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Boleslaw Rutkowski

Publications and source records attributed to Boleslaw Rutkowski.

At least 19 recordsLinked to original sources
PubMed2007

The potential role of sterol regulatory element binding protein transcription factors in renal injury.

The disturbed lipid metabolism is a permanent finding in renal failure. It is supposed to be a main reason for the accelerated atherosclerosis and high cardiovascular and cerebrovascular mortality of patients with renal failure. Sterol regulatory element binding proteins (SREBPs) are the transcription factors involved in the regulation of lipid homeostasis. They are responsible for the transcription activation of genes associated with the synthesis of fatty acids, triglycerides, and cholesterol. SREBP-1 gene expression in adipose tissue and SREBP-2 in liver are significantly elevated in renal failure. This is accompanied with the up-regulation of genes encoding enzymes of both fatty acids and cholesterol synthesis and significant serum lipid enhancement. Moreover, it has been shown that a destructive accumulation of lipids in the kidney structures is associated with enhanced kidney SREBP gene expression and increased lipid production. This was found even in the absence of any abnormalities in serum lipids. One may suppose that SREBP transcription factors play an important role in disturbed lipid metabolism in renal failure.

Disease Progression↗
PubMed2006

Up-regulation of NPY gene expression in hypothalamus of rats with experimental chronic renal failure.

Anorexia is possibly one of the most important causes of malnutrition in uremic patients. The cause of this abnormality is still unknown. Considering that: (a) NPY is one of the most important stimulants of food intake; (b) eating is a central nervous system regulated process and (c) NPY is expressed in hypothalamus, we hypothesized that the decrease of NPY gene expression in the hypothalamus could be an important factor contributing to anorexia associated with uremic state. In contrast to the prediction, the results presented in this paper indicate that the NPY gene expression in the hypothalamus of chronic renal failure (CRF) rats was significantly higher than in the hypothalamus of control (pair-fed) rats. Moreover, we found that serum NPY concentration in CRF rats was higher than in control (pair-fed) animals. The increase of plasma NPY concentration in CRF rats may be due to the greater synthesis of the neuropeptide in liver, since higher level of NPY mRNA was found in liver of CRF rats. The results obtained revealed that experimental chronic renal failure is associated with the increase of NPY gene expression in hypothalamus and liver of rats.

Animals↗
PubMed2006

Increased gene expression of liver SREBP-2 in experimental chronic renal failure.

Sterol regulatory element-binding protein-2 (SREBP-2) is a transcription factor regarded as the main regulator of cholesterol homeostasis. Therefore, increased level of SREBP-2 could be responsible for hypercholesterolemia, which is observed in experimental chronic renal failure (CRF). This study was designed primary to evaluate the impact of experimental CRF (5/6 nephrectomy model) on rat liver SREBP-2 gene expression. In CRF rats, a twofold increase in SREBP-2 mRNA level, as well as in mature SREBP-2 protein abundance was found, when compared to control animals. It was associated with enhanced activity and mRNA abundance of liver HMG-CoA reductase, a rate-limiting enzyme for cholesterol biosynthesis. A twofold increase in liver cholesterologenesis rate was also noted. We conclude that experimental CRF is associated with increased liver SREBP-2 gene expression. This is probably the cause for enhanced HMG-CoA reductase gene expression and, consequently, for increase in liver cholesterol synthesis in CRF rats. Despite increased SREBP-2 gene expression we found LDL-receptor mRNA level to be lower than in controls, suggesting SREBP-2 independent mechanisms of LDL-receptor transcriptional regulation in CRF rats. Enhanced cholesterol synthesis and decreased LDL-receptor mRNA level are probably responsible for an almost fourfold increase in serum cholesterol concentration in CRF rats.

Animals↗
PubMed2006

Smoking as a risk factor for renal injury in essential hypertension.

