metabolic acidosis on leptinaemia in haemodialysis patients with chronic renal failure. - 94 haemodialysed patients (58 M, 36 F; mean age 45 +/- 1 years) were enrolled in this study. 56 patients were on haemodialysis treatment for one year using an acetate dialysis fluid, while 38 patients were haemodialysed at least for 3 months with a dialysate buffered with bicarbonate. Plasma leptin concentration, blood gases and body composition were assessed in all examined subjects. - Patients haemodialysed with an acetate and bicarbonate buffered dialysate did not differ with respect to body weight, body mass index (BMI), total fat mass (TFM) and plasma leptin concentration. Patients haemodialysed with an acetate buffered dialysate were characterized by a significantly more severe metabolic acidosis than patients on bicarbonate haemodialysis. Patients were divided according to the actual hydrogen ion concentration: over 60 nmol/l, 45-60 nmol/l and below 45 nmol/l. These subgroups did not differ significantly by body weight, BMI and TFM. Only a slightly (not significantly), lower median leptinaemia was found in patients with elevated hydrogen ion concentration. No significant correlation was noticed between blood hydrogen or hydrocarbonate ion concentration respectively and logarithmic values of plasma leptin concentration (tau = 0.025, p = 0.72; tau = - 0.021, p = 0.76 respectively). - From results obtained in this study we may conclude that, blood hydrogen ion concentration does not influence substantially or only moderately to plasma leptin concentration in haemodialysed patients.

Acidosis↗
PubMed2001

[Chronic allograft nephropathy].

In spite of improved one year renal allograft survival long-term results of renal transplantation did not change since several years. Progressive decline of graft function developing few years after renal transplantation remains a significant problem in renal replacement therapy. The clinical manifestation of progressive impairment of the kidney transplant is heterogeneous and the differential diagnosis of chronic graft rejection is difficult, even if histopathological examination is performed. Improvement of immunosuppressive therapy and avoidance of nonimmunologic factors which increase the risk of graft failure seem to influence markedly function of kidney grafts.

Graft Rejection↗
PubMed2001

[Levels of carnitine and homocysteine in plasma of long-term hemodialysis patients with chronic renal failure].

Homocysteine and carnitine are the metabolic products of exogenous amino acids. Increased plasma concentration of homocysteine but decreased or normal carnitine concentration are usual findings in haemodialysis patients with chronic renal failure. This study aimed to evaluate the interrelationship (if any) between the above mentioned metabolites in haemodialysis uraemic patients. 44 haemodialyzed patients with chronic renal failure--HD (25 female, 19 male, mean age 47 +/- 12 years) were enrolled into this study. Blood samples for estimation of plasma glucose, cholesterol, triglycerides, albumin, folic acid, vitamin B12, homocysteine (HC), total (TC) and free (FC) carnitine were withdrawn after overnight fasting before subsequent haemodialysis session. In all subjects whole body total fat mass (TFM) and lean mass (TLM) were assessed by dual X-ray absorptiometry (DEXA). Hyperhomocysteinaemia was found in 90.9% patients, while carnitine deficiency in 22.7% of all analysed subjects. Both hyperhomocysteinaemia and carnitine deficiency was found in 18.2% of haemodialysis patients. Folic acid deficiency regardless of prescribed supplementation was observed in 9.5% patients. A significant positive correlation was found between plasma concentration of TC or FC and TLM (tau = 0.332, p < 0.001; tau = 0.298, p < 0.01 respectively). A negative correlation was observed between plasma concentration of folic acid and homocysteine (tau = -0.201, p < 0.05). No significant relationship was noted between homocysteinaemia, total and free plasma carnitine levels and anthropometrical parameters. In conclusion, plasma concentration of homocysteine and carnitine are independent indicators of abnormal amino acid metabolism in uraemic patients.

Adult↗
PubMed1999

Microsatellite analysis reveals deletion of a large region at chromosome 8p in conventional renal cell carcinoma.

Loss of heterozygosity (LOH) at chromosome 8p is associated with the progression of conventional (non-papillary) renal cell carcinomas (RCC). To determine the tumor suppressor gene locus, we carried out a deletion mapping of chromosome 8p at 10 microsatellite loci in 96 RCCs. LOH occurred in 32% of the tumors. The smallest overlapping region of deletion at chromosome 8p11.2-p23.1 corresponds to approximately 34-cM genetic distance. No small interstitial deletion was seen.

Carcinoma, Renal Cell↗
PubMed1999

[Genetic aspects of primary hyperparathyroidism].