BACKGROUND: Smoking is an important player in the pathogenesis of hypertensive nephropathy. To shed more light on this issue, we performed a case-control cross-sectional study and stratification analyses to evaluate the influence of smoking on surrogate markers of kidney injury and oxidative stress in patients supposed to have hypertensive nephropathy. The dependence of kidney lesions on the 'extent' of smoking was determined as well. METHODS: 82 patients with essential hypertension and micro- or macro-albuminuria were recruited. The control group consisted of 41 sex- and age-matched healthy individuals. Urine albumin creatinine ratio and plasma von Willebrand factor activity were analysed as markers of endothelial injury. N-acetyl-beta-D-glucosaminidase, transforming growth factor-beta1 and 15-isoprostane F2t urine excretions were regarded as markers of tubular dysfunction, renal fibrosis and oxidative stress, respectively. Patients' smoking habits were recorded and categorized on the basis of a self-administered questionnaire. RESULTS: In multivariate regression analysis, the independent associations between smoking and urine albumin (p < 0.05; beta = 0.27), von Willebrand factor activity (p < 0.05; beta = 0.29) and urine isoprostanes (p < 0.05; beta = 0.28) were found. When the smokers were stratified according to the number of cigarettes smoked per day and the time from which they started smoking, 'heavy smokers' and 'long-term smokers' presented with higher albumin excretion and higher von Willebrand factor activity than 'light smokers' and 'short-term smokers', respectively. The passive smokers had numerically higher albumin excretion and von Willebrand factor activity than nonsmokers. CONCLUSION: The study showed that smoking induces oxidative stress. Smoking was also found to be a strong predictor for the extent of endothelial injury in patients with hypertensive kidney injury. Subjects who smoke heavily and for a long time, as well as passive smokers, seem to be particularly exposed to endothelial damage.

Albuminuria↗
PubMed2006

Accumulation of poly(ADP-ribose) polymerase inhibitors in children with chronic renal failure.

Nicotinamide, N-methyl-2-pyridone-5-carboxamide (Met2PY) and N-methyl-4-pyridone-3-carboxamide (Met4PY) are biological metabolites of the intracellular coenzyme nicotinamide adenine dinucleotide (NAD) that can potentially inhibit poly(ADP-ribose) polymerase 1 (PARP-1; DNA repair enzyme). Our research was aimed at establishing whether chronic renal failure (CRF) in children leads to the elevation of plasma NAD metabolites sufficient to inhibit PARP-1 activity. Nicotinamide, Met2PY and Met4PY plasma and erythrocyte concentrations were measured in 25 children with CRF and in 19 healthy children. The effect of these NAD metabolites on PARP-1 activity was studied in vitro. We found that plasma concentration of all NAD metabolites (nicotinamide, Met2PY, Met4PY) in children with CRF could reach the concentration of 2, 30 and 10 microM as compared to 0.2, 1 and 0.5 microM, respectively, in healthy children. The concentration of nicotinamide metabolites correlated positively with plasma creatinine concentration and negatively with creatinine clearance in children with CRF. We found that Met2PY, Met4PY and nicotinamide inhibited in vitro PARP-1 activity with IC50 values of 2.1, 0.18 and 0.12 mM, respectively. Our data indicate that NAD metabolites accumulate in plasma of children with CRF and their combined effect could lead to the inhibition of PARP-1 activity. NAD metabolites could be particularly harmful in children due to higher DNA turnover than in adults.

Adolescent↗
PubMed2006

Randomized placebo-controlled study on the effects of losartan and carvedilol on albuminuria in renal transplant recipients.

BACKGROUND: The renoprotective effects of agents inhibiting the renin-angiotensin system in renal transplant recipients have been supposed but not finally proven. To shed more light on this issue, we performed a double-blind, placebo-controlled, crossover study to evaluate the influence of the AT-1 angiotensin II receptor blocker, losartan, on the surrogate marker of kidney injury, albuminuria, in patients after renal transplantation. The safety of this therapy was also evaluated. METHODS: Fourteen of 16 patients (nine male, five female), age 45.36 +/- 3.04 years, 65.5 +/- 10.0 months after kidney transplantation, with hypertension and stable serum creatinine 123 +/- 4 micromol/L without proteinuria, completed the protocol. Each patient underwent two 8-week treatment periods (one with losartan 50-100 mg and one with carvedilol 12.5-25 mg) in random order, allowing an 8-week placebo washout between treatments. The target office trough blood pressure was below 130/85 mmHg. RESULTS: The ambulatory blood pressure did not differ in the treatment periods. Losartan significantly reduced albuminuria relative to placebo and carvedilol (27.62+/-17.58 vs. 49.55 +/- 25.33 v. 44.77 +/- 21.9 mg/g creatinine; P < 0.01). A significant but not clinically relevant decrease in hemoglobin level after losartan was observed (losartan: 129 +/- 3.1 g/l, placebo: 134.2 +/- 3.2, carvedilol: 137.1 +/- 3.7; P < 0.001). Serum potassium, creatinine, creatinine clearance, and trough blood cyclosporine levels were unaffected. CONCLUSION: Losartan decreases microalbuminuria in renal transplant recipients with clinically minimal side effects.

Albuminuria↗
PubMed2006

Blood coagulation unaffected by ozonated autohemotherapy in patients on maintenance hemodialysis.

BACKGROUND: Ozonated autohemotherapy (O(3)-AHT) is a clinically useful therapeutic procedure in hemodialyzed patients with peripheral arterial occlusive disease (PAOD). The majority of patients on dialysis are in a hypercoagulable state. Thrombotic complications are the major cause of morbidity and mortality in hemodialyzed patients. Effects of O(3)-AHT on blood coagulation were evaluated in 11 hemodialyzed patients affected by PAOD. METHODS: We performed an oxygen-controlled, crossover study in which nine sessions of autohemotherapy with oxygen administration (AHT) as a control were followed by nine sessions of O(3)-AHT. Blood coagulation was assessed by antithrombin III, activated partial thromboplastin time, prothrombin time, D-dimer and fibrinogen plasma concentrations. RESULTS: The extents of all the measured parameters after nine sessions of O(3)-AHT did not differ statistically from the values after nine sessions of AHT. Similarly, there were no differences in the measured variables after the first session of O(3)-AHT as compared to the values before therapy. We did not observe any thrombotic accidents during the study. CONCLUSIONS: O(3)-AHT with ozone concentration of 50 microg/mL and citrate as an anticoagulant does not influence blood coagualation parameters in hemodialyzed patients with PAOD.

Aged↗
PubMed2006

Effect of preload reduction by hemodialysis on myocardial ultrasonic characterization, left atrial volume, and Doppler tissue imaging in patients with end-stage renal disease.

The purpose of this study was to investigate the effect of hemodialysis (HD) on myocardial cyclic variation of integrated backscatter (CVIBS), left atrium (LA) volume and tissue Doppler imaging (TDI) in end-stage renal disease (ESRD) patients. We examined 25 patients with ESRD undergoing routine HD and 19 age-matched healthy volunteers. CVIBS, LA volume and left ventricular echocardiographic parameters were measured before and after HD in ESRD patients. CVIBS of both the intervetricular septum and posterior wall were significantly diminished after HD (8.2 +/- 2.5 dB vs. 6.5 +/- 1.8 dB, P < 0.001; 9.2 +/- 2.6 dB vs. 7.6 +/- 2.2dB, p < 0.05 respectively). LA volume decreased significantly after HD (P < 0.05). There was no change in the mitral annulus early diastolic velocity (Em) estimated by TDI. The results of our study demonstrate that HD leads to decrease of CVIBS in ESRD patients and that early mitral annulus velocity (Em) could be preload independent marker of left ventricular diastolic function in ESRD patients.

Echocardiography, Doppler↗
PubMed2006

Interrelationship between uremic toxicity and oxidative stress.

Uremic syndrome is associated with several metabolic disturbances. Oxidative stress is an important factor involved in the pathologic mechanism of these changes. The goal of this study was to understand the relationship between oxidative stress markers and two compounds included among uremic toxins. Two independent studies were performed, one with 29 peritoneal dialysis patients and the other with 43 predialysis subjects. In both groups of patients, known oxidative stress markers, malonyldialdehyde (MDA) and carbonyl groups (CG) formation were measured. Additionally, in the predialysis group, glutathione in erythrocytes (GSH) was estimated. In peritoneal dialysis patients, the concentration of advanced glycation end products (AGEs) was found to be significantly increased and correlated with both markers of oxidative stress. In predialysis patients, the increment of newly described uremic toxin purine nucleotide end products (Me2PY and Me4PY) were found and significant correlation was observed between both compounds versus MDA (positive) and GSH (negative). This relationship was visible especially in patients with more advanced renal failure. CG concentration was within the normal values and did not show any correlation with estimated toxin concentrations. In summary, results of both studies suggest that the interrelationship between uremic toxicity and oxidative stress is an important component of uremic syndrome. Nevertheless, further complex studies are needed to elucidate closer pathogenic links.

Aged↗
PubMed2006

Explosion of renal replacement therapy after the implosion of the Soviet Empire.

After the implosion of the Soviet Empire, renal replacement therapy in Central and Eastern Europe has undergone dramatic transformation and improvement with respect to quantity and quality. While the prevalence (ie, the number of patients on renal replacement therapy) is still lower than in Western Europe, the incidence (ie, the number of patients accepted for renal replacement therapy) has by now reached on average the level seen in Western Europe, albeit with wide differences between the individual countries. The rate of renal transplantation is still highly variable. Substantial differences of organizational structures for renal replacement therapy exist, with private organizations gradually taking over from public services.