The results of the last decade genetic research in the field of oncogenesis of sporadic and familiar parathyroid tumors are summarised. The review of studied focuses on two main topics: multiple endocrine neoplasis syndromes as well as sporadic parathyroid adenomas and carcinomas. The current knowledge of genetic factors associated with the development of these lesions is presented.

Chromosome Aberrations↗
PubMed1999

[Response of vasoactive substance to blood pressure changes during hemodialysis in uremic patients].

UNLABELLED: Ultrafiltration during haemodialysis (HD) may be the cause of blood pressure (BP) decline due to reduction of blood volume. In some patients, however, BP does not decrease or even rises during HD. The aim of the study was to answer the question: do uraemic hypertensive patients, showing a decline of mean blood pressure (MAP) during HD session (group A) differ from those showing a stable MAP during HD session (group B) with respect to hormonal profile of aldosterone (ALD), vasopressin (AVP), atrial natriuretic peptide (ANP), endothelin-1,2 (ET-1,2), blood nitric oxide (NO) and plasma renin activity (PRA). A total of 39 haemodialysed, hypertensive patients (17 female, 22 men) were studied. 24 patients (group A) showed a MAP decline of 10 mm Hg or more, while 15 patients (group B) showed MAP changes of less than +/- 10 mm Hg during HD session. PRA, ALD, AVP, ANP, ET-1,2, NO concentration were assessed in blood samples withdrawn from the arterial blood line before HD and after 60, 120, 180 and 240 minutes of HD session. Plasma ET-1,2 and blood NO concentration were also assessed after 30 minutes of HD. BV was continuously monitored with a Crit-Line equipment, BP was measured before and every 30 minutes on HD. Before HD session both examined groups showed similar baseline plasma levels of ALD, AVP, ANP, ET-1,2, NO, PRA and MAP. A 4-hours HD induced a significant increase in plasma ALD and AVP concentrations and a significant decline in ANP level in both groups of patients. In group A, PRA and blood NO concentration increased significantly, while plasma ET-1,2, level did not change during HD. In group B, no significant changes in PRA and blood NO level were noticed, while plasma ET-1,2 rose markedly. In addition in group B, a significant positive correlation was found between MAP and plasma ET-1,2 level changes, but a significant negative correlation between MAP and blood NO level changes. CONCLUSION: Patients with a decline of MAP over 10 mm Hg during HD differ from those with a stable MAP by a different response of plasma ET and blood NO to HD induced volume changes.

Aldosterone↗
PubMed1998

Lack of genetic changes at specific genomic sites separates renal oncocytomas from renal cell carcinomas.

Morphological similarities between renal oncocytomas and 'oncocytic' renal cell carcinomas (RCCs) make a differential diagnosis in many cases difficult. A series of 41 renal oncocytomas has been analysed by microsatellite markers from chromosomes 1, 2, 3p, 6q, 8p, 9, 10, 13q, 14q, 17, and 21, alterations of which are known to be involved specifically in non-papillary and chromophobe RCCs. Only eight of the 41 renal oncocytomas showed loss of heterozygosity (LOH). LOH at chromosomes 1 and 14 occurred in four tumours each and at chromosomes 2, 8, and 9 in one tumour each. Combined LOH at chromosomes 1, 9, and 14 and also at chromosomes 1 and 14 occurred in one case each. No LOH was seen at any other genomic sites. The lack of combination of LOH at specific chromosomal sites differentiates renal oncocytomas from other renal cell tumours with overlapping phenotypes. Applying the microsatellite assay described here, the diagnosis can be established within 2 days, from fresh as well as from paraffin-embedded material.

Adenoma, Oxyphilic↗
PubMed1998

Lack of interleukin 6 (IL-6) and transforming growth factor alpha (TGF-alpha) expression in chromophobe renal cell carcinomas.

We demonstrate the constitutive expression of interleukin 6 (IL-6), IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF), epidermal growth factor (EGF), transforming growth factor alpha (TGF-alpha) and epidermal growth factor receptor (EGFR) in normal kidney cells, and in the majority of renal oncocytomas, papillary and non-papillary renal cell carcinomas (RCCs) by reverse transcriptase polymerase chain reaction (RT-PCR) technique. No expression of IL-6 and TGF-alpha and variable expression of GM-CSF, IL-8, EGF and EGFR was seen in chromophobe RCCs. The lack of expression of IL-6 and TGF-alpha might be correlated with the growth pattern, poor vascularity and low malignancy of chromophobe RCCs.

Carcinoma, Papillary↗