Adolescent↗
PubMed2005

Highlights of the epidemiology of renal replacement therapy in Central and Eastern Europe.

BACKGROUND: In the past 15 years, dramatic political and economic changes have occurred in Central and Eastern Europe (CEE) which also had a positive impact on the availability of renal replacement therapy. The aim of the present study was to analyse the progress achieved in the new millennium. METHODS: Data from 18 CEE countries collected during two independent surveys (1999 and 2002) were validated using information from national and ERA-EDTA registries, and analysed. RESULTS: The data collected from 18 CEE countries clearly document further development and improvement of renal replacement therapy in this region of Europe. In 63% of countries, the incidence rate had become comparable with that observed in more developed European countries. The two main modalities of dialysis, i.e. haemodialysis and peritoneal dialysis, are used. The frequency of the use of PD varies between 0.5% and nearly 37%. Privatization of dialysis units has started in 18 CEE countries. Currently between 2.5% (Russia) and 90% (Hungary) of patients are treated in non-public centres. Renal transplantation is quite well developed in half of the CEE states. In the states on the territory of the former Soviet Union, substantial progress in renal replacement therapy was achieved in the Baltic states, but the development in Byelorussia and Russia is still unsatisfactory. CONCLUSION: The availability and outcome of renal replacement therapy in the majority of states in CEE have become comparable with what is seen in more developed Western Europe. Nevertheless, large differences exist between individual countries. In particular, definite improvement is urgent in Byelorussia and Russia.

Cross-Sectional Studies↗
PubMed2005

The efficacy and safety of once-weekly and once-fortnightly subcutaneous epoetin beta in peritoneal dialysis patients with chronic renal anaemia.

BACKGROUND: Reducing the dosage frequency of subcutaneous epoetin in peritoneal dialysis (PD) patients is convenient and should improve patient satisfaction and, possibly, compliance. We investigated if a weekly dosage of epoetin beta in PD patients safely maintained haemoglobin (Hb) concentrations equivalent to those obtained with previous twice- or thrice-weekly administration. In addition, we investigated if a fortnightly dosage of epoetin beta was safe and as effective as previous weekly administration. METHODS: After a 4 week run-in period, PD patients were switched to either weekly or fortnightly epoetin beta administration, depending on their previous treatment schedules, for 25 weeks. RESULTS: The per-protocol cohort included 128 patients, of whom 54 received epoetin beta once weekly and 74 once fortnightly. The mean change in Hb concentration from baseline over weeks 13-25 and the 90% confidence intervals (CIs) remained within the target range (10-12 g/dl) and specified equivalence (+/-0.75 g/dl) limits in the weekly (-0.34 g/dl; 90% CI: -0.14 to -0.54 g/dl) and fortnightly (-0.39 g/dl; 90% CI: -0.24 to -0.55 g/dl) cohorts. The mean change from baseline in the epoetin beta dose was 1.4 IU/kg/week (90% CI: -3.8 to 6.6 IU/kg/week; 2%) in the weekly cohort and 4.4 IU/kg/week (90% CI: 1.7-7.2 IU/kg/week; 13%) in the fortnightly cohort. Both treatment regimens were well tolerated. CONCLUSIONS: In stable PD patients switched from twice- or thrice-weekly to weekly epoetin beta treatment, Hb concentrations could be maintained within the specified range over 25 weeks without significant change in their mean epoetin beta doses. In patients switched from weekly to fortnightly treatment, Hb concentrations could also be maintained over 25 weeks. There was a small increase in the mean dose during this period, but >/=50% of patients could be maintained without dose increase. Reducing dosage frequency may improve compliance in PD patients who self-administer their epoetin.

Adult↗
PubMed2005

Methylenetetrahydrofolate reductase gene polymorphisms in essential hypertension relation: with the development of hypertensive end-stage renal disease.

BACKGROUND: The pathogenesis of hypertensive nephropathy is multifactoral and in addition to BP, other factors contribute to the development of this renal pathology and its progression to end-stage renal disease. These include genetic predisposition and increased pleasure level of homocysteine-intermediate protein catabolism product known to induce kidney injury. The 677C --> T polymorphism in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene is associated with elevated homocysteine level in the general population, and therefore it has been hypothesized to be a risk factor for the development of renal failure in the course of essential hypertension. METHODS: In this case-control, cross-sectional study the frequency of the MTHFR 677C --> T and the 1298A --> C polymorphism was compared between patients with hypertension-related chronic renal failure (n = 90), patients with essential hypertension without kidney injury (n = 90), and healthy individuals (n = 90) who were matched for age and gender. In addition, the influence of these polymorphisms on homocysteine concentration in individuals with essential hypertension was examined. RESULTS: The frequency of the MTHFR 677 TT genotype did not differ between groups (4.5%, 12.3%, and 11.1%, respectively). Patients with hypertension and the 677TT genotype showed significantly higher homocysteine levels as compared to individuals having CC and CT. In the multivariate correlation analysis the MTHFR 677TT genotype (P < .01; beta = 0.27), age (P < .001; beta = 0.33), and body mass index (P < .01; beta = 0.3) were independent predictors for total homocysteine level. CONCLUSIONS: Plasma homocysteine levels in individuals with essential hypertension is affected by the MTHFR 677C --> T polymorphism. However, we did not prove the hypothesis that MTHFR 677C --> T influences the risk of development of renal failure in the course of hypertension.

Alleles↗
PubMed2005

Mechanisms of enhanced carbohydrate and lipid metabolism in adipose tissue in uremia.

OBJECTIVE: Hyperlipidemia is a permanent finding in advanced renal failure. It is supposed to be responsible for the accelerated arteriosclerosis and cardiovascular complications observed in patients with that disease. The background is partially determined, however, our knowledge in this matter is not yet satisfactory. METHODS: This study is based on the experimental rat model of chronic renal failure (CRF). Considering white adipose tissue (WAT) lipogenesis upregulation in CRF, along with the determination of acetyl coenzyme A carboxylase (ACC) and fatty acid synthase (FAS) genes expression, we have measured WAT gene expression for sterol regulatory binding protein 1 (SREBP-1) at the level of protein mass and mRNA abundance. Furthermore, we have determined glucose uptake, glucose-to-CO 2 conversion rate, and glucose translocator (GLUT-4) gene expression in WAT. RESULTS: Upregulation of both FAS and ACC gene expression was found in WAT of CRF rats. It was accompanied by WAT SREBP-1 gene overexpression. Moreover, we have observed the increased glucose uptake, glucose to CO 2 conversion rate, and GLUT-4 gene expression in WAT of CRF rats in comparison with controls. CONCLUSION: SREBP-1 gene overexpression may contribute to enhanced lipogenesis upregulation in WAT of CRF rats. It is not excluded that the increased WAT glucose metabolism activity is also induced by this mechanism, although there is no evidence currently to that end. We hypothesize that the increased WAT lipogenesis capacity could be a part of mechanism(s) leading to CRF-induced hyperlipidemia.

Acetyl-CoA Carboxylase↗
PubMed2005

Low-dose dual blockade of the renin-angiotensin system improves tubular status in non-diabetic proteinuric patients.

OBJECTIVE: Treatment with agents that inhibit the renin-angiotensin system is commonly regarded as a gold standard renoprotective strategy in patients with chronic kidney diseases. For maximum antiproteinuric effect, the dose titration of these agents is recommended. This therapeutic strategy is not used for proteinuric patients who are not able to receive high doses of angiotensin-converting enzyme inhibitor or angiotensin II receptor antagonists. MATERIAL AND METHODS: In patients with primary glomerulonephritis (n=24), a randomized, triple-treatment, triple-period, cross-over study was performed to compare the effects of combined therapy with benazepril 5 mg and losartan 25 mg and monotherapy with either agent alone at a two-fold higher dose on the extent of tubular injury as assessed by alpha1-microglobulin (alpha1-m) excretion and the plasma level of transforming growth factor-beta1 (TGF-beta1). RESULTS: Combination therapy significantly reduced alpha1-m excretion compared to either agent used alone: 178.29+/-27.36 to 99.63+/-13.03 mg/g creatinine for losartan + benazepril vs 178.29+/-27.36 to 161.59+/-23.22 mg/g creatinine for benazepril alone (p<0.05; ANOVA) and 178.29+/-27.36 to 99.63+/-13.03 mg/g creatinine for losartan + benazepril vs 178.29+/-27.36 to 173.45+/-27.69 mg/g creatinine for losartan alone (p<0.05; ANOVA). There was a significant correlation between change in alpha1-m excretion and reduction in proteinuria (r=0.704; p=0.023). There were no differences in TGF-beta1 level between the studied treatments. Systemic blood pressure reduction did not differ among the therapies. CONCLUSIONS: Combination therapy with angiotensin-converting enzyme inhibitor and angiotensin II subtype 1 receptor antagonists at very small doses may be superior to monotherapy with these agents at higher doses as far as tubular injury is concerned. We speculate that such a therapeutic strategy may be a useful approach for patients who are known not to be capable of receiving optimal renoprotective doses of these regimens.

Adolescent↗
PubMed2005

Steroid withdrawal at 3 months after kidney transplantation: a comparison of two tacrolimus-based regimens.

The 6 month prospective, randomized study compared the steroid-sparing potential of two tacrolimus-based regimens after renal transplantation. A total of 489 patients were randomized (1:1) to receive tacrolimus/mycophenolate mofetil (MMF)/steroids (n = 243; group Tac/MMF/S) or tacrolimus/azathioprine/steroids (n = 246; group Tac/Aza/S). At 3 months, steroids were tapered off in 267 (54.6%) patients free from steroid-resistant acute rejection and with serum creatinine concentrations <160 micromol/l. The incidence of biopsy-confirmed acute rejection at month 3 was lower in group Tac/MMF/S compared with group Tac/Aza/S (18.1% vs. 26.0%,P = 0.035). Moreover, more patients in the Tac/MMF/S group met the criteria for steroid withdrawal than in the Tac/Aza/S group (60.5% vs. 48.8%; P < 0.01). The incidence of acute rejection during months 4-6 was low in all groups, both for patients on steroid-free dual therapy (Tac/MMF: 2.7%, Tac/Aza: 0.8%) and for patients who continued steroid maintenance therapy (Tac/MMF/S: 3.5%, Tac/Aza/S: 7.1%). Moreover, kidney function was well preserved in steroid-free patients with month 6 median serum creatinine levels of 119.5 micromol/l (Tac/MMF), and 115.1 micromol/l (Tac/Aza). For patients who continued to receive steroids, month 6 median creatinine levels were 130.5 micromol/l (Tac/MMF/S) and 132.8 micromol/l (Tac/Aza/S). The criteria for the selection of patients to discontinue steroids were adequate. Both tacrolimus-based regimens allowed the safe discontinuation of steroids in low-risk patients at month 3. The Tac/MMF combination was superior in the prevention of acute rejections and more patients met the chosen criteria for steroid withdrawal.

Adolescent↗
PubMed2005

Expression of scavenger receptor CD36 in chronic renal failure patients.

BACKGROUND: Patients with chronic renal failure (CRF) are at increased risk of atherosclerosis development. One of the major steps in pathogenesis of atherosclerosis is formation of foam cells. Scavenger receptor CD36 is among the major receptors for oxidized low density lipoproteins (oxLDL) and therefore it plays a crucial role in foam cell formation. The aim of the present study was to investigate the expression of CD36 on blood monocytes of CRF patients. METHODS: Expression of CD36 on blood monocytes of CRF patients treated with hemodialysis (HD), peritoneal dialysis (PD), those not yet on dialysis (predialysis), and controls was assessed with the use of flow cytometry. Additionally, the major lipid peroxidation markers, malondialdehyde (MDA) and 4-hydroxyalkenals (HAE), were measured. Further, impact of treatment with HMG-CoA reductase inhibitors (statins) on CD36 expression in CRF patients was evaluated. RESULTS: Expression of monocyte CD36, measured as mean fluorescence intensity (MFI) was significantly higher in HD and PD patients, when compared to controls without renal insufficiency (respectively: 1011 +/- 288 and 1000 +/- 309 vs. 710 +/- 313; P < 0.01 for both groups). This was not the case in predialysis group (828 +/- 363 vs. 710 +/- 313). Higher concentrations of lipid peroxidation indicators, MDA and HAE were observed in all three subgroups of CRF patients (2.1 +/- 0.51, 2.02 +/- 0.27, and 1.81 +/- 0.53 microm in HD, PD, and predialysis group, respectively, vs. 1.13 +/- 0.59 microm in controls; P < 0.01). Patients treated with statins showed significantly lower CD36 expression than patients without statin therapy. CONCLUSIONS: The present study, for the first time, demonstrates increased expression of CD36 scavenger receptor in CRF patients. This may be a possible risk factor for accelerated atherogenesis observed in this group of patients.

Atherosclerosis↗